Podcast
Questions and Answers
What is the primary function of the kidneys?
What is the primary function of the kidneys?
What can occur if both kidneys fail to function properly?
What can occur if both kidneys fail to function properly?
What characterizes acute kidney injury (AKI)?
What characterizes acute kidney injury (AKI)?
Which of the following is a common cause of acute kidney injury (AKI)?
Which of the following is a common cause of acute kidney injury (AKI)?
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What is azotemia?
What is azotemia?
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Which statement about chronic kidney disease (CKD) is accurate?
Which statement about chronic kidney disease (CKD) is accurate?
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How does renal failure affect heart rate?
How does renal failure affect heart rate?
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What term describes the inability of the kidneys to remove accumulated metabolites from the blood?
What term describes the inability of the kidneys to remove accumulated metabolites from the blood?
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What is the main contributing factor for prerenal acute kidney injury (AKI)?
What is the main contributing factor for prerenal acute kidney injury (AKI)?
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Which type of acute kidney injury (AKI) accounts for approximately 40% of cases?
Which type of acute kidney injury (AKI) accounts for approximately 40% of cases?
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Which statement about postrenal acute kidney injury (AKI) is true?
Which statement about postrenal acute kidney injury (AKI) is true?
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What differentiates intrarenal AKI from prerenal AKI?
What differentiates intrarenal AKI from prerenal AKI?
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What is the relationship between prerenal causes of AKI and the integrity of kidney tissues?
What is the relationship between prerenal causes of AKI and the integrity of kidney tissues?
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Which condition is commonly associated with prerenal acute kidney injury?
Which condition is commonly associated with prerenal acute kidney injury?
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Which type of injury is primarily caused by nephrotoxic drugs?
Which type of injury is primarily caused by nephrotoxic drugs?
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What is a common cause of postrenal acute kidney injury?
What is a common cause of postrenal acute kidney injury?
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Which of the following conditions is NOT a cause of intrarenal acute kidney injury?
Which of the following conditions is NOT a cause of intrarenal acute kidney injury?
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Which example is associated with low cardiac output in prerenal acute kidney injury?
Which example is associated with low cardiac output in prerenal acute kidney injury?
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Which of the following conditions is associated with renal ischemia leading to acute tubular necrosis?
Which of the following conditions is associated with renal ischemia leading to acute tubular necrosis?
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What is the primary cause of ureteral obstruction leading to postrenal acute kidney injury?
What is the primary cause of ureteral obstruction leading to postrenal acute kidney injury?
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Which condition is NOT a direct cause of glomerular/microvascular injury in intrarenal acute kidney injury?
Which condition is NOT a direct cause of glomerular/microvascular injury in intrarenal acute kidney injury?
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Which type of acute kidney injury is primarily caused by low fluid volume to the kidneys?
Which type of acute kidney injury is primarily caused by low fluid volume to the kidneys?
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Which example best illustrates altered vascular resistance as a cause of prerenal acute kidney injury?
Which example best illustrates altered vascular resistance as a cause of prerenal acute kidney injury?
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What is a primary reason for the fall in glomerular filtration rate (GFR) during prerenal acute kidney injury (AKI)?
What is a primary reason for the fall in glomerular filtration rate (GFR) during prerenal acute kidney injury (AKI)?
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Which condition can rapidly reverse prerenal acute kidney injury (AKI)?
Which condition can rapidly reverse prerenal acute kidney injury (AKI)?
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What consequence can unresolved ischemia in prerenal AKI lead to?
What consequence can unresolved ischemia in prerenal AKI lead to?
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Which factor is NOT associated with causing prerenal acute kidney injury?
Which factor is NOT associated with causing prerenal acute kidney injury?
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Which statement is true regarding the energy requirements of kidney cells during prerenal acute kidney injury?
Which statement is true regarding the energy requirements of kidney cells during prerenal acute kidney injury?
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What is the most common intrarenal cause of acute kidney injury (AKI)?
What is the most common intrarenal cause of acute kidney injury (AKI)?
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Which condition can lead to a reduction in renal blood flow and subsequently cause AKI?
Which condition can lead to a reduction in renal blood flow and subsequently cause AKI?
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Which vascular disorder can lead to intrarenal AKI by damaging the nephrons?
Which vascular disorder can lead to intrarenal AKI by damaging the nephrons?
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What is one of the main characteristics of intrarenal acute kidney injury?
What is one of the main characteristics of intrarenal acute kidney injury?
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Which factor is likely to cause nephrons damage leading to intrarenal AKI?
Which factor is likely to cause nephrons damage leading to intrarenal AKI?
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Which factor is the most common precipitating cause of postrenal acute kidney injury (AKI)?
Which factor is the most common precipitating cause of postrenal acute kidney injury (AKI)?
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In children diagnosed with acute kidney injury (AKI), which of the following urine output patterns might indicate a less severe renal injury?
In children diagnosed with acute kidney injury (AKI), which of the following urine output patterns might indicate a less severe renal injury?
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What condition can potentially lead to postrenal acute kidney injury due to obstruction?
What condition can potentially lead to postrenal acute kidney injury due to obstruction?
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Which symptom is most commonly associated with acute kidney injury (AKI) in children?
Which symptom is most commonly associated with acute kidney injury (AKI) in children?
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Which statement accurately reflects the urine output in a scenario indicating postrenal acute kidney injury?
Which statement accurately reflects the urine output in a scenario indicating postrenal acute kidney injury?
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What is the primary cause of acute tubular necrosis (ATN)?
What is the primary cause of acute tubular necrosis (ATN)?
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Which risk factor is NOT associated with ischemic acute tubular necrosis (ATN)?
Which risk factor is NOT associated with ischemic acute tubular necrosis (ATN)?
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What effect does ischemia lasting more than 2 hours have on kidney tubules?
What effect does ischemia lasting more than 2 hours have on kidney tubules?
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Which of the following nephrotoxins is commonly associated with acute tubular necrosis (ATN)?
Which of the following nephrotoxins is commonly associated with acute tubular necrosis (ATN)?
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What physiological mechanism contributes to decreased glomerular filtration rate (GFR) during acute tubular necrosis?
What physiological mechanism contributes to decreased glomerular filtration rate (GFR) during acute tubular necrosis?
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How do nephrotoxins typically damage tubular epithelial cells?
How do nephrotoxins typically damage tubular epithelial cells?
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Which condition is likely to increase the concentration of nephrotoxins in nephrons?
Which condition is likely to increase the concentration of nephrotoxins in nephrons?
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Which of the following demographic groups is at a higher risk for ATN when exposed to nephrotoxic drugs?
Which of the following demographic groups is at a higher risk for ATN when exposed to nephrotoxic drugs?
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What is the approximate mortality rate for AKI in seriously ill patients?
What is the approximate mortality rate for AKI in seriously ill patients?
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In which patient population does the incidence of AKI increase most significantly?
In which patient population does the incidence of AKI increase most significantly?
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What percentage of hospitalized patients are estimated to develop AKI?
What percentage of hospitalized patients are estimated to develop AKI?
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What is a key factor that contributes to the high mortality rate associated with AKI?
What is a key factor that contributes to the high mortality rate associated with AKI?
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What percentage of children in pediatric intensive care units is estimated to develop AKI?
What percentage of children in pediatric intensive care units is estimated to develop AKI?
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Which group has a higher incidence of acute kidney injury (AKI) due to age-related factors?
Which group has a higher incidence of acute kidney injury (AKI) due to age-related factors?
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What common condition is least likely to increase the risk of acute kidney injury?
What common condition is least likely to increase the risk of acute kidney injury?
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Which of the following factors contributes to the increased risk of AKI in older adults?
Which of the following factors contributes to the increased risk of AKI in older adults?
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What is a significant risk factor for children that increases their likelihood of developing AKI during illness?
What is a significant risk factor for children that increases their likelihood of developing AKI during illness?
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Which of the following is a risk factor for acute kidney injury (AKI) related specifically to pharmacological agents?
Which of the following is a risk factor for acute kidney injury (AKI) related specifically to pharmacological agents?
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What is the primary focus of prevention strategies for contrast-induced nephropathy?
What is the primary focus of prevention strategies for contrast-induced nephropathy?
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Which of the following is NOT a recommended strategy for preventing contrast-induced nephropathy?
Which of the following is NOT a recommended strategy for preventing contrast-induced nephropathy?
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How can nurses contribute to the prevention of contrast-induced nephropathy?
How can nurses contribute to the prevention of contrast-induced nephropathy?
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Which of the following is a common characteristic of patients at risk for contrast-induced nephropathy?
Which of the following is a common characteristic of patients at risk for contrast-induced nephropathy?
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What role do oxygen free radicals play in contrast-induced nephropathy?
What role do oxygen free radicals play in contrast-induced nephropathy?
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Which clinical manifestation is least likely to be associated with fluid volume excess in acute kidney injury?
Which clinical manifestation is least likely to be associated with fluid volume excess in acute kidney injury?
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Which therapy is most appropriate for treating hyperkalemia in acute kidney injury?
Which therapy is most appropriate for treating hyperkalemia in acute kidney injury?
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Which clinical manifestation is typically associated with anemia in acute kidney injury?
Which clinical manifestation is typically associated with anemia in acute kidney injury?
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Which of the following is a common complication of acute kidney injury related to potassium levels?
Which of the following is a common complication of acute kidney injury related to potassium levels?
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What is the recommended dietary change for a patient managing hyperkalemia?
What is the recommended dietary change for a patient managing hyperkalemia?
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Which of the following is a potential indicator of pulmonary edema in acute kidney injury?
Which of the following is a potential indicator of pulmonary edema in acute kidney injury?
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What symptom is indicative of fluid volume excess in a patient with acute kidney injury?
What symptom is indicative of fluid volume excess in a patient with acute kidney injury?
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Which intervention is crucial for managing blood pressure in patients with acute kidney injury?
Which intervention is crucial for managing blood pressure in patients with acute kidney injury?
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Which of the following findings in a patient with acute kidney injury suggests the presence of hyperkalemia?
Which of the following findings in a patient with acute kidney injury suggests the presence of hyperkalemia?
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Which therapy is used to address excessive fluid retention in acute kidney injury?
Which therapy is used to address excessive fluid retention in acute kidney injury?
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What is the outcome if acute kidney injury (AKI) is recognized and effectively treated during the initiation phase?
What is the outcome if acute kidney injury (AKI) is recognized and effectively treated during the initiation phase?
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How long does the initiation phase of acute kidney injury typically last?
How long does the initiation phase of acute kidney injury typically last?
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What characterizes the initiation phase of acute kidney injury?
What characterizes the initiation phase of acute kidney injury?
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Which aspect complicates identifying acute kidney injury during the initiation phase?
Which aspect complicates identifying acute kidney injury during the initiation phase?
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What is the significance of the initiating event in the initiation phase of AKI?
What is the significance of the initiating event in the initiation phase of AKI?
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What is a potential consequence of impaired potassium excretion during the maintenance phase of AKI?
What is a potential consequence of impaired potassium excretion during the maintenance phase of AKI?
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Which of the following manifestations is NOT typically associated with the maintenance phase of AKI?
Which of the following manifestations is NOT typically associated with the maintenance phase of AKI?
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How does azotemia contribute to neurological symptoms during the maintenance phase of AKI?
How does azotemia contribute to neurological symptoms during the maintenance phase of AKI?
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What effect does fluid retention during the maintenance phase of AKI have on the heart and lungs?
What effect does fluid retention during the maintenance phase of AKI have on the heart and lungs?
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What is the impact of metabolic acidosis on patients during the maintenance phase of AKI?
What is the impact of metabolic acidosis on patients during the maintenance phase of AKI?
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What happens to diuresis during the recovery phase of acute kidney injury (AKI)?
What happens to diuresis during the recovery phase of acute kidney injury (AKI)?
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What is the typical time frame for rapid renal function improvement during the recovery phase of AKI?
What is the typical time frame for rapid renal function improvement during the recovery phase of AKI?
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What continues to remain high in serum despite increasing urine output during the recovery phase of AKI?
What continues to remain high in serum despite increasing urine output during the recovery phase of AKI?
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What characterizes the recovery phase of AKI?
What characterizes the recovery phase of AKI?
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What can occur as the nephrons recover during the recovery phase of AKI?
What can occur as the nephrons recover during the recovery phase of AKI?
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Which of the following strategies is effective in reducing the risk of acute kidney injury (AKI) when nephrotoxic drugs are necessary?
Which of the following strategies is effective in reducing the risk of acute kidney injury (AKI) when nephrotoxic drugs are necessary?
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What is a primary goal in the management of patients at risk for acute kidney injury (AKI)?
What is a primary goal in the management of patients at risk for acute kidney injury (AKI)?
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Which of the following practices can help avoid the occurrence of acute kidney injury (AKI)?
Which of the following practices can help avoid the occurrence of acute kidney injury (AKI)?
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Which statement about the management of patients' risk for acute kidney injury (AKI) is accurate?
Which statement about the management of patients' risk for acute kidney injury (AKI) is accurate?
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What is a key factor to consider when administering nephrotoxic agents in high-risk patients?
What is a key factor to consider when administering nephrotoxic agents in high-risk patients?
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What is a primary goal in the management of acute kidney injury (AKI)?
What is a primary goal in the management of acute kidney injury (AKI)?
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Which of the following is NOT a goal in the treatment of acute kidney injury (AKI)?
Which of the following is NOT a goal in the treatment of acute kidney injury (AKI)?
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How can kidney function be temporarily supported in patients with acute kidney injury (AKI)?
How can kidney function be temporarily supported in patients with acute kidney injury (AKI)?
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What approach should be taken to avoid further kidney damage in acute kidney injury (AKI)?
What approach should be taken to avoid further kidney damage in acute kidney injury (AKI)?
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What is one of the key components of managing a patient with acute kidney injury (AKI)?
What is one of the key components of managing a patient with acute kidney injury (AKI)?
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What does a fixed specific gravity of 1.010 in urinalysis during AKI indicate?
What does a fixed specific gravity of 1.010 in urinalysis during AKI indicate?
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Which of the following findings in urinalysis is associated with glomerular damage in AKI?
Which of the following findings in urinalysis is associated with glomerular damage in AKI?
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What typically happens to serum creatinine levels in the early stages of AKI?
What typically happens to serum creatinine levels in the early stages of AKI?
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Which serum electrolyte finding is commonly seen in patients with AKI?
Which serum electrolyte finding is commonly seen in patients with AKI?
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Which of the following is a common component of a complete blood count (CBC) in AKI?
Which of the following is a common component of a complete blood count (CBC) in AKI?
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What is a key indicator of recovery from AKI regarding serum creatinine levels?
What is a key indicator of recovery from AKI regarding serum creatinine levels?
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Which imaging technique is commonly used to identify obstructive causes of renal failure in AKI?
Which imaging technique is commonly used to identify obstructive causes of renal failure in AKI?
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What is a potential risk associated with using radiologic contrast media in diagnosing kidney issues?
What is a potential risk associated with using radiologic contrast media in diagnosing kidney issues?
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What is indicated by the presence of cell casts in urinalysis during AKI?
What is indicated by the presence of cell casts in urinalysis during AKI?
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Which condition may lead to anemia in patients with AKI?
Which condition may lead to anemia in patients with AKI?
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What is the primary pharmacologic goal in managing acute kidney injury (AKI)?
What is the primary pharmacologic goal in managing acute kidney injury (AKI)?
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Which medication is administered to increase renal blood flow in low doses?
Which medication is administered to increase renal blood flow in low doses?
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What is a potential consequence of not improving urinary output after restoring renal blood flow?
What is a potential consequence of not improving urinary output after restoring renal blood flow?
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What role do loop diuretics play in the management of AKI?
What role do loop diuretics play in the management of AKI?
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Why are aggressive management of hypertension and use of antihypertensives important in AKI?
Why are aggressive management of hypertension and use of antihypertensives important in AKI?
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What might be ordered to prevent GI bleeding in a patient with AKI?
What might be ordered to prevent GI bleeding in a patient with AKI?
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When hyperkalemia occurs in a patient with AKI, what is a common treatment approach?
When hyperkalemia occurs in a patient with AKI, what is a common treatment approach?
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Which class of drugs must be discontinued during the treatment of AKI due to their nephrotoxic effects?
Which class of drugs must be discontinued during the treatment of AKI due to their nephrotoxic effects?
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What is the mechanism by which potassium-binding exchange resins work?
