Acute Kidney Injury (AKI)

In a patient presenting with elevated BUN and normal creatinine levels, which condition is the most likely underlying cause?

A patient diagnosed with acute tubular necrosis (ATN) is likely to present with which specific urinary finding?

Which class of the following medications is least likely to be implicated in nephrotoxicity leading to intrarenal damage?

A patient presents with signs of heavy metal poisoning, reporting a garlic taste in their mouth. Which specific heavy metal exposure should be immediately investigated as a potential cause of acute kidney injury?

Which of the following conditions primarily affects the kidney by directly damaging the nephrons, potentially leading to a decrease in GFR and subsequent renal dysfunction?

In a patient presenting with clinical signs of dehydration, which of the following changes in the BUN/creatinine ratio would be most indicative of a fluid volume deficit contributing to acute kidney injury?

How does the urine specific gravity change when a urine sample is refrigerated before testing and why?

During the oliguric phase of acute kidney injury (AKI), which of the following mechanisms primarily contributes to the reduction in urine output?

In the context of kidney function, what is the most accurate interpretation of the phrase 'Fluid volume overload' with respect to the BUN/creatinine ratio?

What are the primary characteristics of the oliguric phase of acute kidney injury (AKI)?

In the context of renal failure, which intervention directly targets the regulation of erythropoietin production and oxygen sensing at the cellular level?

How does chronic renal failure primarily differ from acute renal failure in terms of functional recovery?

Which of the following interventions is least likely to directly address the underlying mechanisms of renal failure?

In what primary way does the progression of kidney function loss differ between acute and chronic renal failure?

Considering the multifaceted impact of renal failure, which of the following functions is least directly compromised when the kidneys fail?

A patient presents with acute kidney injury (AKI) due to hypovolemia resulting from severe vomiting and diarrhea. Beyond fluid resuscitation, which of the following interventions would MOST directly address the underlying pre-renal etiology of the AKI?

A patient with a history of chronic heart failure develops pre-renal acute kidney injury (AKI). Which of the following mechanisms contributes MOST significantly to the decreased renal perfusion in this patient?

A patient with severe burns develops pre-renal acute kidney injury (AKI). Which of the following pathophysiological processes BEST explains the development of AKI in this scenario?

Following a motor vehicle accident, a patient develops acute kidney injury (AKI) secondary to hemorrhagic shock. Which of the following compensatory mechanisms is MOST likely to be activated initially to maintain renal perfusion in this pre-renal state?

A patient with acute pancreatitis develops pre-renal acute kidney injury (AKI). Which of the following mechanisms MOST directly contributes to reduced renal perfusion in this patient?

In a patient experiencing acute renal failure, which scenario would lead to the most significant elevation of serum creatinine (S. Creat)?

A patient's lab results show a BUN of 25 mg/dL and S. Creat of 1.4 mg/dL. Considering the provided reference ranges and causes of renal failure, which condition is LEAST likely to be the primary diagnosis?

If a patient's acute renal failure is determined to be caused by a prerenal factor, what would be the MOST effective initial intervention?

In the context of acute renal failure, how does the concept of 'reversible decrease in GFR' relate to the progression of kidney injury?

Which of the following scenarios BEST illustrates the transition from acute kidney injury (AKI) to chronic kidney injury (CKI)?

A patient with acute kidney injury exhibits a sudden weight gain of 2 lbs within 24 hours. Which of the following interventions is MOST appropriate based on this finding?

A patient with metabolic acidosis secondary to kidney injury requires sodium bicarbonate (NaHCO3) administration. If the patient weighs 70 kg and has a bicarbonate deficit of 8 mEq/L, what is the calculated dose of NaHCO3 needed?

A patient with hyperkalemia receives treatment with dextrose and insulin. What is the PRIMARY mechanism by which this intervention reduces serum potassium levels?

A patient with acute kidney injury and hypovolemia has a previous urine output of 400 ml. According to the provided guidelines, what would be the MOST appropriate initial fluid intake?

Which diagnostic test is MOST important for assessing both structural abnormalities and potential obstructions in a patient with kidney dysfunction?

