Moving Points in NephrologyDrug-Induced Glomerular Disease Direct Cellular InjuryMarkowitz, Glen S.*; Bomback, Andrew S.†; Perazella, Mark A.‡ Author Information *Department of Pathology and Cell Biology and †Division of Nephrology, Columbia University Medical Center, New York, New York; and ‡Section of Nephrology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut Correspondence: Dr. Mark A. Perazella, Section of Nephrology, Department of Internal Medicine, Yale University School of Medicine, Boardman Building 122, 330 Cedar Street, New Haven, CT 06520-8029. Email: [email protected] Clinical Journal of the American Society of Nephrology 10(7):p 1291-1299, July 2015. | DOI: 10.2215/CJN.00860115 Buy Metrics Abstract The potential of medications to cause kidney injury is well known. Although nephrotoxicity is most commonly associated with injury in the tubulointerstitial compartment as either acute tubular necrosis or acute interstitial nephritis, a growing body of literature has also highlighted the potential for drug-induced glomerular lesions. This review surveys the three primary patterns of drug-induced glomerular diseases stratified by the cell type at which the glomerular lesion is focused: visceral epithelial cell (or podoctye) injury, endothelial cell injury, and mesangial cell injury. A number of commonly prescribed medications, including IFNs, bisphosphonates, nonsteroidal anti-inflammatory drugs, antiplatelet agents, and antiangiogenesis drugs, that are both prescribed and available over the counter, have been implicated in these iatrogenic forms of glomerular disease. Recognition of these drug-induced etiologies of glomerular disease and rapid discontinuation of the offending agent are critical to maximizing the likelihood of renal function recovery. Copyright © 2015 The Authors. Published by Wolters Kluwer Health, Inc. All rights reserved.