What is the mechanism by which potassium-binding exchange resins work?
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What is a key consideration when administering IV fluids in the management of AKI?
What is a key consideration when administering IV fluids in the management of AKI?
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What is a common method of administering phosphate-binding drugs for patients with kidney issues?
What is a common method of administering phosphate-binding drugs for patients with kidney issues?
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Which of the following drugs is NOT a phosphate-binding medication?
Which of the following drugs is NOT a phosphate-binding medication?
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Why might drug dosages need to be adjusted for patients with acute kidney injury (AKI)?
Why might drug dosages need to be adjusted for patients with acute kidney injury (AKI)?
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What effect does acute kidney injury (AKI) have on the half-life of drugs eliminated by the kidneys?
What effect does acute kidney injury (AKI) have on the half-life of drugs eliminated by the kidneys?
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How long should a retention enema be retained in the bowel before irrigating out?
How long should a retention enema be retained in the bowel before irrigating out?
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Which of the following is a significant nursing implication when prescribing medications for a patient with AKI?
Which of the following is a significant nursing implication when prescribing medications for a patient with AKI?
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What is a possible consequence of using the usual drug dosages for a patient with AKI?
What is a possible consequence of using the usual drug dosages for a patient with AKI?
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Which medication is specifically mentioned as binding to phosphates in the GI tract?
Which medication is specifically mentioned as binding to phosphates in the GI tract?
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What happens to the elimination of drugs from the body when a patient has acute kidney injury?
What happens to the elimination of drugs from the body when a patient has acute kidney injury?
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What is a common route for administer phosphate-binding medications for patients with renal issues?
What is a common route for administer phosphate-binding medications for patients with renal issues?
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What is the recommended method for administering mannitol solutions?
What is the recommended method for administering mannitol solutions?
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Which of the following is NOT a correct practice when administering calcium chloride?
Which of the following is NOT a correct practice when administering calcium chloride?
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What is the purpose of sodium polystyrene sulfonate (SPS) in electrolyte management?
What is the purpose of sodium polystyrene sulfonate (SPS) in electrolyte management?
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What should a patient do if they experience light-headedness after receiving IV calcium?
What should a patient do if they experience light-headedness after receiving IV calcium?
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What is the correct procedure for administering sodium bicarbonate infusion?
What is the correct procedure for administering sodium bicarbonate infusion?
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Which condition may necessitate the discontinuation of a drug during therapy?
Which condition may necessitate the discontinuation of a drug during therapy?
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What is a recommended practice when administering urea intravenously?
What is a recommended practice when administering urea intravenously?
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Why is it advised to monitor vital signs and breath sounds during diuretic therapy?
Why is it advised to monitor vital signs and breath sounds during diuretic therapy?
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How should phosphate binders be administered for best results?
How should phosphate binders be administered for best results?
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Which of the following substances is used to correct acidosis and facilitate potassium movement?
Which of the following substances is used to correct acidosis and facilitate potassium movement?
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What is the primary action mechanism of loop diuretics in treating acute kidney injury?
What is the primary action mechanism of loop diuretics in treating acute kidney injury?
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Which of the following nursing considerations should be prioritized when administering loop diuretics?
Which of the following nursing considerations should be prioritized when administering loop diuretics?
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What potential side effect may arise from high doses of loop diuretics, particularly with ethacrynic acid?
What potential side effect may arise from high doses of loop diuretics, particularly with ethacrynic acid?
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How should furosemide be administered intravenously for optimal effectiveness?
How should furosemide be administered intravenously for optimal effectiveness?
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Why might potassium wasting not be a major concern during acute kidney injury when using specific diuretics?
Why might potassium wasting not be a major concern during acute kidney injury when using specific diuretics?
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What is the purpose of administering thiazide diuretics alongside loop diuretics in AKI treatment?
What is the purpose of administering thiazide diuretics alongside loop diuretics in AKI treatment?
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Which of the following is a major nursing intervention for patients undergoing treatment with loop diuretics?
Which of the following is a major nursing intervention for patients undergoing treatment with loop diuretics?
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What is commonly advised for patients regarding fluid intake while on loop diuretics?
What is commonly advised for patients regarding fluid intake while on loop diuretics?
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What is the expected response time for urine output increase after IV administration of loop diuretics?
What is the expected response time for urine output increase after IV administration of loop diuretics?
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Which laboratory values should be closely monitored during diuretic therapy for AKI?
Which laboratory values should be closely monitored during diuretic therapy for AKI?
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How is the restricted daily fluid intake calculated for a patient recovering from acute kidney injury (AKI)?
How is the restricted daily fluid intake calculated for a patient recovering from acute kidney injury (AKI)?
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What indicators should a nurse primarily monitor to assess fluid balance in a patient with AKI?
What indicators should a nurse primarily monitor to assess fluid balance in a patient with AKI?
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Why is it important to restrict fluid intake in patients with improved vascular volume and renal perfusion?
Why is it important to restrict fluid intake in patients with improved vascular volume and renal perfusion?
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If a patient excretes 450 mL of urine in 24 hours, what is the total fluid intake allowance for the next day?
If a patient excretes 450 mL of urine in 24 hours, what is the total fluid intake allowance for the next day?
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What is the typical role of insensible losses in fluid management for AKI patients?
What is the typical role of insensible losses in fluid management for AKI patients?
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What is the maximum amount of protein intake recommended for patients with acute kidney injury (AKI)?
What is the maximum amount of protein intake recommended for patients with acute kidney injury (AKI)?
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What role do carbohydrates play in the dietary management of a patient with AKI?
What role do carbohydrates play in the dietary management of a patient with AKI?
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What is a primary disadvantage of parenteral nutrition for patients with AKI?
What is a primary disadvantage of parenteral nutrition for patients with AKI?
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Which type of dietary protein is recommended for patients with AKI?
Which type of dietary protein is recommended for patients with AKI?
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What is a potential outcome of inadequate nutrient and calorie intake in patients with acute kidney injury?
What is a potential outcome of inadequate nutrient and calorie intake in patients with acute kidney injury?
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What is the maximum daily protein intake recommended for a patient with acute kidney injury (AKI)?
What is the maximum daily protein intake recommended for a patient with acute kidney injury (AKI)?
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Which type of dietary protein is preferred for patients with renal insufficiency?
Which type of dietary protein is preferred for patients with renal insufficiency?
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What is the primary reason for increasing carbohydrate intake in patients with AKI?
What is the primary reason for increasing carbohydrate intake in patients with AKI?
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Which of the following is a disadvantage of parenteral nutrition in patients with AKI?
Which of the following is a disadvantage of parenteral nutrition in patients with AKI?
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What is a common condition that might lead to the need for parenteral nutrition in patients with AKI?
What is a common condition that might lead to the need for parenteral nutrition in patients with AKI?
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Which condition is a significant problem for patients receiving dialysis due to renal failure?
Which condition is a significant problem for patients receiving dialysis due to renal failure?
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What is the primary purpose of continuous renal replacement therapy (CRRT)?
What is the primary purpose of continuous renal replacement therapy (CRRT)?
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Which form of dialysis uses the peritoneum as a dialyzing membrane?
Which form of dialysis uses the peritoneum as a dialyzing membrane?
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What is the mechanism by which dialysis removes excess metabolic wastes from the blood?
What is the mechanism by which dialysis removes excess metabolic wastes from the blood?
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What is a limitation of dialysis in patients with renal failure?
What is a limitation of dialysis in patients with renal failure?
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What is the primary mechanism used in hemodialysis to remove excess water from the blood?
What is the primary mechanism used in hemodialysis to remove excess water from the blood?
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Which substances can pass through the dialyzer's porous membrane during hemodialysis?
Which substances can pass through the dialyzer's porous membrane during hemodialysis?
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How does the concentration gradient influence solute movement during diffusion in hemodialysis?
How does the concentration gradient influence solute movement during diffusion in hemodialysis?
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What role does the dialysate play in the process of hemodialysis?
What role does the dialysate play in the process of hemodialysis?
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What consequence results from a higher hydrostatic pressure in the blood than in the dialysate during hemodialysis?
What consequence results from a higher hydrostatic pressure in the blood than in the dialysate during hemodialysis?
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What is the most common complication associated with hemodialysis?
What is the most common complication associated with hemodialysis?
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Which factor is NOT a potential cause of hypotension during hemodialysis?
Which factor is NOT a potential cause of hypotension during hemodialysis?
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What infection risk is increased for patients on chronic hemodialysis?
What infection risk is increased for patients on chronic hemodialysis?
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Which complication occurs as a result of altered platelet function in hemodialysis patients?
Which complication occurs as a result of altered platelet function in hemodialysis patients?
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When may patients with AKI switch to fewer hemodialysis sessions per week?
When may patients with AKI switch to fewer hemodialysis sessions per week?
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What is the primary advantage of Continuous Renal Replacement Therapy (CRRT) for patients with AKI?
What is the primary advantage of Continuous Renal Replacement Therapy (CRRT) for patients with AKI?
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During CRRT, which of the following substances is NOT typically removed from the blood?
During CRRT, which of the following substances is NOT typically removed from the blood?
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What role does fluid replacement play during CRRT?
What role does fluid replacement play during CRRT?
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How does CRRT differ from traditional hemodialysis in terms of fluid removal?
How does CRRT differ from traditional hemodialysis in terms of fluid removal?
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Which of the following describes a key characteristic of the hemofilter used in CRRT?
Which of the following describes a key characteristic of the hemofilter used in CRRT?
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Which continuous renal replacement therapy involves arterial blood circulating through a hemofilter surrounded by dialysate?
Which continuous renal replacement therapy involves arterial blood circulating through a hemofilter surrounded by dialysate?
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What is the primary purpose of continuous venovenous hemodialysis (CVVHD)?
What is the primary purpose of continuous venovenous hemodialysis (CVVHD)?
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Which of the following correctly describes the ultrafiltration process in continuous arteriovenous hemofiltration (CAVH)?
Which of the following correctly describes the ultrafiltration process in continuous arteriovenous hemofiltration (CAVH)?
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Which statement accurately describes continuous arteriovenous hemodialysis (CAVHD)?
Which statement accurately describes continuous arteriovenous hemodialysis (CAVHD)?
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What type of blood does continuous venovenous hemodialysis (CVVHD) use for treatment?
What type of blood does continuous venovenous hemodialysis (CVVHD) use for treatment?
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What is the primary requirement for continuous renal replacement therapy related to vascular access?
What is the primary requirement for continuous renal replacement therapy related to vascular access?
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Which of the following statements about vascular access for continuous renal replacement therapy is true?
Which of the following statements about vascular access for continuous renal replacement therapy is true?
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In which setting is continuous renal replacement therapy most commonly performed?
In which setting is continuous renal replacement therapy most commonly performed?
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What is a critical measure to reduce the risk of infection in patients undergoing continuous renal replacement therapy?
What is a critical measure to reduce the risk of infection in patients undergoing continuous renal replacement therapy?
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Which vascular access method requires both arterial and venous lines for some types of continuous renal replacement therapy?
Which vascular access method requires both arterial and venous lines for some types of continuous renal replacement therapy?
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What is the primary purpose of the central partition in a double-lumen catheter used for hemodialysis?
What is the primary purpose of the central partition in a double-lumen catheter used for hemodialysis?
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In which arm is an arteriovenous (AV) fistula typically created for long-term vascular access?
In which arm is an arteriovenous (AV) fistula typically created for long-term vascular access?
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What palpation finding is indicative of a functional arteriovenous (AV) fistula?
What palpation finding is indicative of a functional arteriovenous (AV) fistula?
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How long does it typically take for an arteriovenous (AV) fistula to mature for use in hemodialysis?
How long does it typically take for an arteriovenous (AV) fistula to mature for use in hemodialysis?
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What nursing practice should be followed to protect an AV fistula?
What nursing practice should be followed to protect an AV fistula?
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What is the main advantage of using an AV graft for vascular access in CKD patients?
What is the main advantage of using an AV graft for vascular access in CKD patients?
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Which of the following complications is most commonly associated with AV fistulas and grafts?
Which of the following complications is most commonly associated with AV fistulas and grafts?
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What psychological impact can failure of an AV fistula or graft cause in patients?
What psychological impact can failure of an AV fistula or graft cause in patients?
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When is it ideal to create an AV fistula or graft for CKD patients?
When is it ideal to create an AV fistula or graft for CKD patients?
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Which systemic manifestations can arise from localized complications of AV fistulas or grafts?
Which systemic manifestations can arise from localized complications of AV fistulas or grafts?
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What is the role of the peritoneal membrane in peritoneal dialysis?
What is the role of the peritoneal membrane in peritoneal dialysis?
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What is the process that occurs after the dialysate has been instilled into the peritoneal cavity?
What is the process that occurs after the dialysate has been instilled into the peritoneal cavity?
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What is a key step that follows the dwell time of the solution in the abdomen during peritoneal dialysis?
What is a key step that follows the dwell time of the solution in the abdomen during peritoneal dialysis?
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How often is the process of infusion, dwell time, and drainage typically repeated in peritoneal dialysis?
How often is the process of infusion, dwell time, and drainage typically repeated in peritoneal dialysis?
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What specific feature of the dialysate is critical for its function in peritoneal dialysis?
What specific feature of the dialysate is critical for its function in peritoneal dialysis?
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What is a significant disadvantage of peritoneal dialysis for patients with acute kidney injury (AKI)?
What is a significant disadvantage of peritoneal dialysis for patients with acute kidney injury (AKI)?
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Which condition is a contraindication for peritoneal dialysis?
Which condition is a contraindication for peritoneal dialysis?
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Why is peritoneal dialysis considered less risky for unstable patients compared to other renal replacement therapies?
Why is peritoneal dialysis considered less risky for unstable patients compared to other renal replacement therapies?
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What is one of the principal risks associated with peritoneal dialysis?
What is one of the principal risks associated with peritoneal dialysis?
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Which statement accurately describes the nature of peritoneal dialysis in relation to patients with AKI?
Which statement accurately describes the nature of peritoneal dialysis in relation to patients with AKI?
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What is a common predisposing factor for acute kidney injury (AKI) in infants?
What is a common predisposing factor for acute kidney injury (AKI) in infants?
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Which condition is associated with a higher risk of acute kidney injury (AKI) in preterm newborns?
Which condition is associated with a higher risk of acute kidney injury (AKI) in preterm newborns?
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What is a potential long-term consequence for children who recover from acute kidney injury (AKI)?
What is a potential long-term consequence for children who recover from acute kidney injury (AKI)?
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Which of the following is NOT a commonly recognized cause of acute kidney injury (AKI) in infants?
Which of the following is NOT a commonly recognized cause of acute kidney injury (AKI) in infants?
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What is the estimated incidence of acute kidney injury (AKI) in the neonatal intensive care unit?
What is the estimated incidence of acute kidney injury (AKI) in the neonatal intensive care unit?
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What is a potential clinical manifestation of acute kidney injury (AKI) in children?
What is a potential clinical manifestation of acute kidney injury (AKI) in children?
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Which complication is commonly associated with acute kidney injury (AKI) in pediatric patients?
Which complication is commonly associated with acute kidney injury (AKI) in pediatric patients?
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Which of the following symptoms might prompt evaluation for acute kidney injury (AKI) in a dehydrated child?
Which of the following symptoms might prompt evaluation for acute kidney injury (AKI) in a dehydrated child?
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What percentage of pediatric patients with acute kidney injury (AKI) typically have a reversible condition?
What percentage of pediatric patients with acute kidney injury (AKI) typically have a reversible condition?
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What serious condition can result from unresolved acute kidney injury (AKI) in children?
What serious condition can result from unresolved acute kidney injury (AKI) in children?
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What is a common clinical manifestation of hyperkalemia in children?
What is a common clinical manifestation of hyperkalemia in children?
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Which of the following clinical manifestations is NOT typically associated with hyponatremia?
Which of the following clinical manifestations is NOT typically associated with hyponatremia?
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Which condition can lead to hypocalcemia in children with acute kidney injury?
Which condition can lead to hypocalcemia in children with acute kidney injury?
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What is a possible consequence of severe hypocalcemia that may be masked in a child with metabolic acidosis?
What is a possible consequence of severe hypocalcemia that may be masked in a child with metabolic acidosis?
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What clinical manifestation might indicate hyperkalemia on an electrocardiogram?
What clinical manifestation might indicate hyperkalemia on an electrocardiogram?
