Over the past several years, dramatic progress has been made in
identifying the changes in renal vasculature and underlying mechanisms
for these events in progressive renal disease. The maintenance of normal
vasculature is certainly important for organ function, especially for
the most highly vascularized one, the kidney. Maintenance of glomerular
capillary number is critical for the glomerular filtration whereas
peritubular capillaries (PTC) are essential for providing oxygen and
nutrients to the tubules and interstitial cells.
What happens with the renal vasculature in chronic renal disease?
Morphometric studies have documented that the initial response to a fall in nephron number is glomerular hypertrophy in which glomerular capillaries increase in both number and length. Despite an early proliferative response of the glomerular endothelium, there is a progressive loss of the endothelium due to unchecked apoptosis and impaired proliferation (J Am Soc Nephrol 12:1434-1447, 2001).
A similar finding occurs in the interstitium. Bohle noted that there was a loss of PTC in progressive renal disease in man, and he posited an essential role for impaired blood flow in the etiology of the interstitial fibrosis (Kidney Int 56:794-814, 1999). Our group and others confirmed this observation in a large variety of chronic tubulointerstitial nephritis in human kidneys and animal models of progressive renal disease such as aging kidney, the remnant kidney (RK) and chronic cyclosporine nephropathy (J Am Soc Nephrol 12:1434-1447, 2001; Am J Kidney Dis 37:601-611, 2001; Am J Physiol Renal Physiol 280:F727-F736, 2001).
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