[Drugs renal toxicity]

Drug-induced renal dysfunction is frequent in clinical practice. Outcomes may be severe, with increased morbidity and mortality. Kidneys are particularly vulnerable to drug toxicity, especially since they are highly vascularized, thus receiving about 25% of cardiac output. Furthermore, interstitial accumulation of toxic agents in papilla and the medulla often occurs due to the existence of a corticomedullary osmotic gradient. Moreover, the key role played by the renal tubule in the reabsorption processes of a number of endogenous and exogenous substances further increases the exposure of the kidney to high concentrations of potentially toxic agents, both in the tubular lumen and cells. As a result, drugs may be toxic to all of the four structures of the kidney: glomerulus, tubule, interstitium, and blood vessels. This chapter reviews the main mechanisms of drug-induced renal toxicity and then focuses on the nephrotoxicity of anti-infectious drugs: antibacterial drugs, antifungal agents, antimalariae, and antiviral drugs. NSAID and anticancer drugs renal toxicity are detailed elsewhere in this textbook. Methods used to prevent drug-induced nephrotoxicity, when known, are detailed. Risk factors are also listed, such as high-risk populations, identification and elimination of risk factors, and drug dosage adjustment in patients with baseline abnormal renal function.