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What is the initial therapy recommended for children with severe fluid volume deficit associated with acute kidney injury (AKI)?
What is the initial therapy recommended for children with severe fluid volume deficit associated with acute kidney injury (AKI)?
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What should be monitored to determine if the initial therapy for fluid volume deficit is effective?
What should be monitored to determine if the initial therapy for fluid volume deficit is effective?
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What is the subsequent therapy aimed at after addressing the initial severe fluid volume deficit?
What is the subsequent therapy aimed at after addressing the initial severe fluid volume deficit?
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In a case where blood loss is causing the acute kidney injury (AKI), what additional treatment may be administered?
In a case where blood loss is causing the acute kidney injury (AKI), what additional treatment may be administered?
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What is the acceptable rate for administering the initial IV bolus of isotonic solution for severe fluid volume deficit?
What is the acceptable rate for administering the initial IV bolus of isotonic solution for severe fluid volume deficit?
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What physiological change during pregnancy is associated with acute kidney injury (AKI) in women?
What physiological change during pregnancy is associated with acute kidney injury (AKI) in women?
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Which condition is a unique etiology for AKI that may develop in the first trimester of pregnancy?
Which condition is a unique etiology for AKI that may develop in the first trimester of pregnancy?
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What is a common consequence of the physiologic hydronephrosis experienced by over 90% of pregnant women?
What is a common consequence of the physiologic hydronephrosis experienced by over 90% of pregnant women?
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What condition is a leading cause of AKI in the postpartum period?
What condition is a leading cause of AKI in the postpartum period?
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Which of the following complications could lead to AKI as pregnancy progresses?
Which of the following complications could lead to AKI as pregnancy progresses?
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What is a significant reason for the heightened prevalence of acute kidney injury (AKI) in older adults?
What is a significant reason for the heightened prevalence of acute kidney injury (AKI) in older adults?
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Which of the following comorbidities is NOT associated with a higher risk of AKI in older adults?
Which of the following comorbidities is NOT associated with a higher risk of AKI in older adults?
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Which of the following factors can predispose older adults to acute kidney injury (AKI)?
Which of the following factors can predispose older adults to acute kidney injury (AKI)?
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How does aging directly affect the kidney's function regarding acute kidney injury (AKI)?
How does aging directly affect the kidney's function regarding acute kidney injury (AKI)?
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What impact does a prolonged hospital stay have on older adults regarding acute kidney injury (AKI)?
What impact does a prolonged hospital stay have on older adults regarding acute kidney injury (AKI)?
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What should a nurse do if an adult patient's urine output falls below 30 mL/hr?
What should a nurse do if an adult patient's urine output falls below 30 mL/hr?
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Which situation might lead a nurse to alert the healthcare provider regarding nephrotoxic drugs?
Which situation might lead a nurse to alert the healthcare provider regarding nephrotoxic drugs?
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What is a critical early sign of hypovolemia that a nurse should monitor for?
What is a critical early sign of hypovolemia that a nurse should monitor for?
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Why is it important for a nurse to observe patients receiving blood components closely?
Why is it important for a nurse to observe patients receiving blood components closely?
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In which patient population is the risk of acute kidney injury (AKI) most heightened?
In which patient population is the risk of acute kidney injury (AKI) most heightened?
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What is the minimum urine output that the nurse should report as a concern in adult patients at risk of AKI?
What is the minimum urine output that the nurse should report as a concern in adult patients at risk of AKI?
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Which of the following is a common sign the nurse should monitor for in patients at risk of hypovolemia?
Which of the following is a common sign the nurse should monitor for in patients at risk of hypovolemia?
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What should the nurse do if a patient is receiving multiple nephrotoxic drugs?
What should the nurse do if a patient is receiving multiple nephrotoxic drugs?
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In which situation should the nurse be particularly vigilant for transfusion reactions?
In which situation should the nurse be particularly vigilant for transfusion reactions?
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What is an essential nursing action to minimize the risk of developing AKI in at-risk patients?
What is an essential nursing action to minimize the risk of developing AKI in at-risk patients?
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What vital sign assessments should be performed in a patient with acute kidney injury (AKI)?
What vital sign assessments should be performed in a patient with acute kidney injury (AKI)?
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Which of the following should be included when taking a patient's history for assessing AKI?
Which of the following should be included when taking a patient's history for assessing AKI?
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What symptom might indicate potential renal issues during a physical examination for AKI?
What symptom might indicate potential renal issues during a physical examination for AKI?
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Why is it essential to obtain a thorough history for patients at risk of AKI?
Why is it essential to obtain a thorough history for patients at risk of AKI?
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In addition to the patient, who else should be consulted during assessments for pediatric and older patients with AKI?
In addition to the patient, who else should be consulted during assessments for pediatric and older patients with AKI?
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Which of the following is a priority nursing care need for a patient with acute kidney injury (AKI)?
Which of the following is a priority nursing care need for a patient with acute kidney injury (AKI)?
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What problem is a potential concern for patients with acute kidney injury (AKI) related to nutrition?
What problem is a potential concern for patients with acute kidney injury (AKI) related to nutrition?
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Which of the following problems might indicate potential inadequate renal perfusion in a patient with AKI?
Which of the following problems might indicate potential inadequate renal perfusion in a patient with AKI?
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What nursing intervention can help mitigate the risk of infection in patients with acute kidney injury (AKI)?
What nursing intervention can help mitigate the risk of infection in patients with acute kidney injury (AKI)?
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Which nursing concern should be addressed to support inadequate family coping skills in patients with AKI?
Which nursing concern should be addressed to support inadequate family coping skills in patients with AKI?
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What is a key focus of nursing care in preventing complications for patients?
What is a key focus of nursing care in preventing complications for patients?
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Which of these outcomes should be a collaborative goal for nursing care?
Which of these outcomes should be a collaborative goal for nursing care?
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Which statement accurately represents a goal for maintaining fluid balance in nursing care?
Which statement accurately represents a goal for maintaining fluid balance in nursing care?
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How does good nutritional support contribute to patient outcomes in nursing care?
How does good nutritional support contribute to patient outcomes in nursing care?
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What is an important aspect of emotional support provided by nursing care?
What is an important aspect of emotional support provided by nursing care?
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What is the primary focus for preventing acute kidney injury (AKI)?
What is the primary focus for preventing acute kidney injury (AKI)?
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Which practice is essential in reducing the risk of infection in patients with acute kidney injury (AKI)?
Which practice is essential in reducing the risk of infection in patients with acute kidney injury (AKI)?
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What should be monitored in patients taking potentially nephrotoxic medications to prevent acute kidney injury?
What should be monitored in patients taking potentially nephrotoxic medications to prevent acute kidney injury?
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Which extrarenal loss of fluid should be assessed to manage acute kidney injury (AKI) effectively?
Which extrarenal loss of fluid should be assessed to manage acute kidney injury (AKI) effectively?
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Which of the following is NOT considered a critical aspect of caring for patients at risk for acute kidney injury (AKI)?
Which of the following is NOT considered a critical aspect of caring for patients at risk for acute kidney injury (AKI)?
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What is a critical preventive measure for patients at risk of acute kidney injury (AKI)?
What is a critical preventive measure for patients at risk of acute kidney injury (AKI)?
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Which of the following factors is essential for managing a patient with AKI?
Which of the following factors is essential for managing a patient with AKI?
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Why is meticulous aseptic technique important in patients with AKI?
Why is meticulous aseptic technique important in patients with AKI?
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What should be carefully monitored to manage fluid balance in patients with AKI?
What should be carefully monitored to manage fluid balance in patients with AKI?
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What is a common mistake in managing patients who are at risk for developing AKI?
What is a common mistake in managing patients who are at risk for developing AKI?
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What is the primary importance of maintaining accurate intake and output (I&O) records in the care of a patient with acute kidney injury (AKI)?
What is the primary importance of maintaining accurate intake and output (I&O) records in the care of a patient with acute kidney injury (AKI)?
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Which intervention should be prioritized when a nurse suspects a patient with AKI has developed infections?
Which intervention should be prioritized when a nurse suspects a patient with AKI has developed infections?
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How often should vital signs be assessed in a patient at risk for AKI?
How often should vital signs be assessed in a patient at risk for AKI?
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What role does daily weighing of a patient with AKI play in their care plan?
What role does daily weighing of a patient with AKI play in their care plan?
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What observation is a potential indication of excess fluid volume in a patient with AKI?
What observation is a potential indication of excess fluid volume in a patient with AKI?
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What are the manifestations associated with hyperkalemia in a patient with acute kidney injury?
What are the manifestations associated with hyperkalemia in a patient with acute kidney injury?
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Which electrolyte imbalance is most likely caused by water retention in patients with acute kidney injury?
Which electrolyte imbalance is most likely caused by water retention in patients with acute kidney injury?
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In the context of acute kidney injury, what symptom indicates hyperphosphatemia?
In the context of acute kidney injury, what symptom indicates hyperphosphatemia?
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What should be emphasized in the care of a patient with acute kidney injury to prevent skin breakdown?
What should be emphasized in the care of a patient with acute kidney injury to prevent skin breakdown?
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What is a recommended intervention for patients with acute kidney injury to help manage thirst?
What is a recommended intervention for patients with acute kidney injury to help manage thirst?
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What change is typically observed in weight for patients with acute kidney injury (AKI) despite loss of tissue mass?
What change is typically observed in weight for patients with acute kidney injury (AKI) despite loss of tissue mass?
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How can the involvement of a dietitian benefit patients with nutritional imbalances due to renal failure?
How can the involvement of a dietitian benefit patients with nutritional imbalances due to renal failure?
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What role does engaging patients in daily menu planning play in addressing their nutritional needs?
What role does engaging patients in daily menu planning play in addressing their nutritional needs?
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What is an effective method for monitoring a patient's nutritional status when they have renal failure?
What is an effective method for monitoring a patient's nutritional status when they have renal failure?
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What approach can encourage patients to eat more when facing dietary restrictions due to AKI?
What approach can encourage patients to eat more when facing dietary restrictions due to AKI?
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What is a recommended measure to encourage food intake in patients experiencing fatigue or anorexia?
What is a recommended measure to encourage food intake in patients experiencing fatigue or anorexia?
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Which symptom can lead to decreased food intake in patients with uremia?
Which symptom can lead to decreased food intake in patients with uremia?
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What should be administered if a patient cannot eat or tolerate enteral nutrition?
What should be administered if a patient cannot eat or tolerate enteral nutrition?
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What is an important nursing intervention before meals for patients experiencing nausea?
What is an important nursing intervention before meals for patients experiencing nausea?
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What is the primary purpose of providing frequent small meals to patients with fatigue or anorexia?
What is the primary purpose of providing frequent small meals to patients with fatigue or anorexia?
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What should a nurse assess before providing patient teaching for AKI?
What should a nurse assess before providing patient teaching for AKI?
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During the initial stages of AKI, what type of information should a nurse focus on providing?
During the initial stages of AKI, what type of information should a nurse focus on providing?
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Why is tailoring information to the patient's developmental level important?
Why is tailoring information to the patient's developmental level important?
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What is a key consideration for patient education regarding AKI?
What is a key consideration for patient education regarding AKI?
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What may hinder a patient with AKI from learning effectively?
What may hinder a patient with AKI from learning effectively?
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What precautions should a patient take to avoid complications after an episode of acute kidney injury (AKI)?
What precautions should a patient take to avoid complications after an episode of acute kidney injury (AKI)?
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What information is crucial for patients to understand regarding their urine output after recovering from AKI?
What information is crucial for patients to understand regarding their urine output after recovering from AKI?
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Why is it important to teach patients and their families about diagnostic tests and therapeutic procedures related to AKI?
Why is it important to teach patients and their families about diagnostic tests and therapeutic procedures related to AKI?
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What long-term caution should patients be advised about after experiencing AKI?
What long-term caution should patients be advised about after experiencing AKI?
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Which aspects of health should a patient recovering from AKI actively monitor?
Which aspects of health should a patient recovering from AKI actively monitor?
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What is the main factor evaluated in the management of a patient with acute kidney injury (AKI)?
What is the main factor evaluated in the management of a patient with acute kidney injury (AKI)?
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Which of the following indicators suggests that a patient's nutritional needs are being met?
Which of the following indicators suggests that a patient's nutritional needs are being met?
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What should be done if the expected outcomes of care for a patient with AKI are not being met?
What should be done if the expected outcomes of care for a patient with AKI are not being met?
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Which sign indicates a potential secondary infection in a patient with acute kidney injury?
Which sign indicates a potential secondary infection in a patient with acute kidney injury?
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Why is family involvement important in the care discussions for a patient with AKI?
Why is family involvement important in the care discussions for a patient with AKI?
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Which type of acute kidney injury (AKI) is characterized by direct damage to kidney tissue?
Which type of acute kidney injury (AKI) is characterized by direct damage to kidney tissue?
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During which phase of acute kidney injury does the glomerular filtration rate (GFR) significantly decrease?
During which phase of acute kidney injury does the glomerular filtration rate (GFR) significantly decrease?
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Which of the following is a potential consequence of prolonged acute kidney injury?
Which of the following is a potential consequence of prolonged acute kidney injury?
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What commonly associated symptom of acute kidney injury can severely impact heart function?
What commonly associated symptom of acute kidney injury can severely impact heart function?
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Which phase of AKI is often asymptomatic but marks the start of kidney injury?
Which phase of AKI is often asymptomatic but marks the start of kidney injury?
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What is a common risk factor for acquiring infections in patients with acute kidney injury?
What is a common risk factor for acquiring infections in patients with acute kidney injury?
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Which of the following factors is NOT related to fluid and electrolyte imbalances caused by acute kidney injury?
Which of the following factors is NOT related to fluid and electrolyte imbalances caused by acute kidney injury?
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Which population is particularly vulnerable to developing acute kidney injury?
Which population is particularly vulnerable to developing acute kidney injury?
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What is the normal glomerular filtration rate (GFR) for healthy adults?
What is the normal glomerular filtration rate (GFR) for healthy adults?
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How do kidneys contribute to acid-base homeostasis?
How do kidneys contribute to acid-base homeostasis?
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Which of the following electrolytes is primarily regulated by the kidneys?
Which of the following electrolytes is primarily regulated by the kidneys?
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What is the primary role of erythropoietin produced by the kidneys?
What is the primary role of erythropoietin produced by the kidneys?
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In which condition would blood levels of creatinine typically remain within a balanced range?
In which condition would blood levels of creatinine typically remain within a balanced range?
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Which pathway is initiated by the kidneys to help restore normal blood pressure when it drops?
Which pathway is initiated by the kidneys to help restore normal blood pressure when it drops?
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What typical range does blood urea nitrogen (BUN) fall within in healthy adults?
What typical range does blood urea nitrogen (BUN) fall within in healthy adults?
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How do kidneys respond when the body is adequately hydrated?
How do kidneys respond when the body is adequately hydrated?
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What does the accumulation of urea and other toxins in the blood indicate?
What does the accumulation of urea and other toxins in the blood indicate?
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Which condition is characterized by low sodium levels due to fluid overload?
Which condition is characterized by low sodium levels due to fluid overload?
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What results from impaired excretion of hydrogen ions in kidney dysfunction?
What results from impaired excretion of hydrogen ions in kidney dysfunction?
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What alteration might lead to elevated potassium levels in kidney dysfunction?
What alteration might lead to elevated potassium levels in kidney dysfunction?
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Which of the following is typically observed in patients with oliguria?
Which of the following is typically observed in patients with oliguria?
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What is a consequence of fluid retention in kidney dysfunction?
What is a consequence of fluid retention in kidney dysfunction?
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What can result from decreased erythropoietin production in kidney dysfunction?
What can result from decreased erythropoietin production in kidney dysfunction?
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Which alteration occurs in kidney function leading to protein or blood presence in urine?
Which alteration occurs in kidney function leading to protein or blood presence in urine?
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Which symptom is commonly associated with acute kidney injury (AKI) due to waste product buildup?
Which symptom is commonly associated with acute kidney injury (AKI) due to waste product buildup?
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Which recent exposure should be inquired about to identify potential causes of AKI?
Which recent exposure should be inquired about to identify potential causes of AKI?
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What change in vital signs might indicate fluid overload in a patient with AKI?
What change in vital signs might indicate fluid overload in a patient with AKI?
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Which physical exam finding may suggest poor kidney perfusion?
Which physical exam finding may suggest poor kidney perfusion?
