The role of intraglomerular pressure in the initiation and progression of renal disease.
Reduction in functioning nephron number leads to progressive renal disease. A haemodynamic basis for this process has been suggested by studies of partially nephrectomized rats. In this model compensatory hyperfiltration in the remnant nephrons due to increases in the glomerular capillary hydraulic pressure (-PGC) and plasma flow rate is associated with eventual glomerular sclerosis. Therapeutic attenuation of these haemodynamic adaptations protects against glomerular injury. One such therapy is angiotensin converting enzyme (ACE) inhibition, which lowers systemic blood pressure and -PGC and prevents sclerosis in rats with renal ablation, as well as in the hyperfiltering kidneys of normotensive rats with diabetes mellitus. Control of -PGC with ACE inhibitor is also protective even when therapy is delayed until systemic hypertension and glomerular injury are established. In contrast, the control of systemic hypertension but not -PGC affords no protection in remnant kidney rats. Thus, control of glomerular hypertension slows the progression of renal disease.
D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D004656:Enalapril / Q000627:therapeutic use; D005921:Glomerulonephritis / Q000209:etiology*; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology* / Q000517:prevention & control; D006977:Hypertension, Renal / Q000150:complications* / Q000517:prevention & control; D009392:Nephrectomy; D051381:Rats
D000806:Angiotensin-Converting Enzyme Inhibitors; D004656:Enalapril