Drug nephrotoxicity and its prevention

Drug induced renal disease occurs frequently in patients treated with diagn ostic and therapeutic agents. Drug nephrotoxicity is seen in both inpatient and outpatient settings and presents differently depending on the drug and clinical setting. Loss of renal function is often reversible on discontinu ation of therapy, but may occasionally lead to end-stage renal failure. The ongoing development of more potent and specific drugs provides the potenti al for more nephropathy by an increasing variety of agents and mechanisms. Analysis of these? effects can further our understanding of the mechanisms of renal disease and potentially result in new therapeutic approaches, as d emonstrated by the recent application of angiotensinconverting enzyme (CE) inhibitors to slow down the loss of renal function in progressive renal dis ease. Drug toxicity in hospitalized patients is a frequent adverse event wi th nephrotoxicity accounting for nearly 7% of all drug toxicity Drug nephro toxicity nas identified as the cause of one fifth of all cases in hospital- acquired acute renal failure, with a mortality of 8%. Aminoglycosides, radi ographic contrast media, and cisplatin were most commonly implicated. Among the drugs which contributed to 29% of all acute renal failure in hospitali zed patients the most commonly involved were antibiotics (aminoglycosides, pentamidine and the cepalosporins), non-steroidal antiinflammatory drugs (N SAIDs), ACE: inhibitors, and diuretics. The introduction of newer NSAIDs, a ntihypertensives, and antibiotics and their changed usage, coupled with the decline in use of aminoglycosides, has changed the spectrum of commonly im plicated drugs. For management of individual patients, several guidelines c an help maximize efficacy and safety. Clinicians who remain observant and s trive to understand mechanisms of disease and pharmacology will expand the horizons of pharmacotherapy and thereby improve patients outcomes. Much res earch is necessary to increase our understanding of the pathogenesis of thi s heterogeneous group of disorders to turn apparent adverse effects to diag nostic and therapeutic advantage.