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What is a key indicator of potential uremia observed during a patient interview?
What is a key indicator of potential uremia observed during a patient interview?
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Which characteristic of urine should be assessed to evaluate AKI during a physical exam?
Which characteristic of urine should be assessed to evaluate AKI during a physical exam?
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What is the purpose of performing daily weight checks in patients suspected of AKI?
What is the purpose of performing daily weight checks in patients suspected of AKI?
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Which recent events should be investigated to identify risk factors for AKI?
Which recent events should be investigated to identify risk factors for AKI?
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What may elevated white blood cell (WBC) count indicate in patients with acute kidney injury (AKI)?
What may elevated white blood cell (WBC) count indicate in patients with acute kidney injury (AKI)?
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Which finding on a renal ultrasound suggests acute kidney injury rather than chronic kidney disease?
Which finding on a renal ultrasound suggests acute kidney injury rather than chronic kidney disease?
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What does a renal biopsy help identify in cases of acute kidney injury?
What does a renal biopsy help identify in cases of acute kidney injury?
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Which imaging method is used to confirm blockages that could lead to postrenal acute kidney injury?
Which imaging method is used to confirm blockages that could lead to postrenal acute kidney injury?
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What is the primary implication of low hemoglobin and hematocrit levels in a patient with acute kidney injury?
What is the primary implication of low hemoglobin and hematocrit levels in a patient with acute kidney injury?
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Which finding in urinalysis suggests renal tubular damage?
Which finding in urinalysis suggests renal tubular damage?
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An elevated blood urea nitrogen (BUN) level above what value is often seen in acute kidney injury (AKI)?
An elevated blood urea nitrogen (BUN) level above what value is often seen in acute kidney injury (AKI)?
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Which electrolyte imbalance may lead to muscle weakness and cardiac dysrhythmias?
Which electrolyte imbalance may lead to muscle weakness and cardiac dysrhythmias?
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What does a low pH and low bicarbonate level in arterial blood gases (ABGs) indicate in AKI?
What does a low pH and low bicarbonate level in arterial blood gases (ABGs) indicate in AKI?
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What is a common key finding in serum creatinine levels for patients with acute kidney injury (AKI)?
What is a common key finding in serum creatinine levels for patients with acute kidney injury (AKI)?
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Which condition is indicated by hyperphosphatemia and hypocalcemia in a patient with AKI?
Which condition is indicated by hyperphosphatemia and hypocalcemia in a patient with AKI?
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What abnormal urinalysis finding might indicate glomerular damage?
What abnormal urinalysis finding might indicate glomerular damage?
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What does the presence of casts in the urine signify in a patient with AKI?
What does the presence of casts in the urine signify in a patient with AKI?
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What is the primary role of a nephrologist in the management of acute kidney injury (AKI)?
What is the primary role of a nephrologist in the management of acute kidney injury (AKI)?
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Which surgical intervention might be required for postrenal AKI due to obstructions?
Which surgical intervention might be required for postrenal AKI due to obstructions?
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What type of dialysis is typically used when hemodialysis is contraindicated?
What type of dialysis is typically used when hemodialysis is contraindicated?
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What is a crucial aspect of patient education related to medication management in AKI?
What is a crucial aspect of patient education related to medication management in AKI?
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Which of the following reflects an objective of physical therapy in AKI management?
Which of the following reflects an objective of physical therapy in AKI management?
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In which scenario is Continuous Renal Replacement Therapy (CRRT) most appropriately utilized?
In which scenario is Continuous Renal Replacement Therapy (CRRT) most appropriately utilized?
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What aspect is essential for minimizing infection risk in patients with central lines for dialysis?
What aspect is essential for minimizing infection risk in patients with central lines for dialysis?
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Which of the following is a common symptom that patients should be educated to recognize as a sign of potential complications in AKI?
Which of the following is a common symptom that patients should be educated to recognize as a sign of potential complications in AKI?
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Which surgery may be indicated in severe cases of AKI due to intrinsic damage from infection?
Which surgery may be indicated in severe cases of AKI due to intrinsic damage from infection?
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What is one of the goals of comprehensive care approaches for managing AKI?
What is one of the goals of comprehensive care approaches for managing AKI?
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What is the primary purpose of using diuretics in the management of acute kidney injury (AKI)?
What is the primary purpose of using diuretics in the management of acute kidney injury (AKI)?
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Which dietary modification is crucial for managing patients with acute kidney injury (AKI)?
Which dietary modification is crucial for managing patients with acute kidney injury (AKI)?
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What role do potassium-binding agents play in the treatment of AKI?
What role do potassium-binding agents play in the treatment of AKI?
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Which of the following interventions is primarily non-pharmacologic in nature?
Which of the following interventions is primarily non-pharmacologic in nature?
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What is the purpose of dietary electrolyte management in patients with AKI?
What is the purpose of dietary electrolyte management in patients with AKI?
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Which pharmacologic intervention is typically used to manage symptoms of nausea in AKI patients?
Which pharmacologic intervention is typically used to manage symptoms of nausea in AKI patients?
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What benefit do positioning strategies, such as semi-Fowler's position, offer to patients with AKI?
What benefit do positioning strategies, such as semi-Fowler's position, offer to patients with AKI?
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Which collaborative intervention is essential for addressing the dietary needs of AKI patients?
Which collaborative intervention is essential for addressing the dietary needs of AKI patients?
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What is the function of phosphate binders in the treatment of AKI?
What is the function of phosphate binders in the treatment of AKI?
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Which of the following statements accurately describes why antihypertensives are used in AKI management?
Which of the following statements accurately describes why antihypertensives are used in AKI management?
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Which sign indicates a patient may be experiencing inadequate nutritional intake related to acute kidney injury?
Which sign indicates a patient may be experiencing inadequate nutritional intake related to acute kidney injury?
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What complication might arise from poor self-care adherence in patients with acute kidney injury?
What complication might arise from poor self-care adherence in patients with acute kidney injury?
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What is a common indication of worsening kidney function that may prompt the need for dialysis or advanced support?
What is a common indication of worsening kidney function that may prompt the need for dialysis or advanced support?
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Which sign suggests the emergence of secondary complications due to acute kidney injury?
Which sign suggests the emergence of secondary complications due to acute kidney injury?
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What approach should be taken if initial strategies to manage acute kidney injury are ineffective?
What approach should be taken if initial strategies to manage acute kidney injury are ineffective?
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What is a sign that indicates effective kidney function recovery during intervention for AKI?
What is a sign that indicates effective kidney function recovery during intervention for AKI?
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Which condition is indicative of ineffective intervention for AKI?
Which condition is indicative of ineffective intervention for AKI?
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Which of the following findings would indicate that a patient has maintained their nutritional needs after an AKI intervention?
Which of the following findings would indicate that a patient has maintained their nutritional needs after an AKI intervention?
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What abnormal finding could suggest fluid or electrolyte imbalances during evaluation of AKI treatment?
What abnormal finding could suggest fluid or electrolyte imbalances during evaluation of AKI treatment?
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Which aspect does NOT indicate effective treatment outcomes for a patient with AKI?
Which aspect does NOT indicate effective treatment outcomes for a patient with AKI?
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What would be an appropriate nursing action if a patient with AKI fails to show improvement in kidney function?
What would be an appropriate nursing action if a patient with AKI fails to show improvement in kidney function?
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Which of the following is a crucial indicator of restored electrolyte balance in patients recovering from AKI?
Which of the following is a crucial indicator of restored electrolyte balance in patients recovering from AKI?
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When evaluating for secondary complications during AKI recovery, which sign would not be concerning?
When evaluating for secondary complications during AKI recovery, which sign would not be concerning?
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What is one of the main reasons older adults are at a higher risk for acute kidney injury (AKI)?
What is one of the main reasons older adults are at a higher risk for acute kidney injury (AKI)?
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Which factor does not contribute to the risk of AKI in older adults?
Which factor does not contribute to the risk of AKI in older adults?
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What is a common symptom of acute kidney injury (AKI) in older adults?
What is a common symptom of acute kidney injury (AKI) in older adults?
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How should medication dosages be managed for older adults with reduced kidney function?
How should medication dosages be managed for older adults with reduced kidney function?
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Why is family education important in the management of acute kidney injury (AKI) in older adults?
Why is family education important in the management of acute kidney injury (AKI) in older adults?
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What is a characteristic of managing acute kidney injury (AKI) across different age groups?
What is a characteristic of managing acute kidney injury (AKI) across different age groups?
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What is the impact of hydration management in the prevention of acute kidney injury (AKI)?
What is the impact of hydration management in the prevention of acute kidney injury (AKI)?
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Which of the following is not considered a contributing factor to AKI risk in older adults?
Which of the following is not considered a contributing factor to AKI risk in older adults?
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What physiological change during pregnancy can complicate the diagnosis of AKI?
What physiological change during pregnancy can complicate the diagnosis of AKI?
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Which condition is most commonly associated with kidney strain during the later stages of pregnancy?
Which condition is most commonly associated with kidney strain during the later stages of pregnancy?
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In children, which underlying issue is least likely to cause acute kidney injury (AKI)?
In children, which underlying issue is least likely to cause acute kidney injury (AKI)?
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What nutritional consideration is particularly important for children with AKI?
What nutritional consideration is particularly important for children with AKI?
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Which symptom is least commonly seen in children with acute kidney injury (AKI)?
Which symptom is least commonly seen in children with acute kidney injury (AKI)?
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What potential complication related to pregnancy significantly raises the risk of AKI?
What potential complication related to pregnancy significantly raises the risk of AKI?
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Which of the following management strategies is essential for pregnant women at risk of AKI?
Which of the following management strategies is essential for pregnant women at risk of AKI?
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What is a notable risk factor for infants that may lead to acute kidney injury (AKI)?
What is a notable risk factor for infants that may lead to acute kidney injury (AKI)?
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What is the primary goal of patient education for those with acute kidney injury (AKI)?
What is the primary goal of patient education for those with acute kidney injury (AKI)?
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Which dietary modification is often necessary for patients with acute kidney injury (AKI)?
Which dietary modification is often necessary for patients with acute kidney injury (AKI)?
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What is a symptom of fluid overload that patients with AKI should monitor for?
What is a symptom of fluid overload that patients with AKI should monitor for?
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What type of medications should patients with AKI avoid to protect their kidneys?
What type of medications should patients with AKI avoid to protect their kidneys?
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How should patients with AKI manage their fluid intake?
How should patients with AKI manage their fluid intake?
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Which of the following is a sign of electrolyte imbalance that patients with AKI should recognize?
Which of the following is a sign of electrolyte imbalance that patients with AKI should recognize?
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What daily monitoring is recommended for patients recovering from AKI?
What daily monitoring is recommended for patients recovering from AKI?
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What dietary approach may help patients with AKI who experience nausea or poor appetite?
What dietary approach may help patients with AKI who experience nausea or poor appetite?
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What is a crucial aspect of preventing future episodes of acute kidney injury (AKI)?
What is a crucial aspect of preventing future episodes of acute kidney injury (AKI)?
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Which practice is important for managing electrolyte imbalances effectively?
Which practice is important for managing electrolyte imbalances effectively?
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What should individuals do if they experience potential side effects from prescribed medications?
What should individuals do if they experience potential side effects from prescribed medications?
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Which dietary habit should be encouraged to protect long-term kidney health?
Which dietary habit should be encouraged to protect long-term kidney health?
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What is an essential recommendation for caregivers involved in a patient's recovery from AKI?
What is an essential recommendation for caregivers involved in a patient's recovery from AKI?
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Why is regular follow-up important after experiencing AKI?
Why is regular follow-up important after experiencing AKI?
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What should be avoided by pregnant women to protect both their health and that of the fetus concerning kidney function?
What should be avoided by pregnant women to protect both their health and that of the fetus concerning kidney function?
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What is the significance of involving family members in the care of a patient recovering from AKI?
What is the significance of involving family members in the care of a patient recovering from AKI?
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Study Notes
Kidney Function
- Kidneys maintain homeostasis by controlling fluid and electrolyte balance, as well as acid-base balance.
- They also help regulate blood pressure.
- Only one functioning kidney is needed to maintain homeostasis, as demonstrated by patients with a single transplanted kidney.
Renal Failure
- Occurs when kidneys fail to remove accumulated metabolites from the blood.
- This leads to altered fluid, electrolyte, and acid-base balance.
- Can be caused by primary kidney disorders, systemic diseases, or other urologic defects.
- Two types: acute and chronic.
Acute Kidney Injury (AKI)
- Characterized by a rapid decline in renal function.
- This causes decreased excretion of waste products, leading to increased creatinine and urea levels.
- Affects 13-18% of hospitalized patients.
- Most common causes are ischemia (insufficient blood supply) and exposure to nephrotoxins (substances that damage kidney tissue).
- Other causes include major surgery, sepsis, and severe pneumonia.
Acute Kidney Injury (AKI) Causes
- AKI causes fall into three categories: prerenal, intrarenal, and postrenal
- Prerenal is the most common cause, accounting for 55% of cases
- In prerenal AKI, decreased blood flow to the kidneys causes AKI without directly damaging kidney tissue
- Intrarenal AKI is caused by direct damage to functional kidney tissue
- Intrarenal AKI accounts for 40% of cases
- Postrenal AKI is the least common cause at approximately 5%
- Postrenal AKI is caused by urinary tract obstructions, which damage the kidneys
Causes of Acute Kidney Injury
-
Prerenal AKI: This is caused by factors that reduce blood flow to the kidneys, leading to decreased filtration.
- Hypovolemia: Conditions that lead to decreased blood volume, such as hemorrhage, dehydration, severe burns or wounds, and excessive fluid loss from the gastrointestinal tract.
- Low cardiac output: Conditions that impair the heart's ability to pump blood, like heart failure and cardiogenic shock.
- Altered vascular resistance: Conditions that cause changes in blood vessel diameter, such as sepsis, anaphylaxis, and medications that affect blood vessels.
-
Intrarenal AKI: This is caused by damage to the kidneys themselves.
- Glomerular/microvascular injury: Damage to the filtration units of the kidneys, caused by conditions such as glomerulonephritis, disseminated intravascular coagulation, vasculitis, hypertension, preeclampsia, and hemolytic uremic syndrome.
- Acute tubular necrosis: Damage to the kidney tubules, which is often caused by ischemia (lack of blood flow) due to prerenal AKI, toxins like drugs and heavy metals, hemolysis, and rhabdomyolysis.
- Interstitial nephritis: Inflammation of the kidney tissue, which can be triggered by nephrotoxic drugs, infections, immune disorders, or unknown causes.
-
Postrenal AKI: This is caused by obstruction of the urinary tract, preventing urine flow from the kidneys.
- Ureteral obstruction: Blockage of the tubes connecting the kidneys to the bladder, caused by stones (calculi), cancer, or pressure from external sources.
- Urethral obstruction: Blockage of the tube that carries urine out of the body, caused by enlarged prostate, stones, cancer, narrowing (stricture), or blood clots.
Causes of Acute Kidney Injury (AKI)
-
Prerenal AKI: Caused by factors that reduce blood flow to the kidneys.
- Hypovolemia (low blood volume): Can be due to hemorrhage, dehydration, fluid loss from the GI tract, burns, and wounds.
- Low Cardiac Output: Can arise from heart failure or cardiogenic shock.
- Altered Vascular Resistance: Seen in conditions like sepsis, anaphylaxis, and the use of vasoactive drugs.
-
Intrarenal AKI: Damage to the kidneys themselves.
- Glomerular/Microvascular Injury: Conditions causing this include glomerulonephritis, disseminated intravascular coagulation, vasculitis, hypertension, preeclampsia, and hemolytic uremic syndrome.
- Acute Tubular Necrosis (ATN): Ischemic damage to the kidney tubules due to conditions associated with prerenal AKI, toxins like drugs and heavy metals, hemolysis, and rhabdomyolysis.
- Interstitial Nephritis: Inflammation of the kidney tissue caused by nephrotoxic drugs, infections, immune disorders, or unknown causes.
-
Postrenal AKI: Obstruction of the urinary tract.
- Ureteral Obstruction: Can be due to kidney stones, cancer, or external compression.
- Urethral Obstruction: Causes include prostate enlargement, stones, cancer, strictures, and blood clots.
Prerenal AKI
- Prerenal AKI is characterized by reduced renal blood flow and perfusion.
- Factors that can decrease vascular volume, cardiac output, or systemic vascular resistance contribute to prerenal AKI.
