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Articles in PresS, published online ahead of print October 1, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00169.2002
Submitted on May 1, 2002
Accepted on September 19, 2002
1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, Vietnam
* To whom correspondence should be addressed. E-mail: dbasile{at}mcw.edu.
Ischemic ARF results in the permanent loss of peritubular capillaries and predisposes the progression of chronic renal failure. The current study was undertaken to determine whether renal hypoxia, which may represent an important mediator in disease progression, is persistently exacerbated following recovery from ARF. Rats were subjected to ischemia/reperfusion (IR) injury and allowed to recover for 5 weeks or 20 weeks. Immunohistochemistry of the hypoxia sensitive marker, 2-pimonidizole, at 5 weeks revealed an overall increase in incorporation in the outermedullary region following recovery from ARF when compared with sham-operated controls. Unilateral nephrectomy, in combination with I/R injury resulted in greater 2-pimonidizole staining than observed in the bilateral injury model. In addition, in the unilateral ischemia/nephrectomy model, proteinuria, interstitial fibrosis and renal functional loss developed significantly faster than in the bilateral model of ARF when animals were allowed to recover for 20 weeks. L-arginine in the drinking water (~0.5 g/day) increased total renal blood flow ~30%, decreased pimonidizole staining and attenuated manifestations of chronic renal disease. These data suggest that a reduction in the peritubular capillary density following ARF results in a persistent reduction in renal pO2 and that hypoxia may play an important role in progression of chronic renal disease following ARF.
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