Clinical management scenarios for acute kidney injury workup, chronic kidney disease staging, and dialysis decisions tested on USMLE Step 2 CK.
About this set
40 mixed cards for USMLE Step 2 CK Renal. It opens with "What absolute serum creatinine rise, within what time frame, meets KDIGO" and "What relative serum creatinine rise, within what time frame, meets KDIGO". Study it alongside the other USMLE Step 2 CK sets below.
40 cards · mixed cards · AI-written, checked twice. Edit anything.
- What absolute serum creatinine rise, within what time frame, meets KDIGO criteria for AKI?
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An increase of at least 0.3 mg/dL within 48 hours- What relative serum creatinine rise, within what time frame, meets KDIGO criteria for AKI?
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At least 1.5 times the baseline value within 7 days- What urine output threshold meets KDIGO criteria for AKI?
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Less than 0.5 mL/kg/hr for at least 6 hours- A FENa below what value suggests prerenal azotemia?
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Less than 1 percent- A FENa above what value suggests intrinsic AKI such as acute tubular necrosis?
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Greater than 2 percent- Why is FENa unreliable for classifying AKI in a patient on diuretics, and what index should be used instead?
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Diuretics force sodium excretion regardless of cause, so FEUrea should be used instead- What urine microscopy finding is classic for acute tubular necrosis?
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Muddy brown granular casts- What urine microscopy finding suggests acute interstitial nephritis?
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White blood cell casts- What urine microscopy finding suggests glomerulonephritis as the cause of AKI?
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Red blood cell casts (dysmorphic RBCs)- A BUN to creatinine ratio greater than what value suggests prerenal azotemia?
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Greater than 20 to 1- What is the most common cause of hospital-acquired AKI?
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Acute tubular necrosis (ischemic or nephrotoxic)- What two common drug classes cause AKI by altering glomerular hemodynamics rather than direct toxicity?
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NSAIDs and ACE inhibitors/ARBs- By what mechanism do NSAIDs cause AKI?
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They inhibit prostaglandins that dilate the afferent arteriole, lowering GFR- By what mechanism do ACE inhibitors precipitate AKI in a patient with bilateral renal artery stenosis?
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Loss of angiotensin II-mediated efferent arteriolar constriction causes GFR to drop- What is the classic clinical triad of drug-induced acute interstitial nephritis?
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Fever, rash, and eosinophilia
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