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Am J Physiol Renal Physiol (August 9, 2001). doi:10.1152/ajprenal.0050.2001
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Articles in PresS, published online ahead of print August 9, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0050.2001
Submitted on February 16, 2001
Accepted on July 3, 2001

Renal ischemic injury results in permanent damage to the peritubular capillaries and influences long-term function

David P Basile1*, Deborah Donohoe1, Kelly Roethe1, and Jeffrey L Osborn1

1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA

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

Acute episodes of severe renal ischemia result in acute renal failure (ARF). This episode is followed by a characteristic recovery and repair response in which tubular morphology and renal function appear completely restored within approximately 1 month. However, the chronic effects of such an injury have not been well-studied. Male rats were subjected to 60 min bilateral ischemia followed by reperfusion yielding a characteristic injury. Post-ischemic animals manifested severe diuresis peaking at 1 week post-injury (V>45 ml/day, ARF vs. 18 ml/day, sham; P <0.05). Urine flow subsequently declined but remained significantly elevated vs. shams for the 40 week period. The prolonged alteration in urinary concentrating ability was attributed in part to a diminished capacity to generate a hypertonic medullary interstitium. By week 16, proteinuria developed in the post-ARF group and progressed for the duration of the study. Histological examination revealed essentially normal tubular morphology at 4 and 8 wks post-injury but the development of tubulointerstitial fibrosis at 40 wks. TGF-ß1 expression was elevated at 40 weeks, but not at 4 and 8 weeks post-injury. Microfil analysis revealed an approximate 30-50% reduction in the peritubular capillary density in the inner stripe of the outer medulla at 4, 8 and 40 wks of post ARF groups vs. shams. In addition, post-ARF rats manifested a significant pressor response to a low-dose of Ang II (15 ng/kg/min). We hypothesize that severe ischemic injury results in a permanent alteration in renal capillary density contributing to a urinary concentrating defect and predisposing the development of renal fibrosis.




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