• Pieter Evenepoel.
• Division of Nephrology, Department of Medicine, University Hospital Leuven, B-3000 Leuven, Belgium. pieter.evenepoel@uz.kuleuven.ac.be
• Best Pract Res Clin Anaesthesiol. 2004 Mar 1; 18 (1): 37-52.

AbstractAcute renal failure (ARF) is a common problem in intensive care medicine. Even modest degrees of ARF not requiring dialysis treatment increase the risk of death approximately fivefold. Despite the widespread appreciation of the role of nephrotoxic drugs in their contribution to ARF, these drugs continue to have an ongoing aetiological role. Potentially nephrotoxic drugs include non-steroidal anti-inflammatory drugs, radiocontrast agents, antimicrobial and anaesthetic agents. Endogenous compounds such as myoglobin and haemoglobin may furthermore cause toxic nephropathy. Tubular injury initiated by toxins often results from a combination of acute renal vasoconstriction and direct cellular toxicity due to intracellular accumulation of the toxin, or, alternatively, may be mediated immunologically in case of interstitial nephritis. Patients with reduced renal functional reserve, cardiovascular co-morbidity, diabetes mellitus, and advanced age are at increased risk. Awareness of the range of toxins on the one hand and simple measures such as adequate pre-hydration of the patient and drug monitoring on the other hand may be sufficient to avoid drug-induced ARF or minimize its clinical severity in susceptible patients.

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