Progression of chronic renal failure in focal segmental glomerulosclerosis: consequence of podocyte damage or of tubulointerstitial fibrosis?
W Kriz - Pediatric Nephrology, 2003 - Springer
W Kriz
Pediatric Nephrology, 2003•SpringerThe decline in renal function in chronic renal failure is based on the progressive loss of
viable nephrons. The pathways to nephron loss in conjunction with chronic renal disease
generally start in the glomerulus, extending onto the tubulointerstitium via the urinary pole.
Pathways to nephron degeneration starting focally in the tubulointerstitium have yet to be
described. The deleterious effects of protein leakage on progression appear to be a result of
podocyte damage, the beneficial effects of ACE inhibitors a result of podocyte protection.
viable nephrons. The pathways to nephron loss in conjunction with chronic renal disease
generally start in the glomerulus, extending onto the tubulointerstitium via the urinary pole.
Pathways to nephron degeneration starting focally in the tubulointerstitium have yet to be
described. The deleterious effects of protein leakage on progression appear to be a result of
podocyte damage, the beneficial effects of ACE inhibitors a result of podocyte protection.
Abstract
The decline in renal function in chronic renal failure is based on the progressive loss of viable nephrons. The pathways to nephron loss in conjunction with chronic renal disease generally start in the glomerulus, extending onto the tubulointerstitium via the urinary pole. Pathways to nephron degeneration starting focally in the tubulointerstitium have yet to be described. The deleterious effects of protein leakage on progression appear to be a result of podocyte damage, the beneficial effects of ACE inhibitors a result of podocyte protection.
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