Pathophysiology of ischemic nephropathy

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Loss of renal function beyond a renal vascular lesion presents a complex challenge to clinicians. This article summarizes current understanding of critical vascular lesions to the kidney and putative mechanisms by which loss of perfusion activates fibrogenic mechanisms in the kidney. The authors emphasize alterations in vasoactive pathways, including disturbed oxidative stress, activation of endothelin, and reduced nitric oxide, which modulate cytokines and inflammatory mediators within the renal parenchyma. Improved understanding of these mechanisms is essential in preventing irreversible interstitial fibrosis and restoring renal perfusion.

Original languageEnglish (US)
Pages (from-to)793-803
Number of pages11
JournalUrologic Clinics of North America
Volume28
Issue number4
StatePublished - 2001

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Kidney
Blood Vessels
Perfusion
Endothelins
Nitric Oxide
Oxidative Stress
Fibrosis
Cytokines

ASJC Scopus subject areas

  • Urology

Cite this

Pathophysiology of ischemic nephropathy. / Lerman, Lilach O; Textor, Stephen C.

In: Urologic Clinics of North America, Vol. 28, No. 4, 2001, p. 793-803.

Research output: Contribution to journalArticle

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