Skip to main content
. Author manuscript; available in PMC: 2014 Feb 10.
Published in final edited form as: Compr Physiol. 2012 Apr;2(2):1303–1353. doi: 10.1002/cphy.c110041

Figure 3. Interplay between tubular and vascular injury leading to sustained reductions of GFR in the extension phase of AKI.

Figure 3

Injury induced by ischemia can results in damage to both the tubular as well as the microvascular compartment. Resolution of vasoconstriction appears effective at reducing injury when administered prophylactically, but not following established injury. Resistance may be due to exacerbated inflammation, which may impart reductions in RBF and GFR insensitive to vasodilator therapies. Of central importance in this process is the activation of inflammatory processes which are influenced by factors released by damaged proximal tubules as well as adhesion of damaged microvascular cells. Infiltrating leukocytes may impinge on RBF either by secreting vasoactive factors, or by contributing to the disruption of flow by physical interference. In addition, exacerbated hypoxia leading to tubular obstruction may contribute to reductions in GFR independent of vasodilator therapy. From citation (531)