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Multiple Choice

Nephrotoxic drugs cause which class of acute renal failure?

Nephrotoxic drugs injure the kidney tissue directly, causing intrinsic (intrarenal) acute kidney injury. This is most commonly acute tubular necrosis from agents like aminoglycosides, radiocontrast, amphotericin B, and cisplatin, where the damage is inside the renal parenchyma—especially the tubules. Because the injury is to the kidney tissue itself, the hallmark is a failure of tubular function and a drop in GFR from within the kidney, rather than from reduced blood flow or urinary obstruction. This differs from pre-renal AKI, which results from decreased kidney perfusion, and from post-renal (obstructive) AKI, which stems from obstruction to urine flow. In intrinsic AKI due to nephrotoxins, the nephron tubules are the primary site of injury, leading to characteristic lab patterns such as higher FENa (often >2%) and granular casts on urine study. Stop the offending drug and provide supportive care to allow recovery of tubular function.

Nephrotoxic drugs injure the kidney tissue directly, causing intrinsic (intrarenal) acute kidney injury. This is most commonly acute tubular necrosis from agents like aminoglycosides, radiocontrast, amphotericin B, and cisplatin, where the damage is inside the renal parenchyma—especially the tubules. Because the injury is to the kidney tissue itself, the hallmark is a failure of tubular function and a drop in GFR from within the kidney, rather than from reduced blood flow or urinary obstruction. This differs from pre-renal AKI, which results from decreased kidney perfusion, and from post-renal (obstructive) AKI, which stems from obstruction to urine flow. In intrinsic AKI due to nephrotoxins, the nephron tubules are the primary site of injury, leading to characteristic lab patterns such as higher FENa (often >2%) and granular casts on urine study. Stop the offending drug and provide supportive care to allow recovery of tubular function.