Drug-induced prerenal acute kidney injury: Differentiation from renal acute kidney injury and identification of causative drugs

Abstract

Drug-induced prerenal acute kidney injury (AKI) is characterized by a decrease in glomerular filtration rate and associated oliguria resulting from a decrease in renal blood flow, or in intraglomerular pressure caused by the administration of the drug. Fewer drugs are known to cause this type of AKI than those known to cause renal AKI. Attention must be paid to the increasing incidence of drug-induced prerenal AKI in patients with risk factors for renal ischemia, such as hemorrhage, dehydration, shock, heart failure, arteriosclerosis and advanced age. For patients with these risk factors who are treated with nephrotoxic drugs, it is important to distinguish between renal and prerenal AKI. In addition to increased serum creatinine and decreased urinary output (which are used as diagnostic criteria for both types of AKI), prerenal AKI can be differentiated from renal AKI based on a fractional excretion of sodium (FENa) of less than 1%, decreased urine sodium concentration and/or increased urine osmotic pressure. However, it should be noted that these tests are not routinely performed in clinical practice and consequently prerenal AKI is often misdiagnosed as renal AKI. This review describes the causative drugs of prerenal AKI, focusing particularly on non-steroidal anti-inflammatory drugs (NSAIDs), calcineurin inhibitors, renin-angiotensin system inhibitors and diuretics.