Role of medullary blood flow in the pathogenesis of renal ischemia-reperfusion injury

Abstract

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.

Figure 1. Effect of renal ischemia-reperfusion injury on regional blood flow in the kidney

Sprague-Dawley rats underwent 30 minutes renal ischemia and 180 minutes of reperfusion. Cortical blood flow (CBF) and outer medullary blood flow (MBF) were measured by laser-Doppler flowmetry. CBF and MBF decreased dramatically during the ischemic period and CBF rapidly recovered to baseline levels following reperfusion. In contrast, a transient improvement in MBF was seen immediately after reperfusion followed by a gradual decline to approximately 50% of baseline that was sustained for the 3 hour period of the experiment. Adapted from Regner et al. (19)