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Am J Physiol Renal Physiol (September 17, 2008). doi:10.1152/ajprenal.00099.2008
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Submitted on February 26, 2008
Accepted on September 10, 2008

VEGF121 preserves renal microvascular structure and ammeliorates secondary renal disease following acute kidney injury

Ellen C Leonard1, Jessica L Friedrich1, and David P. Basile1*

1 Department of Cellular and Integrative Physiology, Indiana University, Indianaoplis, Indiana, United States

* To whom correspondence should be addressed. E-mail: dpbasile{at}iupui.edu.

Acute kidney injury induced by renal ischemia reperfusion (I/R) compromises microvascular density and predisposes chronic kidney disease (CKD) and sodium dependent hypertension. Vascular endothelial cell growth factor-121 (VEGF-121) was administered to rats on a 0.4% sodium diet at various times following recovery from I/R for up to 35 days. VEGF-121 had no effect on the initial loss of renal function as indicated by serum creatinine levels measured 24 hours post-injury. Serum creatinine values declined thereafter indicative of renal repair. Rats were then switched to an elevated sodium diet, 4.0%, for an additional 28 days to induce CKD. The elevated sodium diet enhanced renal hypertrophy, interstitial volume, albuminuria and cardiac hypertrophy relative to post-ischemic animals maintained on standard salt-diet. Administration of VEGF-121 from either day 0-14, 0-35, or 3-35 relative to I/R injury suppressed the effects of sodium diet on CKD development, while delayed administration of VEGF-121 from day 21-35 had no effect. eNOS protein levels were up-regulated in post-ischemic animals and this effect was significantly increased by elevated salt diet but not influenced by prior VEGF treatment. Conversely, microvascular density was preserved in post-ischemic animals treated with VEGF-121 relative to vehicle treated post-ischemic animals. These data suggest that early, but not delayed, treatment with VEGF-121 can preserve vascular structure post-ischemia and influence chronic renal function in response to elevated sodium intake.




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