Format

Send to

Choose Destination
Clin J Am Soc Nephrol. 2015 Jul 7;10(7):1291-9. doi: 10.2215/CJN.00860115. Epub 2015 Apr 10.

Drug-induced glomerular disease: direct cellular injury.

Author information

1
Department of Pathology and Cell Biology and.
2
Division of Nephrology, Columbia University Medical Center, New York, New York; and.
3
Section of Nephrology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut mark.perazella@yale.edu.

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.

KEYWORDS:

GN; drug nephrotoxicity; glomerular disease

PMID:
25862776
PMCID:
PMC4491280
DOI:
10.2215/CJN.00860115
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center