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suck abstract from ncbi


10.2215/CJN.00860115

http://scihub22266oqcxt.onion/10.2215/CJN.00860115
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25862776!4491280!25862776
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suck abstract from ncbi

pmid25862776      Clin+J+Am+Soc+Nephrol 2015 ; 10 (7): 1291-9
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  • Drug-induced glomerular disease: direct cellular injury #MMPMID25862776
  • Markowitz GS; Bomback AS; Perazella MA
  • Clin J Am Soc Nephrol 2015[Jul]; 10 (7): 1291-9 PMID25862776show ga
  • 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.
  • |Animals[MESH]
  • |Drug-Related Side Effects and Adverse Reactions/diagnosis/*etiology/physiopathology/therapy[MESH]
  • |Endothelial Cells/drug effects/pathology[MESH]
  • |Epithelial Cells/drug effects/pathology[MESH]
  • |Glomerulonephritis/*chemically induced/diagnosis/physiopathology/therapy[MESH]
  • |Humans[MESH]
  • |Kidney Glomerulus/*drug effects/pathology/physiopathology[MESH]
  • |Mesangial Cells/drug effects/pathology[MESH]
  • |Prognosis[MESH]
  • |Risk Assessment[MESH]


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