Role of medullary blood flow in the pathogenesis of renal ischemia-reperfusion injury. Curr Opin Nephrol Hypertens 2012 Jan;21(1):33-8
Date
11/15/2011Pubmed ID
22080855Pubmed Central ID
PMC3612396DOI
10.1097/MNH.0b013e32834d085aScopus ID
2-s2.0-83055186460 (requires institutional sign-in at Scopus site) 69 CitationsAbstract
PURPOSE OF REVIEW: Renal ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI). Alterations in renal medullary blood flow (MBF) contribute to the pathogenesis of renal IRI. Here we review recent insights into the mechanisms of altered MBF in the pathogenesis of IRI.
RECENT FINDINGS: Although cortical blood flow fully recovers following 30-45 min of bilateral IRI, recent studies have indicated that there is a prolonged secondary fall in MBF that is associated with a long-term decline in renal function. Recent findings indicate that angiopoietin-1, atrial natriuretic peptide, heme oxygenase-1, and the gasotransmitters CO and H(2)S, may limit the severity of IRI by preserving MBF. Additional studies have also suggested a role for cytochrome P450-derived 20-HETE in the postischemic fall in MBF.
SUMMARY: Impaired MBF contributes to the pathogenesis of renal IRI. Measurement of renal MBF provides valuable insight into the underlying mechanisms of many renoprotective pathways. Identification of molecules that preserve renal MBF in IRI may lead to new therapies for AKI.
Author List
Regner KR, Roman RJAuthor
Kevin R. Regner MD Interim Chair, Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Acute Kidney InjuryAngiopoietin-1
Animals
Atrial Natriuretic Factor
Carbon Monoxide
Heme Oxygenase-1
Humans
Hydrogen Sulfide
Hydroxyeicosatetraenoic Acids
Kidney Medulla
Renal Circulation
Reperfusion Injury
