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Questions and Answers
What is a common consequence of acute kidney injury (AKI) on bodily functions?
Which of the following factors can lead to acute kidney injury?
What differentiates acute kidney injury (AKI) from chronic kidney disease (CKD)?
In renal failure, what bodily imbalance can occur as a result of kidney dysfunction?
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What physiological response occurs in the body to accommodate the excess fluid due to renal failure?
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How does acute kidney injury typically present in hospitalized patients?
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What changes in laboratory findings are usually observed in cases of acute kidney injury?
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Which of the following conditions is NOT typically a cause of acute kidney injury?
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What is the nature of acute kidney injury (AKI)?
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Which statement accurately reflects a cause of acute kidney injury (AKI)?
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How is acute kidney injury (AKI) characterized in terms of laboratory findings?
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Which of these conditions is least likely to contribute to the onset of acute kidney injury (AKI)?
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What is a significant risk factor that increases the vulnerability of kidneys to injury?
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What is a potential physiological consequence of decreased red blood cells (RBCs)?
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Which treatment is most commonly associated with addressing fluid volume excess in patients with AKI?
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What is a clinical manifestation indicative of hyperkalemia?
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Which of the following interventions is least likely to be used for managing hyperkalemia?
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What phase of acute kidney injury (AKI) begins with the initiating event and ends with tubular injury?
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Which symptom is directly associated with respiratory distress in a patient with fluid volume excess?
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Which of the following indicates a potential renal complication involving cardiac function?
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What is a common clinical approach for treating low red blood cell counts in patients?
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What is a primary concern in the maintenance phase of acute kidney injury (AKI)?
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Which symptom is indicative of severe hyperkalemia during the maintenance phase of AKI?
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What characterizes the recovery phase of acute kidney injury (AKI)?
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Which of the following complications is most likely due to electrolyte imbalances in the maintenance phase of AKI?
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How do electrolytes such as phosphate and calcium change in the maintenance phase of acute kidney injury?
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What is a common central nervous system effect seen during the maintenance phase of AKI?
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Which is a characteristic of nonoliguric acute kidney injury (AKI)?
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What is likely to occur in the absence of intervention during the prolonged maintenance phase of AKI?
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What is a common laboratory finding associated with acute kidney injury (AKI)?
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Which imaging technique is preferred to assess kidney structure with minimal nephrotoxic effects?
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Which electrolyte imbalance is commonly observed in patients with acute kidney injury?
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What does an increased serum potassium level during acute kidney injury typically indicate?
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What is likely to show on arterial blood gas (ABG) studies in patients with acute kidney injury?
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What is the key goal when managing a patient who has developed acute kidney injury (AKI)?
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Which of the following is an important aspect of preventing acute kidney injury (AKI) when nephrotoxic drugs must be used?
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What abnormal finding is typically observed in urinalysis of a patient with AKI?
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Which of the following serum changes is expected shortly after the onset of acute kidney injury (AKI)?
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What activity should be encouraged for patients upon discharge after an AKI event regarding nephrotoxic drugs?
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Which is a critical component of managing acute kidney injury (AKI)?
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What type of urine casts might be present in cases of acute kidney injury (AKI)?
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Which of the following actions can help reduce the risk of AKI when nephrotoxic agents must be utilized?
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Study Notes
Renal Function
- Kidneys control fluid and electrolyte balance, acid-base balance and blood pressure; they are vital for homeostasis.
- One functioning kidney is sufficient for maintaining homeostasis; this is common in patients with a single transplanted kidney.
- Renal failure occurs when both kidneys fail to function; this results in fluid accumulation, electrolyte imbalances, and altered blood values like hemoglobin, hematocrit, BUN and creatinine.
- Heart rate increases as the body tries to accommodate excess fluid; muscle function is affected by electrolyte imbalances.
- Cerebral edema can occur; untreated renal failure leads to death within a few days.
Renal Failure
- Renal failure is characterized by the kidneys' inability to remove accumulated metabolites, leading to altered fluid, electrolyte, and acid-base balance.
- Causes include primary kidney disorders, systemic diseases, and urological defects.
- The condition can be acute or chronic.
- Acute renal failure has a sudden onset and may be reversible with prompt intervention.
