Drug-induced acute kidney injury

The purpose of this review is to describe the most prevalent mechanisms of drug-induced acute kidney injury, to define the risk factors for nephrotoxicity, and to analyze the available evidence for preventive measures.

Drug toxicity remains an important cause of acute kidney injury that, in many circumstances, can be prevented or at least minimized by vigilance and early intervention. Recent studies have resulted in increased insight into the subcellular mechanisms of drug nephrotoxicity. Further improvement is to be expected from the identification of early markers of nephrotoxicity and an increasing involvement of a clinical pharmacist.

The main mechanisms of nephrotoxicity are vasoconstriction, altered intraglomerular hemodynamics, tubular cell toxicity, interstitial nephritis, crystal deposition, thrombotic microangiopathy, and osmotic nephrosis. Before prescribing a potentially nephrotoxic drug, the risk-to-benefit ratio and the availability of alternative drugs should be considered. Modifiable risk factors should be corrected. The correct drug dosage should be prescribed. Patients should be pre-hydrated and the glomerular filtration rate should be frequently monitored during the administration of a potentially nephrotoxic drug. Studies are needed to further elucidate the mechanisms of nephrotoxicity to design more-rational prevention and treatment strategies. Computer-based prescriber-order entry and an appropriately trained intensive care unit pharmacist are particularly helpful to minimize medication errors and adverse drug events.