- Prerenal AKI is prevalent in patients who have experienced trauma, surgery, or critical illness.
- The kidneys typically receive 20-25% of the cardiac output to sustain a normal glomerular filtration rate (GFR).
- A reduction in renal blood flow below 20% of the normal value leads to a decrease in GFR.
- Reduced filtration by the glomeruli results in decreased tubular reabsorption.
- The slowing of kidney cell metabolism conserves energy and oxygen.
- Prompt restoration of blood flow can rapidly reverse prerenal AKI, leaving the renal parenchyma intact.
- Prolonged ischemia can cause tubular cell necrosis and significant nephron damage.
- Sustained ischemia may lead to intrarenal AKI caused by ischemic injury.
Intrarenal AKI
- Characterized by acute damage to the renal parenchyma and nephrons
- Caused by diseases of the kidney itself
- Acute tubular necrosis is the most common intrarenal cause of AKI
- In acute glomerulonephritis, glomerular inflammation can reduce renal blood flow and cause AKI.
- Vascular disorders affecting the kidney, such as vasculitis, malignant HTN, and arterial or venous occlusion, can damage nephrons and cause AKI.
Postrenal AKI
- Obstructive causes of AKI are classified as postrenal.
- Any condition preventing urine excretion can cause postrenal AKI.
- Benign prostatic hypertrophy is the most frequent cause.
- Other causes include kidney or urinary tract stones (calculi) and tumors.
- Children with AKI might experience oliguria (reduced urine output) or normal to increased urine output.
- Renal failure without oliguria usually means a less severe kidney injury.
Acute Tubular Necrosis (ATN)
- ATN is the destruction of tubular epithelial cells, causing a rapid decline in renal function.
- Prolonged ischemia is the primary cause of ATN.
- Ischemia and nephrotoxin exposure together significantly increase ATN risk.
- Risk factors for ischemic ATN include:
- Major surgery
- Severe hypovolemia
- Sepsis
- Trauma
- Burns
- Toxins from bacteria or damaged tissue in sepsis, trauma, and burns worsen ischemia.
- ATN is the most common cause of intrinsic renal failure in children.
- Ischemia exceeding 2 hours causes irreversible kidney tubule damage, with cell necrosis and sloughing.
- Reduced GFR due to ischemia, activated renin-angiotensin system, and cellular debris blocking tubules increases pressure in the glomerular capsule.
- Common nephrotoxins associated with ATN:
- Aminoglycoside antibiotics
- Radiologic contrast media
- Nephrotoxins damage tubular cells directly or indirectly.
- Damaged tubular cells increase permeability, leading to filtrate reabsorption and decreased waste elimination.
- Other nephrotoxins include:
- NSAIDs
- Chemotherapeutic drugs
- Heavy metals (mercury, gold)
- Common chemicals (ethylene glycol)
- Ibuprofen and acetaminophen are particularly problematic in children.
- ATN risk is higher in older patients, those with pre-existing renal insufficiency, and when combined with other nephrotoxins.
- Dehydration increases ATN risk by concentrating toxins in nephrons.
Etiology of AKI
- AKI can occur at any age
- Around 5% of hospitalized patients develop AKI
- 4.5% of children in pediatric intensive care develop AKI
- 8% of infants in neonatal intensive care develop AKI
- The incidence of AKI increases with the severity of the patient’s illness.
- Mortality rate for AKI in seriously ill patients may be 75%
- The high mortality rate is likely due to the populations affected by AKI (the elderly and critically ill), rather than the disorder itself.
Risk Factors for AKI
- Major trauma, surgery, infection, hemorrhage, severe heart failure, severe liver disease, and lower urinary tract obstruction can increase the risk of AKI.
- Drugs and radiologic contrast media that are toxic to the kidney also increase the risk of AKI.
- Older adults are at higher risk for AKI due to increased incidence of serious illness, hypotension, major surgeries, diagnostic procedures, and treatment with nephrotoxic drugs.
- Older adults are also at greater risk due to a decrease in kidney function associated with aging.
- Children with renal insufficiency are at greater risk for fluid loss with illness, particularly during acute gastrointestinal illness, increasing their susceptibility to dehydration and AKI.
Contrast-induced nephropathy
- Third most common cause of hospital-acquired AKI (acute kidney injury)
- Occurs after decreased renal perfusion and nephrotoxic medication administration
- Preventive strategies can reduce incidence
Prevention Strategies
- Focus on counteracting vasoconstriction
- Enhance blood flow through nephron
- Protect against oxygen free radical injury
Nursing Role
- Nurse needs to know adverse effects of contrast media infusion
- Nurses should identify patients at risk
- Apply evidence-based prevention strategies to prevent contrast-induced nephropathy
Decreased RBCs
- Fatigue
- Pallor
- Dizziness, confusion, lethargy
- Tachycardia, tachypnea, hypotension
- Iron supplementation
- Administration of epoetin
- Blood transfusion
- Therapies aimed at treating the underlying cause of AKI
Fluid Volume Excess
- Dependent pitting edema
- Respiratory crackles
- Dyspnea, pulmonary edema, hypoxemia
- Weight gain
- Tachycardia
- Jugular vein distention
- Fluid restriction
- Sodium-restricted diet
- Diuretics
- Dialysis
Hyperkalemia
- Ventricular arrhythmias
- Tall, peaked T waves; widened QRS
- Cardiac arrest
- Smooth muscle hyperactivity
- Nausea and vomiting
- Abdominal cramping
- Diarrhea
- Muscle weakness
- Paresthesias
- Flaccid paralysis
- Removal of all potassium from IV solutions
- Low-potassium diet
- Administration of glucose and insulin to increase the cells’ utilization of glucose while stimulating the cellular pump that increases the uptake of excess from the blood into the cell
- Potassium-absorbing oral or enema solutions
- Dialysis
Initiation Phase of AKI
- The initiation phase can last for hours to days.
- Starts with an initiating event like hemorrhage.
- Ends with tubular injury.
- If AKI is identified and the initiating event is effectively treated during this phase, the prognosis is positive.
- The initiation phase is often asymptomatic, making early detection difficult.
Maintenance Phase of AKI
-
Characterized by:
- Significant decrease in Glomerular Filtration Rate (GFR)
- Tubular necrosis
-
Oliguria:
- May develop, but many patients continue to produce normal or near-normal urine.
- Regardless of urine output, the kidneys are unable to effectively eliminate metabolic wastes, water, electrolytes, and acids.
-
Consequences:
- Azotemia: Increased levels of nitrogenous waste products in the blood.
- Fluid Retention: Edema, increased risk of heart failure and pulmonary edema.
-
Electrolyte Imbalances:
- Hyperkalemia: Increased potassium levels (above 6.0-6.5 mEq/L) can lead to muscle weakness, nausea, diarrhea, electrocardiographic changes, and even cardiac arrest.
- Hyperphosphatemia: Increased phosphate levels.
- Hypocalcemia: Decreased calcium levels.
- Metabolic Acidosis: Impaired hydrogen ion elimination by the kidneys.
- Anemia: Develops after several days due to suppressed erythropoietin secretion.
- Impaired Immune Function: Increased risk of infections.
-
Other Manifestations:
- Neurological: Confusion, disorientation, agitation, lethargy, hyperreflexia, seizures, and coma due to azotemia and electrolyte/acid-base imbalances.
- Gastrointestinal: Anorexia, nausea, vomiting, and decreased or absent bowel sounds.
- Uremic Syndrome: If AKI persists, it can lead to uremic syndrome, characterized by a buildup of waste products in the blood.
Recovery Phase of AKI
- Characterized by tubule cell repair and regeneration
- Gradual return of GFR to normal or pre-AKI levels
- Diuresis, or increased urine excretion, occurs as nephrons and GFR recover
- Excretion of retained salt, water, and solutes
- Serum creatinine, BUN, potassium, and phosphate levels remain high and may continue to rise despite increased urine output
- Renal function improves rapidly during the first 5 to 25 days of recovery
- Continued improvement for up to 1 year
Preventing AKI
- Maintaining adequate vascular volume, cardiac output, and blood pressure is key to preventing AKI.
- Avoid nephrotoxic drugs whenever possible.
- Minimize the dosage when nephrotoxic drugs are necessary.
- Hydration is important when using nephrotoxic drugs.
- Eliminate other nephrotoxins from medication regimens.
Managing Acute Kidney Injury (AKI)
- Maintaining fluid and electrolyte balance is a crucial aspect of AKI management.
- Identifying and addressing the underlying cause of AKI is essential for effective treatment.
- Preventing further damage to the kidneys is a vital goal to minimize long-term consequences.
- Restoring urine output and kidney function is a primary objective.
- Compensating for kidney impairment until kidney function recovers is essential to support overall patient well-being.
Diagnostic Tests for AKI
- Diagnostic tests are crucial for identifying the cause of AKI and monitoring its impact on homeostasis.
-
Urinalysis reveals abnormal findings in AKI:
- Fixed specific gravity of 1.010 due to impaired tubular concentration.
- Proteinuria indicates glomerular damage as the cause of AKI.
- Presence of RBCs, WBCs, and renal tubular epithelial cells point to glomerular dysfunction, inflammation, and ATN, respectively.
- Cell casts, including RBC, WBC, and renal tubular epithelial casts, reflect tubular damage. Brownish-pigmented casts and positive occult blood tests indicate hemoglobinuria or myoglobinuria.
-
Serum creatinine and BUN are used to assess renal function.
- In AKI, serum creatinine levels rise rapidly within 24-48 hours of onset, peaking within 5-10 days.
- Creatinine and BUN levels increase more gradually when urine output is maintained.
- Recovery is marked by a halt in the rise of serum creatinine and BUN.
-
Serum electrolytes are monitored to evaluate fluid and electrolyte balance.
- Increased serum potassium may necessitate dialysis.
- Hyponatremia is common due to water excess associated with AKI.
- ABG studies often indicate metabolic acidosis caused by the kidneys' inability to eliminate metabolic wastes and hydrogen ions.
- CBC shows reduced RBCs, moderate anemia, and low hematocrit due to AKI's impact on erythropoietin secretion, RBC production, and impaired iron and folate absorption.
-
Renal ultrasonography helps identify obstructive causes of renal failure and differentiate AKI from ESRD.
- Enlarged kidneys may indicate AKI, while small, shrunken kidneys suggest CKD.
- CT scan is performed to evaluate kidney size and identify potential obstructions.
-
IV pyelography, retrograde pyelography, and antegrade pyelography are used to assess kidney structure and function.
- Radiologic contrast media are cautiously used due to their nephrotoxic potential.
- Retrograde and antegrade pyelography are preferred over IV pyelography for their reduced nephrotoxicity.
- Renal biopsy may be required to differentiate between acute and chronic kidney disease.
- Imaging studies assist in assessing kidney structures, renal blood flow, perfusion, and function, aiding in differentiating AKI and CKD in children.
Pharmacologic Therapy for AKI
- The primary goal of drug management in AKI is to restore renal perfusion and remove nephrotoxic drugs from the regimen.
- IV fluids and blood volume expanders are used to restore renal perfusion.
- Low-dose dopamine IV infusion increases renal blood flow by improving cardiac output and dilating mesenteric and kidney blood vessels.
- Furosemide (Lasix), a powerful loop diuretic, may be given alongside IV fluids if renal blood flow restoration doesn't improve urine output.
- Furosemide aims to wash out nephrons, reducing toxin concentration and preventing oliguria, azotemia, fluid, and electrolyte imbalances.
- Aggressive management of hypertension is crucial in AKI associated with conditions like toxemia and gestational hypertension.
- ACE inhibitors or other antihypertensive medications are used to control blood pressure.
- All nephrotoxic drugs or drugs interfering with renal perfusion are discontinued, including NSAIDs, nephrotoxic antibiotics, and other potentially harmful drugs.
- Patients with AKI have an increased risk of GI bleeding due to the stress response and impaired platelet function.
- Antacids, histamine-receptor antagonists (e.g., famotidine), or proton pump inhibitors (e.g., omeprazole) are often prescribed to prevent GI hemorrhage.
- Hyperkalemia management includes restricted potassium intake and active intervention for serum levels above 6.5 mEq/L to prevent cardiovascular adverse effects.
- Insulin and glucose intravenous administration can reduce serum potassium levels by moving potassium into the cells in cases of significant hyperkalemia.
- Oral or enema administration of potassium-binding exchange resin, like SPS, helps remove potassium from the body by exchanging sodium for potassium in the large intestine, often combined with sorbitol to avoid constipation.
- Phosphate-binding drugs like calcium acetate, ferric citrate, lanthanum carbonate, and sevelamer bind phosphates in the GI tract for fecal excretion.
- Drug dosages may need adjustments for AKI patients as kidney elimination is impaired, potentially leading to toxic blood levels due to prolonged half-life.
Loop Diuretics
- Drug Examples: bumetanide (Bumex), ethacrynic acid (Edecrin), furosemide (Lasix), torsemide (Demadex)
- Mechanism of Action: Act on the loop of Henle, increasing urine output.
- Nursing Considerations:
- Administration: Furosemide - undiluted at a rate of no more than 20 mg/min. Ethacrynic acid - 50 mg diluted with 50 mL normal saline, at a rate of no more than 10 mg/min. Bumetanide - undiluted over at least 1 min or diluted in lactated Ringer solution, normal saline, or 5% dextrose in water for infusion. Torsemide - undiluted over at least 2 min.
- Monitoring: Assess weight and vital signs, monitor intake and output, daily weight, vital signs, skin turgor. Assess for orthostatic hypotension and monitor laboratory results, especially serum electrolyte, glucose, BUN, and creatinine levels.
- Ototoxicity: High doses, especially ethacrynic acid, increase the risk of ototoxicity, which may be reversible if detected early. Avoid concurrent administration with ototoxic agents like aminoglycosides and cisplatin.
Thiazide Diuretics
- Drug Examples: chlorothiazide (Diuril), hydrochlorothiazide, indapamide, methyclothiazide
- Mechanism of Action: Act on the distal convoluted tubule, increasing urine output.
- Nursing Considerations:
- Administration: Administer as ordered.
- Monitoring: Assess weight and vital signs, monitor intake and output, daily weight, vital signs, skin turgor. Assess for orthostatic hypotension and monitor laboratory results, especially serum electrolyte, glucose, BUN, and creatinine levels.
Mannitol
- Mechanism of Action: Works as an osmotic diuretic
- Nursing Considerations:
- Administration: Administer intravenously, diluting before use if indicated. Check solution for crystallization and dissolve crystals by warming slightly. Infuse 15–25% mannitol solutions through a filter over 30–90 min.
- Monitoring: Monitor vital signs, breath sounds, and urinary output. Discontinue if signs of heart failure or pulmonary edema develop or if renal function continues to decline.
- Patient Education: Report shortness of breath, headache, chest pain, or dizziness immediately.
Urea
- Mechanism of Action: Used as an osmotic diuretic
- Nursing Considerations:
- Administration: Administer intravenously, diluting in 100 mL of 5 or 10% dextrose in water for every 30 g of urea. Administer no faster than 4 mL/min through a filter.
- Monitoring: Monitor vital signs, breath sounds, and urinary output. Discontinue if signs of heart failure or pulmonary edema develop or if renal function continues to decline.
Electrolytes and Electrolyte Modifiers
- Drug Examples: Calcium chloride, calcium gluconate, sodium bicarbonate, sodium polystyrene sulfonate (SPS)
- Mechanism of Action: Various mechanisms to correct electrolyte imbalances.
- Nursing Considerations:
- Administration:
- IV calcium chloride at less than 1 mL/min; IV calcium gluconate at 0.5 mL/min. Inject into a large vein through a small-bore needle; avoid infiltration because extravasation of IV solution will cause tissue necrosis.
- IV sodium bicarbonate infusion over 4–8 hr; oral tablets as prescribed.
- SPS as an oral solution mixed with sorbitol to prevent constipation, or as a retention enema mixed with warm water. Leave in the bowel for 30–60 min, irrigate using a small tap-water enema.
- Monitoring: Assess serum electrolyte levels before and during therapy. Report rapid shifts or adverse responses to the HCP. Monitor for adverse reactions, such as dysrhythmias, electrolyte imbalances, and metabolic alkalosis.
Phosphate Binders
- Drug Examples: Calcium acetate (Calphron, Phoslyra), ferric citrate (Auryxia), lanthanum carbonate (Fosrenol), sevelamer (Renagel, Renvela)
- Mechanism of Action: Bind to excess phosphate in the gut, preventing absorption.
