期刊
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
卷 21, 期 1, 页码 33-38出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MNH.0b013e32834d085a
关键词
acute kidney injury; hemodynamics; kidney; renal medulla
资金
- National Institutes of Health [HL36279, HL29587, DK090123]
- Clinical Translational Science Institute of Southeast Wisconsin
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R37HL036279, P01HL029587, R01HL036279] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK090123] Funding Source: NIH RePORTER
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 H2S, 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.
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