Although common causes of acute renal failure, as in uninfected hospitalized patients, are prerenal azotemia and acute tubular necrosis (5–6), recent studies highlight an increased incidence of HIV-associated thrombotic microangiopathies and rhabdomyolysis (7–9); the latter may stem from statin use in patients with complications of antiretroviral therapy (10–14). Opportunistic infections complicating the viral illness, such as tuberculosis, cytomegalovirus infection, and fungal infections, and complications, such as lymphoma and Kaposi sarcoma, are associated with structural anatomic abnormalities, renal insufficiency, and acute renal failure (6, 8). Chronic kidney disease, such as thrombotic thrombocytopenic purpura, associated with HIV infection, can also mimic acute renal failure (4, 6, 15). Drugs used to treat superinfections associated with HIV infection (for example, antibiotics, antifungals, and antivirals) and antiretroviral drugs to treat HIV infection (for example, indinavir and ritonavir) (16) are associated with the development of interstitial nephritis and nephrotoxicity. Antibiotics commonly cause acute interstitial nephritis, while aminoglycosides, amphotericin, and foscarnet cause acute tubular necrosis. The nucleoside phosphonate analogues adefovir and cidofovir cause proximal renal tubular injury (16). Abacavir (17) and tenofovir (18–19) are implicated in the development of tubular injury and renal failure. Sulfadiazine, acyclovir, and indinavir cause crystalluria and, occasionally, intrarenal obstruction (20). Indinavir is associated with several nephrologic syndromes, such as dysuria, acute and chronic interstitial nephritis (including tubular atrophy and interstitial fibrosis), and nephrolithiasis; nelfinavir has been linked to the development of nephrolithiasis (10, 16, 21–23). Leukocyturia is associated with progressive renal disease in patients treated with indinavir (22, 24).