- Chronic Kidney Disease (CKD) is a silent condition with gradual progression and few symptoms until severe kidney damage occurs.
Acute Kidney Injury (AKI)
- Previously referred to as Acute Renal Failure (ARF), AKI is a rapid decline in kidney function.
- It is characterized by a decrease in kidney excretory function, alongside increases in creatinine and urea levels.
- AKI affects ~13-18% of hospital admissions.
- The most common causes are ischemia (insufficient blood supply) and exposure to nephrotoxins (substances damaging nerves or nerve tissue).
- The kidneys are vulnerable to these factors due to their high blood flow.
- Other causes of AKI include major surgery, sepsis, and severe pneumonia.
Renal Failure
- Renal failure is a condition where the kidneys cannot remove waste products from the blood, leading to fluid, electrolyte, and acid-base imbalances.
- Renal failure can be caused by primary kidney problems or secondary issues arising from systemic diseases or urological defects.
- Renal failure can be acute or chronic.
- Acute renal failure (ARF) has a sudden onset and can often be reversed with immediate treatment.
- Chronic kidney disease (CKD) progresses gradually with few symptoms until the kidneys are severely damaged.
Acute Kidney Injury (AKI)
- AKI, previously called ARF, is a rapid decrease in kidney function accompanied by increased creatinine and urea levels in the blood.
- AKI affects 13-18% of hospitalized patients.
- The most common causes of AKI are ischemia (lack of blood supply) and exposure to nephrotoxins (substances that damage kidneys).
- Kidneys are susceptible to these factors because of the large volume of blood flowing through them.
- Low blood pressure or volume can cause kidney tissue ischemia.
- Nephrotoxins in the bloodstream directly damage renal tissue.
- Other causes of AKI include major surgery, sepsis, and severe pneumonia.
Decreased RBCs
- Decreased red blood cell count can lead to fatigue, pallor, dizziness, confusion, lethargy, tachycardia, tachypnea, and hypotension.
- Treatment options include iron supplementation, administration of epoetin, and blood transfusion.
Fluid Volume Excess
- Fluid volume excess can lead to dependent pitting edema, respiratory crackles, dyspnea, pulmonary edema, hypoxemia, weight gain, tachycardia, and jugular vein distention.
- Treatment options include fluid restriction, sodium-restricted diet, diuretics, and dialysis.
Hyperkalemia
- Hyperkalemia can cause ventricular arrhythmias, tall, peaked T waves, widened QRS, cardiac arrest, smooth muscle hyperactivity, nausea and vomiting, abdominal cramping, diarrhea, muscle weakness, paresthesias, and flaccid paralysis.
- Treatment options include removal of potassium from IV solutions, a low-potassium diet, administration of glucose and insulin to increase cellular glucose uptake, potassium-absorbing oral or enema solutions, and dialysis.
Initiation Phase of AKI
- This phase may last hours to days.
- Begins with the initiating event (e.g., hemorrhage).
- Ends when tubular injury occurs.
- Prognosis is good if the initiating event is treated effectively.
- Often Asymptomatic, making it difficult to identify AKI before the maintenance phase.
Maintenance Phase of AKI
- Characterized by a significant fall in GFR and tubular necrosis.
- Oliguria may develop, although many patients continue to produce normal or near-normal amounts of urine (nonoliguric AKI).
- Kidney cannot efficiently eliminate metabolic wastes, water, electrolytes, and acids from the body.
- Azotemia, fluid retention, electrolyte imbalances, and metabolic acidosis develop.
- More severe in patients with oliguria, leading to a poorer prognosis.
- Salt retention and water retention cause edema, increasing the risk for heart failure and pulmonary edema.
- Impaired potassium excretion leads to hyperkalemia
- When serum potassium level is greater than 6.0 to 6.5 mEq/L, manifestations of its effect on neuromuscular function develop, including muscle weakness, nausea and diarrhea, electrocardiographic changes, and possible cardiac arrest.
- Other electrolyte imbalances include hyperphosphatemia and hypocalcemia.
- Metabolic acidosis results from impaired hydrogen ion elimination by the kidneys.
- Anemia develops after several days of AKI due to suppressed erythropoietin secretion by the kidneys.
