Biologia, Bratislava, 55/Suppl. 8: 95-102, 2000.

ISSN 0006-3088 (Biologia). ISSN 1335-6399 (Biologia. Section Cellular and Molecular Biology).



Drug nephrotoxicity and its prevention.


Jozef Novotny1* & Martin Novotny2

1 Trnava University, School of Public Health and Social Welfare, Departments of Clinical Medicine and Clinical Pharmacology, Hornopotocna 23, SK-91743, Trnava, Slovakia

2 Department of Neurosurgery, School of Medicine, Comenius University, Derer´s Faculty Hospital and Policlinics, Limbova 5, SK-83305, Bratislava, Slovakia

* corresponding author

Received: August 1, 2000 / Accepted: October 24, 2000



Drug induced renal disease occurs frequently in patients treated with diagnostic 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 discontinuation of therapy, but may occasionally lead to end-stage renal failure. The ongoing development of more potent and specific drugs provides the potential 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 demonstrated by the recent application of angiotensin-converting enzyme (ACE) inhibitors to slow down the loss of renal function in progressive renal disease. Drug toxicity in hospitalized patients is a frequent adverse event with nephrotoxicity accounting for nearly 7% of all drug toxicity. Drug nephrotoxicity was identified as the cause of one fifth of all cases in hospital-acquired acute renal failure, with a mortality of 8%. Aminoglycosides, radiographic contrast media, and cisplatin were most commonly implicated. Among the drugs which contributed to 29% of all acute renal failure in hospitalized patients the most commonly involved were antibiotics (aminoglycosides, pentamidine and the cepalosporins), nonsteroidal antiinflammatory drugs (NSAIDs), ACE inhibitors, and diuretics. The introduction of newer NSAIDs, antihypertensives, and antibiotics and their changed usage, coupled with the decline in use of aminoglycosides, has changed the spectrum of commonly implicated drugs. For management of individual patients, several guidelines can help maximize efficacy and safety. Clinicians who remain observant and strive to understand mechanisms of disease and pharmacology will expand the horizons of pharmacotherapy and thereby improve patients outcomes. Much research is necessary to increase our understanding of the pathogenesis of this heterogeneous group of disorders to turn apparent adverse effects to diagnostic and therapeutic advantage.