Nephrotoxicity of antiinfective drugs

Antiinfective drugs may show the same mechanisms of nephrotoxicity as other drugs, and these can be subgrouped into vascular, tubulotoxic, tubulo-obstructive, and immunologic effects. While vascular effects of antiinfective drugs are rare, tubulotoxicity is a well known phenomenon, especially in connection with aminoglycosides and amphotericin B as well as cephalosporins, pentamidine, foscarnet, and cidovir. The tubulo-obstructive effect caused by precipitation of the drug and first observed after treatment with sulfonamides in the 1940s, has become a renascent problem now that high doses of sulfonamides are being given to immunocompromised patients (sulfadiazine, cotrimoxazole). Moreover, this effect has also been associated with newer antiviral drugs like acyclovir and indinavir. We describe a transplant patient who received high doses of cotrimoxazole for pneumocystis carinii pneumonia and lost transplant function mainly due to bioptically proven glomerular and tubular crystallization with tubular degeneration caused by sulfamethoxazole. Acute interstitial nephritis is the main immunologic effect of antiinfective drugs (especially rifampicin but also cephalosporins, quinolones, sulfonamides, and penicillins). Immune stimulation by cytokine treatment (mainly interferon-alpha) involves several kinds of autoimmune renal diseases like acute interstitial nephritis or glomerulonephritis as well as interstitial and vascular rejection of renal transplants.