Evaluate the following clinical vignettes describing patients who developed acute kidney injury (AKI) in various clinical settings. Match each patient's clinical presentation to the most accurate pathophysiological diagnosis.
- A 68-year-old man with heart failure undergoes aggressive diuresis with intravenous furosemide. He develops AKI with a BUN of 72 mg/dL and a creatinine of 2.4 mg/dL. Urinalysis shows abundant hyaline casts.Hemodynamic prerenal azotemia due to decreased effective arterial blood volume
- A 55-year-old woman with decompensated cirrhosis develops oliguria and a creatinine of 3.1 mg/dL. Urine sodium is 6 mEq/L. Renal function does not improve after 48 hours of intravenous albumin therapy and diuretic withdrawal.Hepatorenal syndrome driven by splanchnic vasodilation and severe renal vasoconstriction
- A 60-year-old man undergoes a contrast-enhanced CT scan. Two days later, his serum creatinine increases from 1.0 mg/dL to 2.2 mg/dL. Urinalysis shows granular casts, and the fractional excretion of sodium (FENa) is 0.6%.Contrast-induced nephropathy featuring direct tubular toxicity and unique renal vasoconstriction
- A 72-year-old man undergoes coronary angiography. Five days later, he develops AKI, a purplish mottling on his feet, and new-onset peripheral eosinophilia. Urinalysis reveals eosinophils.Atheroembolic renal disease resulting from cholesterol crystal embolization
Cevap
The presentations map to distinct mechanisms: overdiuresis causes classic prerenal azotemia, cirrhosis with albumin-unresponsive AKI represents hepatorenal syndrome, post-contrast AKI is contrast-induced nephropathy (notable for FENa < 1%), and post-angiography AKI with livedo reticularis is atheroembolic renal disease.
The correct matches rely on synthesizing the patient history with specific diagnostic markers. Furosemide diuresis predictably shrinks the effective arterial blood volume, leading to a classic prerenal pattern characterized by a high BUN/Cr ratio and hyaline casts. Hepatorenal syndrome is distinguished from simple prerenal azotemia by its complete failure to improve after withdrawing diuretics and administering a dedicated volume expansion trial with intravenous albumin. Contrast-induced nephropathy represents a toxic injury to the tubules, but unlike classic ischemic acute tubular necrosis (which typically exhibits a FENa > 2%), the profound vasoconstrictive effect of the contrast media classically yields a FENa < 1%. Finally, atheroembolic renal disease is distinguished by its delayed onset (days to weeks post-procedure) alongside systemic signs of crystal embolization, such as livedo reticularis, blue toe syndrome, and eosinophilia.
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Anahtar Kavram
Differentiating etiologies of acute kidney injury requires recognizing classic clinical contexts and appropriately interpreting urine indices, while maintaining high suspicion for exceptions such as contrast nephropathy, which typically presents with a FENa < 1%.
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