- Nursing Considerations:
- Administration: Administer as prescribed.
- Monitoring: Monitor serum phosphate levels.
Patient Education:
-
Loop Diuretics:
-
Maintain a fluid intake of 2–3 L per day unless contraindicated.
-
Rise slowly from lying or sitting positions to prevent light-headedness.
-
Take in the morning and, if ordered twice a day, in the late afternoon to avoid sleep disturbance.
-
Take with food or milk to prevent gastric distress.
-
Avoid NSAIDs.
-
Electrolytes and Electrolyte Modifiers:
-
IV calcium may make you light-headed; remain in bed for at least 30 min after administration.
-
Chew sodium bicarbonate tablets and follow with 8 oz of water. Do not take with milk.
-
Retain the SPS enema as long as possible.
Fluid Management in Acute Kidney Injury (AKI)
- Fluid restriction is typically implemented once vascular volume and renal perfusion are restored in patients with AKI.
- The daily fluid intake is calculated by accounting for insensible losses and urine output.
- Insensible losses, including respiration, perspiration, and bowel losses, are estimated at 500 mL daily.
- The amount of urine excreted in the previous 24 hours is added to the insensible loss to determine the total allowed fluid intake.
- For example, a patient excreting 325 mL of urine in 24 hours should be allowed a total fluid intake of 825 mL (500 mL for insensible loss + 325 mL urine output).
- Fluid balance is carefully monitored using accurate weight measurements and serum sodium levels as primary indicators.
Renal Insufficiency and Nutrition
- Renal insufficiency and underlying disease processes increase catabolism and decrease anabolism.
- Adequate nutrients and calories are needed to prevent catabolism in patients with acute kidney injury (AKI).
- Protein intake should be limited to 0.6 g/kg of body weight per day to minimize azotemia.
- Dietary proteins should be of high biological value, meaning they are rich in essential amino acids.
- Carbohydrate intake should be increased to maintain adequate calorie intake and provide a protein-sparing effect.
- Parenteral nutrition may be used when patients cannot consume adequate oral intake due to nausea, vomiting, or critical illness.
- Parenteral nutrition provides amino acids, concentrated carbohydrates, and fats.
- Disadvantages of parenteral nutrition in AKI patients include the high volume of fluid required and the risk of infection through the venous line.
Nutrition Management in Renal Insufficiency
- Renal insufficiency and underlying disease processes increase catabolism and decrease anabolism.
- Patients with AKI need adequate nutrients and calories to prevent catabolism.
- Protein intake should be limited to 0.6 g/kg of body weight per day to minimize azotemia.
- High biological value proteins (rich in essential amino acids) are preferred.
- Carbohydrate intake should be increased to maintain calorie intake and provide a protein-sparing effect.
- Parenteral nutrition with amino acids, concentrated carbohydrates, and fats may be used when patients are unable to consume adequate oral diets.
- Disadvantages of parenteral nutrition in AKI include high fluid volume requirements and increased risk of infection through the venous line.
Renal Replacement Therapy
- Renal replacement therapy is necessary for patients with renal failure, characterized by uremia, organ dysfunction, severe fluid overload, hyperkalemia, or metabolic acidosis.
- Dialysis is a process where solute molecules diffuse across a semipermeable membrane from an area of higher concentration to lower concentration.
- Dialysis removes excess fluid and waste products in renal failure.
- Dialysis is also used to rapidly remove nephrotoxins in acute tubular necrosis (ATN).
- Dialysis does not replace erythropoietin production, resulting in persistent anemia in dialysis patients.
- Hemodialysis is a common dialysis form where blood flows through vascular catheters, is pumped through a dialyzer unit, and returned to the patient.
- Peritoneal dialysis utilizes the peritoneum as the dialyzing membrane.
- Continuous renal replacement therapy (CRRT) continuously circulates blood through a highly porous hemofilter.
- CRRT can be used to treat AKI.
Hemodialysis
- Hemodialysis uses diffusion and ultrafiltration to remove waste products, excess water, and electrolytes from the blood
- Blood is extracted from the patient and pumped to the dialyzer
- The dialyzer contains a porous membrane that allows small molecules to pass through while blocking larger molecules
- Dialysate is a solution with a similar composition and temperature to normal extracellular fluid, and it flows along the other side of the membrane
- Small solute molecules can move freely across the membrane by diffusion
- The direction of movement is determined by the concentrations of substances in the blood and dialysate
- Electrolytes and waste products diffuse from the blood into the dialysate
- Substances like calcium can be added to the dialysate to diffuse into the blood
- Ultrafiltration is the process of removing excess water from the blood by creating a higher hydrostatic pressure in the blood that moves through the dialyzer, flowing in the opposite direction of the dialysate
Hemodialysis for AKI
- Patients with AKI typically undergo daily hemodialysis initially.
- As patients improve, they may change to three to four sessions per week.
- Hemodialysis is not used if the patient is hemodynamically unstable (e.g., hypotension or low cardiac output).
Complications of Hemodialysis
-
Hypotension is the most frequent complication.
- Potential causes include changes in serum osmolality, rapid removal of fluid from the vascular compartment, and vasodilation.
- Bleeding can occur due to altered platelet function associated with uremia and heparin use during dialysis.
-
Infection (local or systemic) can result from WBC damage and immune system suppression.
- Staphylococcus aureus septicemia commonly arises from contamination of the vascular access site.
- Patients on chronic hemodialysis have higher rates of hepatitis B, hepatitis C, cytomegalovirus, and HIV infection than the general population.
Continuous Renal Replacement Therapy (CRRT)
- CRRT is a type of dialysis that removes fluid and waste products from the blood more gradually than hemodialysis.
- It's used for patients with acute kidney injury (AKI) who are hemodynamically unstable and cannot tolerate rapid fluid removal.
- CRRT involves continuous circulation of blood through a hemofilter for 12 hours or more.
- Excess water and solutes like electrolytes, urea, creatinine, uric acid, and glucose are removed and drained.
- During CRRT, fluid can be replaced with saline or balanced electrolyte solutions.
- The slow removal of fluid and solutes helps maintain hemodynamic stability.
- CRRT helps prevent complications associated with abrupt changes in extracellular fluid (ECF) composition.
Continuous Renal Replacement Therapies
- Continuous arteriovenous hemofiltration (CAVH) removes fluid and some solutes. It involves circulating arterial blood through a hemofilter, then returning it to the patient through a venous line. Ultrafiltrate collects in a drainage bag.
- Continuous arteriovenous hemodialysis (CAVHD) removes fluid and waste products. It involves circulating arterial blood through a hemofilter surrounded by dialysate, then returning it to the patient through a venous line. Ultrafiltrate collects in a drainage bag.
- Continuous venovenous hemodialysis (CVVHD) removes fluid and waste products. It involves circulating venous blood through a hemofilter surrounded by dialysate, then returning it to the patient through a double-lumen venous catheter. Ultrafiltrate collects in a drainage bag.
Continuous Renal Replacement Therapy
- CRRT is typically performed in an ICU or specialized nephrology unit.
- Some types of CRRT require both arterial and venous lines.
- Other types of CRRT use a double-lumen venous catheter.
- Strict aseptic technique is necessary to reduce the risk of infection at vascular access points.
Acute vascular access
- Double-lumen catheters are inserted into the subclavian, jugular, or femoral vein
- The double-lumen catheter has a central partition to separate blood withdrawal and return
- Blood is withdrawn through openings in the proximal portion of the catheter
- Blood is returned to the circulation through an opening in the distal end of the catheter
Long-term vascular access
- An arteriovenous (AV) fistula is created in the nondominant arm
- The nondominant arm should not be used for venipuncture or blood pressure measurement
- The fistula is created by surgical anastomosis of an artery and vein, usually the radial artery and cephalic vein
- The fistula takes about a month to mature
- A functional AV fistula has a palpable pulsation and a bruit on auscultation
- The nurse should avoid venipunctures and blood pressures on the arm with the fistula
Vascular Access in CKD
-
AV graft: Most common type of vascular access in CKD
- Made from Gore-Tex material
- Surgically implanted to connect artery and vein
- Blood flows from artery to vein
-
External AV shunt: Alternative option for vascular access
- Connects peripheral artery to peripheral vein
- Ideal timing: Creating AV fistula or graft is recommended early on when long-term dialysis is anticipated.
-
Complications: Catheter access has higher rates of complications and mortality than AV fistulas or grafts.
- Local complications: Infection, clotting (thrombosis), and aneurysms
- Systemic manifestations: Septicemia and embolization (from infection and thrombosis)
- Consequences: Local complications can lead to fistula or graft failure, requiring a new access site.
- Psychological impact: AV fistula or graft failure can have a significant negative impact on mental health, potentially leading to depression and low self-esteem.
Peritoneal Dialysis
- Peritoneal Dialysis uses the peritoneal membrane as a dialyzing surface
- The peritoneal membrane is highly vascular
- Sterile dialysate is warmed before infusion
- Dialysate is infused through a catheter inserted into the peritoneal cavity
- While the dialysate is in the abdomen metabolic waste products and excess electrolytes diffuse into the dialysate
- After dwell time the used fluid is drained by gravity
- Drained fluid is collected in a sterile bag and disposed of
- The process of dialysate infusion, dwell time, and drainage is repeated at prescribed intervals
Peritoneal Dialysis Benefits
- Peritoneal dialysis is a slower removal of excess fluid and solutes, making it safer for unstable patients than other methods.
Peritoneal Dialysis Drawbacks
- The slower removal rate of metabolites during peritoneal dialysis can be a disadvantage for patients with acute kidney injury (AKI) as it reduces waste removal.
Peritoneal Dialysis Risk Factors
- Peritoneal dialysis increases the risk of peritonitis.
- Peritoneal dialysis is contraindicated for patients with recent abdominal surgery, significant lung disease, or peritonitis.
Acute Kidney Injury in Infants
- AKI is common in preterm infants, affecting up to 56% of infants in neonatal intensive care units.
- Causes of AKI in infants include:
- Hemolytic uremic syndrome
- Acute glomerulonephritis
- Sepsis
- Poisoning
- Hypovolemia
- Obstructive uropathy
- Complications of cardiac surgery
- Asphyxia before and during delivery
- Predisposing factors include:
- Low Apgar score
- Hypothermia
- Nephrotoxic drugs
- Dehydration
- Congenital heart anomalies, particularly patent ductus arteriosus
- Low birth weight
- Hematologic-oncologic complications, bone marrow transplantation, and respiratory failure are increasingly recognized as causes of AKI in children.
- AKI is associated with high mortality in preterm newborns.
- Children who recover from AKI may experience residual kidney damage and impaired renal function.
Acute Kidney Injury in Children and Adolescents
- Acute kidney injury (AKI) is not common in children, but outcomes are impacted by the cause, associated findings, and the speed of diagnosis and treatment.
- AKI often develops in children already critically ill.
- The cause of oliguria may not always be immediately clear.
- AKI is typically reversible, but severe deviations in kidney function can be life-threatening, leading to high mortality rates.
- Clinical signs of AKI in children include nausea, vomiting, edema, hypertension, lethargy, and visible blood in the urine.
- Decreased urination and lethargy in dehydrated children, children in shock, or those who have recently undergone surgery are critical indicators that require investigation for possible AKI.
- Children with AKI can experience electrolyte imbalances, fluid overload, uremia (high blood urea level), and azotemia (elevated BUN and serum creatinine levels).
Hyperkalemia (Excess Potassium in the Blood)
- Caused by the inability to excrete potassium from diet and catabolized cells.
- Potassium also moves from intracellular fluid to extracellular fluid in metabolic acidosis.
- Clinical manifestations include:
- Peaked T waves
- Widening of QRS waves on electrocardiogram (ECG)
- Dysrhythmias
- Muscle weakness
Hyponatremia (Decreased Sodium in the Blood)
- Occurs during the acute oliguric phase of kidney failure due to fluid accumulation exceeding solute.
- Clinical manifestations include:
- Change in level of consciousness (LOC)
- Muscle cramps
- Anorexia
- Depressed abdominal and deep tendon reflexes
- Cheyne-Stokes respirations
- Seizures
Hypocalcemia (Decreased Calcium in the Blood)
- Phosphate retention (hyperphosphatemia) causes impaired renal function, which decreases calcium ion concentration in the serum.
- Calcium is deposited in injured cells.
- Hyperkalemia and metabolic acidosis can mask symptoms of severe hypocalcemia.
- Clinical manifestations include:
- Muscle tingling
- Changes in muscle tone
- Seizures
- Muscle cramps and twitching
- Positive Chvostek sign: Facial muscle contraction after tapping the facial nerve anterior to the parotid gland.
Initial Therapy for Children with Severe FVD and AKI
- Isotonic solution IV bolus, 20 mL/kg over 5-20 minutes
- Repeat bolus if necessary, based on child's response
- Subsequent therapy addresses fluid deficits, maintenance needs, and ongoing losses
Blood Loss as Cause for AKI
- Albumin may be administered if blood loss is the primary cause of AKI
Pregnancy and AKI
- During pregnancy, glomerular filtration rate (GFR) increases by as much as 50%.
- This increase in GFR leads to a decrease in serum creatinine levels.
- AKI in pregnant women is often caused by the same factors as in the general population.
- Pregnancy-specific factors can lead to AKI:
- Physiologic hydronephrosis: affects over 90% of pregnant women, can cause urinary stasis, UTIs, and AKI.
- First trimester: hyperemesis gravidarum and placenta previa can lead to AKI.
- Later pregnancy: gestational hypertension, preeclampsia, and eclampsia can stress the kidneys, causing proteinuria, hydronephrosis, and AKI.
- Unsafe abortion can lead to sepsis and AKI.
- Puerperal sepsis and postpartum hemorrhage are leading causes of AKI in the postpartum period.
AKI and Age
- Older adults experience AKI more frequently than younger individuals.
- Aging kidneys have reduced capacity to adapt to fluctuations in fluid volumes, solute levels, and heart output.
- GFR naturally decreases as we age.
- Factors increasing AKI risk in older adults include sepsis, surgical procedures, extended hospital stays, and existing health issues like hypertension, diabetes, heart disease, chronic kidney disease, and liver disease.
Preventing AKI
- Maintaining fluid volume and cardiac output can prevent AKI.
- Reducing exposure to nephrotoxins can prevent AKI.
- Monitor critically ill, postoperative, and older adult patients for early signs of hypovolemia.
Early Signs of Hypovolemia
- Low urine output
- Altered mental status
- Changes in vital signs, skin color, or temperature
Reporting Hypovolemia
- Report a fall in urine output to less than 30 mL/hr in adult patients.
- Report other evidence of decreased cardiac output.
Nurse Responsibilities
- Maintain IV fluids as prescribed.
- Alert the HCP about any patient receiving more than one nephrotoxic drug.
- Alert the HCP if a nephrotoxic drug is ordered for a dehydrated patient.
- Closely observe patients receiving blood or blood components for early signs of a transfusion reaction.
- Intervene appropriately as needed.
Preventing AKI
- Early intervention is key: Monitor critically ill, postoperative, and older adult patients for early signs of hypovolemia.
- Signs of Hypovolemia: Low urine output, altered mental status, changes in vital signs, skin color, or temperature.
- Alert for Low Urine Output: Report a fall in urine output to less than 30 mL/hr in adult patients.
- Maintaining Cardiac Output: Maintain IV fluids as prescribed.
- Nephrotoxin Awareness: Alert the HCP if the patient is receiving more than one nephrotoxic drug or if a nephrotoxic drug is ordered for a dehydrated patient.
- Transfusion Safety: Closely observe patients receiving blood or blood components for early signs of transfusion reaction and intervene promptly as needed.
Assessing AKI
- Both subjective and objective data are useful in assessing patients with AKI.
- A thorough history is crucial to identify the cause of AKI, as even brief periods of impaired perfusion can lead to renal ischemia.
- It's important to involve family members or caregivers in the assessment of pediatric and older patients.
Gathering Subjective Data
- Inquire about symptoms like anorexia, nausea, weight gain, or edema.
- Ask about recent exposure to nephrotoxins, such as aminoglycoside antibiotics or contrast media used in radiology.
- Elicit information on prior transfusion reactions and chronic diseases such as diabetes, heart failure, or kidney disease.
Gathering Objective Data
- Monitor vital signs, including temperature.