- Immune function may be impaired, increasing the risk for infection.
- Other manifestations include confusion, disorientation, agitation, or lethargy; hyperreflexia; and possible seizures or coma because of azotemia and electrolyte and acid–base imbalances.
- Anorexia, nausea, vomiting, and decreased or absent bowel sounds.
- Uremic syndrome (if AKI is prolonged).
Recovery Phase of AKI
- Characterized by a process of tubule cell repair and regeneration and gradual return of the GFR to normal or pre-AKI levels.
- Diuresis (excretion of abnormally large quantities of urine) may occur as the nephrons and GFR recover, promoting the excretion of retained salt, water, and solutes.
- Serum creatinine, BUN, potassium, and phosphate levels remain high and may continue to rise in spite of increasing urine output.
- Renal function improves rapidly during the first 5 to 25 days of the recovery phase and continues to improve for up to 1 year.
AKI - Maintaining Adequate Renal Perfusion
- Maintaining adequate vascular volume, cardiac output and blood pressure key in preserving kidney perfusion
- Avoiding nephrotoxic drugs whenever possible
Reducing Risk of AKI with Nephrotoxic Drugs
- Using minimum effective dose of nephrotoxic drugs
- Maintaining hydration
- Eliminating other known nephrotoxins from the medication regimen
Discharging Patients with Instructions to Avoid Nephrotoxic Drugs
- Nurse should encourage patients to contact their pharmacist to add this information to the patient’s pharmacy history
- This will help the patient to avoid nephrotoxic drugs that may be prescribed in the future.
Fluid and Electrolyte Balance in AKI
- Maintaining the fluid and electrolyte balance is a key goal in managing AKI
Goals in the Treatment of AKI
- Identifying and correcting the underlying cause
- Preventing additional kidney damage
- Restoring the urine output and kidney function
- Compensating for renal impairment until kidney function is restored
Diagnostic Tests for AKI
- Urinalysis often reveals abnormalities such as:
- A fixed specific gravity of 1.010
- Proteinuria
- Presence of red blood cells (RBCs), white blood cells (WBCs), and renal tubular epithelial cells
- Cell casts
Serum Creatinine and BUN
- Used to evaluate renal function
- Serum creatinine levels increase rapidly within 24 to 48 hours of onset
- Creatinine levels generally peak within 5 to 10 days
- Creatinine and BUN levels tend to increase more slowly when urine output is maintained
- The onset of recovery is marked by a halt in the rise of the serum creatinine and BUN
Serum Electrolytes
- Monitored to evaluate the fluid and electrolyte status
- Serum potassium rises at a moderate rate
- Hyponatremia is common due to the water excess associated with AKI
Arterial Blood Gas (ABG) Studies
- Often show a metabolic acidosis caused by the kidneys’ inability to adequately eliminate metabolic wastes and hydrogen ions
Complete Blood Count (CBC)
- Shows reduced RBCs, moderate anemia, and a low hematocrit
- AKI affects erythropoietin secretion and RBC production
- Iron and folate absorption may also be impaired, further contributing to anemia
Renal Ultrasonography
- Used to identify obstructive causes of renal failure
- Differentiates AKI from end-stage renal disease (ESRD)
- In AKI, the kidneys may be enlarged, whereas in CKD, they typically appear small and shrunken.
Computed Tomography (CT) Scan
- Evaluates kidney size and identifies possible obstructions
IV Pyelography, Retrograde Pyelography, and Antegrade Pyelography
- Used to evaluate kidney structure and function
- Radiologic contrast media used with extreme caution due to potential nephrotoxicity
- Retrograde pyelography and antegrade pyelography are preferred because they have fewer nephrotoxic effects than IV pyelography
Renal Biopsy
- May be necessary to differentiate between acute and chronic kidney disease
Imaging Studies in Children
- Assist with the assessment of kidney structures, renal blood flow, and renal perfusion and function
- Determine whether a child has AKI or CKD
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Description
This quiz explores the vital roles of the kidneys in maintaining homeostasis, including fluid and electrolyte balance, acid-base balance, and blood pressure regulation. It also covers the causes and implications of renal failure, including acute and chronic forms and their effects on the body. Test your knowledge on kidney function and failure.
