• Sean Pickthorn, Peter Thorne, and Nattawat Klomjit.
• Division of Nephrology and Hypertension, University of Minnesota, Minneapolis, Minnesota, United States
• Pol. Arch. Med. Wewn. 2024 Sep 27; 134 (9).

AbstractMedications are a common cause of acute kidney injury (AKI). There are various mechanisms in which medications can induce AKI, and better understanding of their pathophysiology can aid in clinical recognition, treatment, and prevention of this condition. Hemodynamic‑mediated AKI is often associated with drugs that alter renal perfusion and its autoregulation. Acute tubular injury is a result of direct renal tubular cell toxicity. Acute interstitial nephritis is a T‑cell-mediated immune hypersensitivity reaction to drugs leading to tubule‑interstitial inflammation and AKI. Crystalline nephropathy can be caused by crystallization of medications or by altered urinary chemistry caused by medications. Some medications can evoke AKI through uncommon mechanisms, such as glomerulonephritis and thrombotic microangiopathy. Notably, some medications may cause a phenomenon called "pseudo‑AKI," where serum creatinine is elevated without actual reduction in kidney function. Medications commonly used in clinical practice are reviewed with a focus on their mechanisms of injury, diagnosis, treatment, and prevention. Recognizing common medications associated with AKI is an important first step in reducing the risk of this condition. For each medication, understanding general and specific risk factors for AKI allows for early identification and timely discontinuation of offending agents. These measures can help mitigate the risk of AKI and promote renal recovery.

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