- Analyze urine output, noting volume, color, clarity, specific gravity, and presence of blood cells or protein.
- Assess weight, skin color, peripheral pulses, edema (both periorbital and dependent), and lung, heart, and bowel sounds.
Nursing Care for AKI
- Fluid volume excess is a common problem in AKI due to the kidneys' inability to filter and remove waste products and excess fluid.
- Undernutrition is another concern as AKI can affect the body's ability to absorb nutrients.
- Inadequate renal perfusion is a serious risk as it can lead to further kidney damage. Close monitoring of blood pressure and urine output is crucial.
- Impaired skin integrity is a potential problem due to fluid retention and possible prolonged bed rest.
- Decreased cardiac perfusion is a risk factor due to fluid overload and potential electrolyte imbalances.
- Infection is a risk as AKI weakens the immune system and makes the body more susceptible.
- Inadequate family coping skills can impact the effectiveness of patient care and recovery. Providing support and resources to families is important.
Planning Nursing Care
- Aims to prevent complications, maintain fluid balance, administer medications, meet nutritional needs, prevent infection, and provide emotional support.
- Outcomes are created in collaboration with the patient and family.
- Possible outcomes focus on restoring patient's health indicators to baseline measurements.
- Patient's weight will return to baseline measurement.
- Patient's urine output will be greater than 30 mL/hr. This indicates proper renal function and hydration.
- Patient's hemoglobin and hematocrit values will be within normal limits. This reflects adequate red blood cell count and oxygen-carrying capacity.
- Patient's serum electrolytes will be within normal limits. This ensures proper fluid and mineral balance.
- Patient's pulse rate, volume, and rhythm will return to baseline. This indicates a stable cardiovascular system.
Preventing and Recognizing AKI
- Early identification and prevention are vital in AKI management.
- Closely monitor the patient's weight, fluid intake and output, and electrolyte balance.
- Assess and document extrarenal fluid losses from vomiting, diarrhea, hemorrhage, and increased insensible losses.
- Monitor kidney function in patients taking potentially nephrotoxic medications.
- Meticulous aseptic technique is crucial due to infection being a leading cause of death in AKI.
Preventing and Recognizing AKI
- Early detection and prevention are crucial in managing AKI.
- Monitor weight, fluid intake and output, and electrolyte balance.
- Assess and record fluid losses from vomiting, diarrhea, hemorrhage, and increased insensible losses.
- Monitor kidney function in patients taking potentially nephrotoxic medications.
- Infections are the leading cause of death in AKI, so meticulous aseptic technique is essential.
AKI Prevention and Recognition
- Prevention and early identification are key for treating AKI.
- Closely monitor weight, intake, output, and fluid and electrolyte balance.
- Assess and document fluid loss from sources like vomiting, diarrhea, bleeding, and sweating.
- Carefully monitor kidney function in patients taking potentially nephrotoxic medications.
- Infection is the leading cause of death in AKI, so meticulous infection control is crucial.
Nursing Interventions for AKI
- Maintain hourly intake and output (I&O) records to guide fluid management, especially restrictions.
- Weigh the patient daily or more frequently based on their condition.
- Use consistent methods (same scale, clothing) for accurate weight measurements.
- Rapid weight changes are a strong indicator of fluid volume status, especially with low urine output.
- Monitor vital signs at least every 4 hours. High blood pressure, fast heart rate, and rapid breathing can indicate fluid overload.
- Assess breath and heart sounds, neck vein fullness, and edema in the back and extremities. Report unusual findings.
- If not contraindicated, position the patient in a semi-Fowler's position to help cardiac and respiratory function.
Electrolyte Imbalances in AKI
-
Hyperkalemia:
- Impaired potassium excretion
- Manifestations:
- Irritability
- Nausea
- Diarrhea
- Abdominal cramping
- Cardiac dysrhythmias
- Electrocardiographic changes
-
Hyponatremia:
- Water retention
- Manifestations:
- Nausea
- Vomiting
- Headache
- CNS manifestations:
- Lethargy
- Confusion
- Seizures
- Coma
-
Hyperphosphatemia:
- Decreased phosphate excretion
- Manifestations:
- Hyperreflexia
- Paresthesias
- Tetany (tonic muscle spasms)
AKI Patient Management
- Fluid restriction
- Frequent mouth care
- Hard candies to decrease thirst
- Ice chips (include water content as intake)
- Administer medications with meals
Nutritional Imbalances in Renal Failure
- Anorexia and nausea are common in renal failure and can interfere with food intake and nutrition.
- AKI can increase nutritional needs for healing, while simultaneously decreasing food intake.
- Monitor and record food intake to assess nutritional status and guide supplementation decisions.
- Daily weight monitoring is crucial for tracking nutritional status.
- Weight may remain stable or increase in AKI due to fluid retention, even with tissue mass loss.
- Consult with a registered dietitian to plan meals within prescribed limitations, considering cultural or religious food preferences.
- Unpalatable diets restricted in protein, salt, and potassium can improve with the inclusion of preferred foods.
- Engage patients in daily menu planning to promote a sense of control and autonomy.
- Allow family members to prepare meals within dietary restrictions to encourage eating and enjoyment.
- Family mealtimes provide familiar foods and social interaction, stimulating appetite and enjoyment.
### AKI Nutritional Care
- Provide frequent, small meals or between-meal snacks.
- This helps patients who are fatigued or have anorexia to eat more.
- Administer antiemetics as prescribed and provide mouth care before meals.
- Nausea and a metallic taste in the mouth are common symptoms of uremia that can decrease food intake.
- If a patient is unable to eat or tolerate enteral nutrition, administer parenteral nutrition as ordered.
- This is important for preventing or slowing tissue catabolism in patients with AKI.
Patient Teaching for AKI
- Patient teaching is crucial for resolving AKI and preventing complications.
- Assess patient's anxiety level and ability to comprehend instructions before providing information.
- Consider the patient's physical, mental, and emotional status.
- Tailor information and presentation to the patient's developmental level.
- During the initial stages of AKI, focus on immediate concerns like treating the underlying cause of kidney failure.
- Uremic effects can hinder learning, so adjust information delivery accordingly.
Patient Education for AKI
- Assess patient understanding: Relate information to previous learning experiences to enhance understanding and retention.
- Teach about diagnostic tests and procedures: Explain procedures to reduce anxiety and improve patient cooperation.
- Discuss dietary and fluid restrictions: Explain restrictions and emphasize their importance for continued management after discharge.
- Teach signs and symptoms of complications: Explain potential issues like fluid volume overload, dehydration, heart failure, and electrolyte imbalance, especially if discharged before complete recovery.
- Explain urine output changes: Emphasize the potential for impaired concentrating ability and electrolyte excretion, increasing the risk of fluid loss and imbalances.
- Teach self-monitoring: Instruct patients to monitor weight, blood pressure, and pulse to assess fluid status.
- Avoid nephrotoxic substances: Advise patients to avoid nephrotoxic drugs and chemicals for up to a year following AKI, as nephrons are vulnerable during recovery. This includes NSAIDs, some antibiotics, radiologic contrast media, and heavy metals.
- Discourage alcohol consumption: Alcohol increases the nephrotoxicity of certain substances, so it should be avoided.
Evaluating AKI Patients
- Assessing AKI patients includes monitoring for symptom resolution and preventing complications.
- Data points to evaluate include:
- Weight
- Cardiac rhythm
- Vital signs
- Breath sounds
- Oxygen saturation
- Serum electrolyte levels
- Intake and output
- Hemoglobin and hematocrit
- Evaluation should include patient response to treatment, understanding of the disease process, and self-care requirements.
- Expected outcomes of nursing care include:
- Maintaining fluid, electrolyte, and acid-base balance, evidenced by the absence of signs and symptoms of imbalance.
- Meeting nutritional needs, evidenced by dietary recall, return to appropriate weight, and absence of signs and symptoms of nutritional imbalance.
- Avoiding secondary infections.
- Referral to other specialists may be necessary if expected outcomes are not met.
- Dietitian: for dietary concerns and malnutrition.
- Healthcare provider (HCP): for symptoms of infections such as elevated body temperature, elevated white blood cell count, or increasing malaise.
- Psychologic support may be needed and can include referrals to:
- Social worker
- Chaplain or clergy.
- Family members should be included in discussions regarding care and referral.
Acute Kidney Injury (AKI)
- Sudden decline in kidney function, impacting filtration, fluid balance, and electrolyte/acid-base regulation.
- Leads to waste product accumulation (urea, creatinine) known as azotemia.
Types of AKI
- Prerenal AKI: Reduced blood flow to kidneys (e.g., hypovolemia)
- Intrarenal AKI: Direct kidney tissue damage (e.g., nephrotoxins, infections, ischemia leading to acute tubular necrosis [ATN]).
- Postrenal AKI: Obstruction in urine flow (e.g., stones, tumors).
Phases of AKI
- Initiation Phase: Initial injury, often asymptomatic.
- Maintenance Phase: Significant GFR reduction, leading to fluid retention, electrolyte imbalance, and metabolic acidosis.
- Recovery Phase: Gradual improvement in renal function, urine output increases as tubular cells regenerate.
Critical Issues in AKI
- Fluid and Electrolyte Imbalances: Can cause hyperkalemia, hyperphosphatemia, hyponatremia, and metabolic acidosis. Impacts cardiac & neurological health.
- Systemic Impact: Fluid retention causes hypertension, edema, pulmonary congestion. Electrolyte imbalances cause muscle weakness, cardiac dysrhythmias, and mental status changes.
- Infection Risk: Increased susceptibility to infections due to compromised immunity.
Outcomes and Prognosis
- Reversibility: AKI often reversible with early identification and treatment.
- Prolonged AKI or repeated episodes increase risk of chronic kidney disease (CKD).
- Vulnerable Populations: Older adults, children, and pregnant women. Older adults have age-related GFR decline, increasing AKI risk when exposed to stressors (surgery, sepsis, nephrotoxic medications).
Normal Kidney Function
- Filters blood and removes waste products: The kidneys filter about 120-130 mL/minute of blood plasma, removing urea, creatinine, and other waste products.
- Regulates fluid and electrolyte balance: Kidneys adjust urine concentration to maintain hydration, and selectively reabsorb or excrete electrolytes like sodium, potassium, calcium, and phosphorus.
- Maintains acid-base homeostasis: They excrete hydrogen ions and reabsorb bicarbonate to regulate blood pH.
- Regulates blood pressure through the RAAS system: Kidneys produce renin, an enzyme that helps control blood pressure and fluid balance, by influencing the release of aldosterone.
- Produces erythropoietin: This hormone stimulates red blood cell production in the bone marrow.
- Activates vitamin D: This is essential for calcium absorption and bone health.
-
Normal lab values:
- Serum creatinine: 0.6-1.2 mg/dL.
- Blood urea nitrogen (BUN): 7-20 mg/dL.
- Electrolytes: sodium (135-145 mEq/L), potassium (3.5-5.0 mEq/L), calcium (8.5-10.2 mg/dL), phosphorus (2.5-4.5 mg/dL).
- Normal urine characteristics: Clear, amber-colored, pH around 6.0, free of blood cells, protein, or glucose.
Filtration and Waste Removal Alterations
- Decreased Glomerular Filtration Rate (GFR): A decline in GFR indicates the kidneys are not filtering blood efficiently, resulting in waste product buildup.
- Azotemia: Elevated blood urea nitrogen (BUN) and creatinine levels are hallmarks of azotemia, a sign of impaired waste elimination by the kidneys.
- Uremia: The accumulation of urea and other toxins in the blood due to impaired kidney function manifests as uremia, leading to symptoms such as fatigue, nausea, and changes in mental status.
Fluid and Electrolyte Imbalance
- Fluid Volume Excess (FVE): Impaired kidney function can lead to fluid overload, causing edema, hypertension, and pulmonary congestion.
- Hyperkalemia: Increased potassium levels in the blood are a consequence of the kidneys' inability to excrete potassium effectively, potentially causing muscle weakness and cardiac arrhythmias.
- Hyponatremia: Fluid overload can contribute to low sodium levels, leading to symptoms such as confusion, seizures, and coma.
- Hyperphosphatemia and Hypocalcemia: Kidney dysfunction affects phosphate excretion and calcium absorption, leading to high phosphate and low calcium levels, which can compromise bone health.
- Metabolic Acidosis: Reduced excretion of hydrogen ions and bicarbonate reabsorption leads to a buildup of acids in the blood, resulting in metabolic acidosis.
Acid-Base Balance Alterations
- Metabolic Acidosis: The buildup of acids in metabolic acidosis is a direct consequence of the kidneys' diminished ability to excrete hydrogen ions and retain bicarbonate.
Blood Pressure Dysregulation
- Hypertension: Fluid retention and activation of the renin-angiotensin-aldosterone system (RAAS) contribute to hypertension, potentially exacerbating kidney damage.
- Hypotension: Reduced blood volume or cardiac output in some cases impacts renal perfusion and function, leading to hypotension.
Hormone Production Alterations
- Anemia: Reduced erythropoietin production by the kidneys leads to a decrease in red blood cell production, causing fatigue and pallor.
- Vitamin D Deficiency: The kidneys' inability to effectively convert vitamin D to its active form leads to impaired calcium absorption and bone health issues.
Urine Output Alterations
- Oliguria: A low urine output, often less than 400 mL per day, indicates impaired kidney function.
- Anuria: Extremely low or no urine output is indicative of severe kidney impairment.
- Proteinuria and Hematuria: The presence of protein or blood in the urine reflects damage to the glomeruli.
- Changes in Urine Concentration and Specific Gravity: Altered ability to concentrate or dilute urine results in abnormal urine osmolarity.
Immune System Alterations
- Increased Infection Risk: Patients with AKI are more susceptible to infections due to impaired immunity and potential catheter use.
Skin and Tissue Changes
- Edema and Skin Integrity Issues: Fluid retention can lead to edema, particularly around the eyes, extremities, or areas dependent on gravity, increasing the risk of skin breakdown.
- Pruritus (Itching): Uremia often causes pruritus due to accumulation of toxins.
Observation/Patient Interview
- Anorexia, Nausea, and Vomiting: These symptoms are common in AKI due to the buildup of waste products, which can cause a metallic taste and gastrointestinal upset.
- Weight Gain or Edema: Fluid retention is a hallmark of AKI.
- Fatigue and Weakness: This is often attributed to anemia, fluid imbalances, or the effect of uremia, a buildup of waste products in the blood.
- Exposure to Nephrotoxins: It is essential to inquire about the recent use of medications or procedures involving contrast media, such as NSAIDs or aminoglycosides, as they can damage the kidneys.
- Medical History: Check for chronic conditions like diabetes, hypertension, heart disease, or kidney disease, which can predispose the patient to AKI.
- Recent Procedures or Transfusion Reactions: Surgery, trauma, or reactions to blood transfusions are risk factors for AKI.
- Fluid Loss Events: Episodes of vomiting, diarrhea, or hemorrhage can lead to hypovolemia and reduced kidney perfusion.
Physical Exam
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Blood Pressure: Hypertension is common in fluid overload, while hypotension may indicate hypovolemia.
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Heart Rate and Rhythm: Tachycardia (rapid heartbeat) points to fluid volume changes. Irregular heart rhythms can indicate electrolyte imbalances.
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Respiratory Rate: Tachypnea (rapid breathing) can suggest metabolic acidosis.
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Urine Output and Characteristics: Monitor for oliguria (low output) or anuria (almost no output). Assess the clarity and specific gravity of urine. Hematuria (blood in urine) and proteinuria indicate kidney damage.
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Weight: Daily weight checks are vital for monitoring fluid shifts.
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Skin and Edema: A pale complexion (pallor) may indicate anemia. Cool or mottled skin suggests poor perfusion. Look for periorbital, peripheral, or dependent edema (swelling) as indicators of fluid overload.
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Peripheral Pulses and Neck Veins: Assess pulse quality for weakness or bounding, providing clues about fluid status. Jugular vein distention (JVD) suggests fluid overload and potential heart involvement.
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Auscultation: Listen for crackles or rales in the lungs, which can indicate pulmonary edema. Irregular heart sounds might suggest electrolyte imbalances or fluid overload. Decreased bowel sounds can occur with AKI, especially in cases of uremia.