Why is calcium gluconate administered in the treatment of hyperkalemia, and how does it counteract the effects of elevated potassium levels?

What is the primary mechanism by which sodium polystyrene sulfonate (Kayexalate) lowers serum potassium levels, and what critical consideration should guide its use?

How do phosphate binders, such as aluminum hydroxide and calcium carbonate, reduce hyperphosphatemia, and what potential complication is associated with aluminum hydroxide?

What is the rationale behind administering erythropoietin (EPO) in certain clinical scenarios, and what are the key considerations before initiating this treatment?

During the diuretic phase of acute kidney injury (AKI), which electrolyte imbalance poses the greatest risk for cardiac arrhythmias?

In the management of hypermagnesemia, why is calcium gluconate administered, and what is its primary mechanism of action in this context?

A patient in the diuretic phase of AKI experiences a rapid increase in urine output. Which combination of findings would warrant the MOST immediate intervention?

In the recovery phase of AKI, what laboratory finding BEST indicates the kidneys are returning to their baseline function?

Why is a 24-hour urine analysis ordered during the recovery phase of AKI?

During the recovery phase of AKI, a patient's Total Protein S and Albumin levels are monitored. How do these values assist in evaluating the patient's recovery?

In the context of Acute Interstitial Nephritis (AIN), what immunological mechanism is most likely to initiate the inflammatory response within the kidney, leading to the infiltration of WBCs?

Which of the following best describes the compensatory response of the kidneys to a post-renal obstruction, such as that caused by BPH, in the early stages?

A patient with prostatic cancer develops a post-renal obstruction. If the obstruction is prolonged and left untreated, which of the following is the most likely long-term consequence on renal function?

During the oliguric phase of acute kidney injury (AKI) caused by post-renal obstruction, what is the primary mechanism contributing to the decreased urine output?

In the context of post-renal acute kidney injury (AKI), how does the fractional excretion of sodium (FENa) typically present, and what does this value indicate about the kidney's handling of sodium?

A patient with acute kidney injury and fluid overload is prescribed IV Albumin. Which dietary modification is least appropriate given the patient's conditions?

A patient with a history of heart failure and a UTI is being treated for fluid overload. What finding would be the most concerning and necessitate immediate intervention?

A patient receiving treatment for fluid overload has an order for intake and output (I/O) monitoring. Which method would provide the most accurate and consistent measurement of output?

A nurse is providing skin care for a patient with fluid overload. Which intervention is least appropriate to prevent pruritus?

A patient with acute kidney injury and fluid overload is undergoing cardiac monitoring. Why is cardiac monitoring considered essential in this case?

Renal Failure

Acute Renal Failure

Chronic Renal Failure

Reversibility of Acute Renal Failure

Irreversibility of Chronic Renal Failure

Creatinine

BUN (Blood Urea Nitrogen)

Elevated BUN Causes

Intra-Renal Cause

Acute Tubular Necrosis (ATN)

Normal BUN Range

Normal S. Creat Range

Azotemia

Prerenal Cause

Low BUN/Cr ratio

High BUN/Cr ratio

Refrigerating urine sample

Oligouric Phase

Decreased urine output in oligouric phase

Hypovolemia

Reduced Cardiac Output

Renal Artery Occlusion

Causes of Hypovolemia

Potassium Shift

Calcium Gluconate (for hyperkalemia)

Potassium Binders

Hyperphosphatemia Treatment

Erythropoietin (EPO)

Rapid Weight Gain & Fluid Retention

Fluid Intake & Hypovolemia

Fluid Intake & Severe Hypovolemia

Loop Diuretics

Treating Hyperkalemia: Insulin & Dextrose

IV Albumin

Renal Diet

I/O Monitoring

Daily Weight Monitoring

Lung & Edema Monitoring

Diuretic Phase of ARF

Electrolyte Losses in Diuretic Phase

BUN and Creatinine in Diuretic Phase

Recovery Phase of ARF

Recovery Time for Kidneys

Acute Interstitial Nephritis (AIN)

Post-Renal Causes

Functionally Decreased GFR

Increased Nitrogenous Substances