Table 2.

Features of drug-induced nephrotoxicity

	ATN	AIN	Crystal nephropathy
Mechanism of injury	direct cytotoxicity on tubular epithelial cells, most often proximal tubules	immunologically mediated damage to the interstitium	precipitation of drug as crystals causes damage to the tubular epithelium and/or tubular obstruction
Dose dependence	yes	no	yes; may also be infusion rate-dependent
Time course	days	usually 7–14 days, but can be sooner in previously sensitized individuals	any time during treatment; can occur as soon as following a single dose
Clinical features	elevated serum creatinine ±oliguria increased fractional excretion of sodium microscopic haematuria muddy brown casts proteinuria (usually mild) hypoalbuminaemia	elevated serum creatinine peripheral eosinophilia fever rash sterile pyuria, WBC casts microscopic haematuria tubular proteinuria (low molecular weight proteins) eosinophiluria (poor sensitivity)	elevated serum creatinine (acute or chronic) clinical signs of dehydration/volume depletion elevated urine specific gravity
Antimicrobials most commonly implicated	aminoglycosides amphotericin B cidofovir foscarnet polymyxins vancomycin	β-lactam agents fluoroquinolones rifamycins sulphonamides	aciclovir atazanavir foscarnet ganciclovir indinavir sulfamethoxazole