Urinalysis
- Examines urine for signs of kidney dysfunction and underlying causes
- Fixed Specific Gravity (around 1.010): Indicates inability of the kidneys to concentrate urine, a sign of renal tubular damage
- Proteinuria: Presence of protein may suggest glomerular damage
- Hematuria: Blood in the urine can indicate glomerular injury or inflammation
- Casts (RBC, WBC, or epithelial casts): Suggests acute tubular necrosis (ATN) or other forms of renal damage, as casts are formed from cellular debris in damaged tubules
Serum Creatinine
- Measures kidney function and the ability to filter waste from the blood
- Elevated Levels: Rapidly rising creatinine (over days) is a hallmark of AKI, as kidneys fail to clear creatinine from the blood effectively
- Normal creatinine levels are typically 0.6–1.2 mg/dL in adults
Blood Urea Nitrogen (BUN)
- Indicates waste buildup in the blood
- Increased Levels: Elevated BUN suggests impaired kidney function and reduced excretion of nitrogenous wastes
- A BUN level above 20 mg/dL is often seen in AKI
Serum Electrolytes
- Evaluates fluid and electrolyte imbalances
- Hyperkalemia (Potassium > 5.0 mEq/L): Indicates impaired potassium excretion, which can lead to muscle weakness and cardiac dysrhythmias
- Hyponatremia (Sodium < 135 mEq/L): Reflects fluid retention or dilution, common in AKI, leading to confusion and potential seizures
- Hyperphosphatemia (Phosphorus > 4.5 mg/dL) and Hypocalcemia (Calcium < 8.5 mg/dL): High phosphate levels with low calcium can result from impaired kidney excretion and lead to muscle cramps, tingling, and tetany
Arterial Blood Gases (ABGs)
- Assesses for metabolic acidosis, a common complication of AKI
- Metabolic Acidosis (Low pH < 7.35, low bicarbonate): Indicates kidney failure to excrete hydrogen ions or reabsorb bicarbonate, affecting acid-base balance
Complete Blood Count (CBC)
- Evaluates for anemia and infection
- Low Hemoglobin and Hematocrit: Suggests anemia, which can occur due to decreased erythropoietin production in AKI
- Elevated White Blood Cell (WBC) Count: May indicate infection, which is a leading cause of death in AKI patients
Renal Ultrasound
- Visualizes kidney size, structure, and any possible obstructions
- Enlarged Kidneys: Could indicate acute kidney injury or inflammation
- Small, Shrunken Kidneys: More suggestive of chronic kidney disease (CKD) rather than AKI
- Obstructions: Detects stones, tumors, or other blockages in the urinary tract, potentially indicating postrenal AKI
CT Scan (without contrast)
- Provides a detailed image of kidney structures and assesses for masses or obstructions
- Kidney Enlargement or Masses: May suggest intrinsic kidney damage or pathology
- Obstructions: Confirms blockages that could contribute to postrenal AKI
Renal Biopsy (if necessary)
- Identifies specific causes of kidney injury, particularly if glomerular or other specific tissue damage is suspected
- Glomerulonephritis or Tubular Necrosis: Provides histological evidence of damage to kidney tissues, helping to diagnose specific types of intrinsic AKI
Pharmacologic Interventions
- Diuretics like Furosemide and Bumetanide are used to increase urine output when renal perfusion is restored but urine production remains low. They can also help clear nephrotoxins from the kidneys if they are the cause of AKI.
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Electrolyte Modifiers are used to manage electrolyte imbalances:
- Potassium-Binding Agents like Sodium Polystyrene Sulfonate remove potassium from the body to manage hyperkalemia.
- Calcium Gluconate or a combination of Insulin and Glucose temporarily shift potassium into cells, lowering serum potassium levels in hyperkalemia.
- Antihypertensives like ACE Inhibitors help control blood pressure to prevent further renal damage and reduce strain on the heart.
- Phosphate Binders like Sevelamer are used to control elevated phosphate levels in hyperphosphatemia.
- Erythropoietin is given to treat anemia caused by decreased erythropoietin production, though this is more common in chronic kidney conditions.
- Antiemetics and GI Medications like Famotidine manage nausea and prevent gastrointestinal bleeding, which is common in AKI patients.
Non-Pharmacologic Interventions
- Fluid Management involves adjusting fluid intake based on the patient's fluid volume status. Fluid may be restricted for fluid overload, or given cautiously to maintain perfusion for hypovolemic patients.
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Dietary Modifications are crucial:
- Protein Restriction helps reduce nitrogenous waste load on the kidneys. Protein intake is often limited to high-biological-value proteins.
- Electrolyte Management involves restricting potassium, phosphorus, and sodium intake as needed.
- Increased Carbohydrate Intake provides calories while sparing protein for healing.
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Monitoring and Vital Sign Assessment are critical for early detection of imbalances:
- Hourly Intake and Output monitoring
- Daily Weights
- Frequent Electrolyte Checks
- Positioning in the semi-Fowler's position can improve respiratory function, especially in cases of fluid overload and risk of pulmonary edema.
Collaborative Interventions
- Nutritional Consultation with a dietitian ensures meals meet specific needs for protein, calories, and electrolyte restrictions while considering cultural and personal preferences for better adherence.
- Nephrology Consult provides specialized guidance for AKI management, particularly if dialysis or other advanced interventions are needed.
- Infection Control Team minimizes infection risk, especially when central lines or catheters are in place, ensuring aseptic technique during procedures.
- Physical Therapy maintains mobility and muscle strength, particularly for patients with fluid retention or fatigue limiting movement.
Surgical Interventions
- Placement of Vascular Access for Dialysis involves surgical placement of a central line or an arteriovenous fistula/graft for hemodialysis or continuous renal replacement therapy (CRRT) when required.
- Treatment of Underlying Obstructions in postrenal AKI involves surgical removal of stones, tumors, or other blockages in the urinary tract.
- Nephrectomy or Partial Nephrectomy may be necessary to remove part of a kidney in severe cases with intrinsic damage due to infection or necrosis.
Dialysis and Renal Replacement Therapies
- Hemodialysis rapidly removes waste products and fluid, used for life-threatening electrolyte imbalances or uremia not manageable otherwise.
- Peritoneal Dialysis provides gradual fluid and solute removal, usually when hemodialysis is contraindicated due to hemodynamic instability.
- Continuous Renal Replacement Therapy (CRRT) is a slower, continuous dialysis option for critically ill patients unable to tolerate standard hemodialysis.
Patient and Family Education
- Understanding Medications and Side Effects: Patients are educated on nephrotoxic medications to avoid, the importance of medication adherence, and potential side effects.
- Self-Monitoring Techniques: Patients learn how to monitor blood pressure, weight, and fluid intake.
- Signs of Complications: Patients are taught to recognize symptoms of fluid overload, electrolyte imbalances, and infection, encouraging early reporting.
Evaluating the Outcomes of Interventions for AKI
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Effective Interventions:
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Fluid, Electrolyte, and Acid-Base Balance Restored:
- Normal Urine output (greater than 30 mL/hr for adults), stable weight, normal skin turgor, and absence of edema or dehydration.
- Stable serum potassium, sodium, calcium, and phosphorus levels and balanced blood pH (7.35–7.45).
- Stable vital signs, including blood pressure, heart rate, and respiratory rate.
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Improved Kidney Function Indicators:
- Stable or decreasing serum creatinine and BUN levels.
- Urine is clear, normal color and specific gravity, without proteinuria or hematuria.
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Nutritional and Hydration Needs Met:
- Patient maintains or returns to baseline weight, has an adequate appetite, and displays no symptoms of malnutrition or fluid imbalance.
- Patient consumes meals and snacks as recommended.
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Absence of Secondary Complications:
- No signs of infection (fever or elevated WBC count).
- Skin integrity maintained.
- Patient and family demonstrate an understanding of the disease process, self-monitoring skills, and adherence to fluid, dietary, and medication guidelines.
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Fluid, Electrolyte, and Acid-Base Balance Restored:
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Ineffective Interventions
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Persistent Fluid or Electrolyte Imbalances:
- Continued edema, weight fluctuations, or abnormal urine output (oliguria or anuria).
- Abnormal potassium, sodium, calcium, or phosphorus levels, or imbalanced blood pH potentially leading to muscle weakness, cardiac dysrhythmias, or neurological issues.
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Kidney Function Not Improving:
- Persistent elevation in waste levels (rising serum creatinine and BUN) indicates ongoing kidney dysfunction.
- Decreased or worsening urine output (reduced, dark, or concentrated urine, possibly with persistent protein or blood present).
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Inadequate Nutritional Intake and Weight Loss:
- Ongoing anorexia, nausea, or visible weight loss, indicating unmet nutritional needs.
- Insufficient dietary intake that does not meet protein and calorie needs.
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Emergence of Secondary Complications:
- Elevated temperature, WBC count, or evidence of localized infection (e.g., at vascular access sites).
- Skin breakdown or pressure ulcers.
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Knowledge Deficits or Poor Self-Care Adherence:
- Difficulty following dietary, fluid or medication guidelines, increasing risk of recurrent or worsening AKI.
- Patient does not consistently monitor blood pressure, weight, or fluid balance, leading to undetected complications.
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Persistent Fluid or Electrolyte Imbalances:
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Next Steps if Interventions are Ineffective:
- Reassess Treatment Plan: Review fluid management, medication effectiveness, and dietary strategies, collaborate with specialists.
- Increase Monitoring Frequency: Tighten monitoring of vital signs, electrolytes, I&O, and weight.
- Consider Dialysis or Advanced Support: Discuss initiation of dialysis or CRRT if kidney function continues to decline.
- Provide Additional Education: Reinforce patient and family education on self-care, emphasizing critical signs to report and steps to improve adherence.
AKI in Pregnancy
- Pregnancy increases glomerular filtration rate (GFR) by up to 50%, making AKI diagnosis challenging.
- Pregnant patients may experience fluid-related complications due to increased blood volume.
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First Trimester:
- Hyperemesis gravidarum (severe nausea/vomiting) and placenta previa increase AKI risk by causing dehydration and blood loss.
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Later Stages of Pregnancy:
- Gestational hypertension, preeclampsia, and eclampsia can strain the kidneys, leading to proteinuria, hydronephrosis, and AKI.
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Postpartum Period:
- AKI can result from postpartum hemorrhage or infections like puerperal sepsis.
- Over 90% of pregnant women experience physiological hydronephrosis, increasing the risk of urinary stasis and infection, further raising AKI risk.
- Management: Close monitoring of blood pressure, fluid status, and renal function is essential. Treatment options must be carefully chosen to avoid harming both the mother and fetus, and nephrotoxic medications should be avoided or used cautiously.
AKI in Children and Adolescents
- AKI is rare in childhood but has a high mortality rate, especially when linked to severe underlying illness.
- Infants: AKI is often related to prematurity, congenital anomalies, or complications like asphyxia during birth.
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Children: AKI can result from:
- Hemolytic Uremic Syndrome (HUS).
- Acute Glomerulonephritis.
- Sepsis, dehydration, or trauma.
- Children may present with nausea, vomiting, edema, hypertension, lethargy, and gross hematuria. Electrolyte imbalances, fluid overload, uremia, and azotemia are common.
- Nutritional Needs: Growing children may require additional calories and protein, especially high-biological-value proteins (e.g., eggs, poultry, fish) to support growth. However, protein intake should still be moderated to reduce nitrogenous waste.
- Management: Fluid and electrolyte imbalances are carefully monitored. Treatment often includes frequent, small meals, antiemetics, and possibly parenteral nutrition if needed. Family education on signs of complications and fluid restrictions is crucial.
AKI in Older Adults
- Older adults are more susceptible to AKI due to age-related decline in kidney function and reduced ability to compensate for fluid and electrolyte changes.
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Contributing Factors:
- Age-Related Decline in GFR: Reduces kidney resilience and ability to filter efficiently.
- Comorbidities: Conditions like hypertension, diabetes, heart disease, chronic kidney disease (CKD), and liver disease, increase AKI risk.
- Hospitalization and Procedures: Prolonged hospital stays, surgery, and exposure to nephrotoxic drugs or contrast media raise AKI risk.
- Older adults may not present typical AKI symptoms; instead, they might show changes in mental status, fatigue, or mild gastrointestinal symptoms.
- Medication Caution: Reduced kidney function affects drug clearance, so dosages of nephrotoxic and other medications need careful adjustment.
- Management: Frequent monitoring of weight, I&O, and serum electrolytes is essential. Special attention to blood pressure management and the prevention of dehydration is critical, as is avoiding nephrotoxic medications whenever possible.
Understanding AKI and Its Causes
- AKI is a temporary but serious reduction in kidney function.
- This impacts the kidneys' ability to filter waste, balance fluids, and regulate electrolytes.
- Causes can be diverse and specific to the patient, such as dehydration, medications, infections, and underlying health conditions.
Managing Fluid and Dietary Restrictions
- Fluid Intake: Patients may be given specific fluid restrictions to prevent fluid overload. Measuring and monitoring intake is important.
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Dietary Modifications:
- Protein: Depending on the patient's situation, there might be restrictions on protein intake, with emphasis on high-biological-value proteins when necessary.
- Low-Potassium and Low-Phosphorus Foods: Patients may be advised to avoid foods high in potassium (e.g., bananas, oranges, potatoes) and phosphorus (e.g., dairy, nuts).
- Sodium: Limiting salty foods and processed foods is important for patients on a sodium-restricted diet.
- Healthy Eating Habits: It's suggested to eat small, frequent meals and snacks to manage nausea or a poor appetite.
Monitoring for Complications
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Fluid Imbalance:
- Overload: Symptoms include swelling in the legs or face, shortness of breath, rapid weight gain, and elevated blood pressure.
- Deficiency: Symptoms include dizziness, dry mouth, decreased urine output, and sudden weight loss.
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Electrolyte Imbalance:
- Hyperkalemia: Muscle weakness, irregular heartbeat, numbness or tingling.
- Hyponatremia: Confusion, headache, seizures.
- Hypocalcemia: Muscle cramps, tingling in fingers, seizures.
- Daily Monitoring: Patients should check their weight, blood pressure, and pulse daily to monitor for changes.
Medication Education
- Nephrotoxic Drugs: Patients should be informed about medications that can harm their kidneys, such as NSAIDs, certain antibiotics, and contrast dyes. These should be avoided during recovery.
- Prescription Adherence: Patients should follow their prescribed medication regimens, especially antihypertensives and medications to manage electrolyte imbalances.
- Side Effects: Patients should be informed about potential side effects of their medications and when to contact their healthcare provider.
Preventing Future Episodes of AKI
- Hydration: Staying hydrated is important, but overhydration should be avoided, especially during physical activity or illness.
- Infection Prevention: Good handwashing practices, limiting close contact with sick individuals, and following post-discharge infection control guidelines are vital.
- Regular Follow-up: Regular follow-up appointments for monitoring kidney function and ongoing care are essential.
Educating on Recovery and Lifestyle Modifications
- Temporary Nature of AKI: Most cases of AKI are reversible, but lifestyle changes may be necessary to prevent further kidney stress.
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Dietary and Fluid Adjustments:
- Some dietary and fluid restrictions may continue after discharge.
- Long-term adjustments may be needed based on the patient's kidney function.
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Long-Term Kidney Health:
- Maintaining a balanced diet, managing chronic conditions (e.g., diabetes, hypertension), and limiting alcohol are vital for long-term kidney health.
Involving Family and Caregivers
- Support with Monitoring: Family members should understand the patient's fluid and dietary needs to help with meal planning and intake monitoring.
- Recognizing Warning Signs: Caregivers should be informed about signs of complications and encouraged to promptly contact the healthcare team if symptoms arise.
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Emotional Support:
- AKI and hospitalization can be emotionally distressing, so families should provide emotional support and help the patient with lifestyle changes.
Additional Guidance for Specific Populations
- Pregnant Women: Manage blood pressure carefully and avoid nephrotoxic medications to protect both mother and fetus.
- Children and Adolescents: Use age-appropriate language and involve parents in understanding fluid restrictions, diet needs, and signs of AKI complications.
- Older Adults: Focus on preventing dehydration, managing existing health conditions, and avoiding medications that could harm kidney function.
Key Point:
- Empowering patients and their families with knowledge about AKI management and prevention is crucial for better adherence to treatment and improved outcomes.
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Test your knowledge on kidney functions, renal failure, and acute kidney injury (AKI). This quiz covers critical aspects of how kidneys maintain homeostasis, the types of renal failure, and the causes of AKI. Perfect for students of human biology and healthcare professionals.