Abstract
Experimental data are summarized that provide evidence that enhanced transmission of systemic hypertension to the glomerulus occurs in the setting of reduced renal mass. It is proposed that similar adaptive glomerular hemodynamic alterations occur in parenchymal renal disease in humans, favoring the development of intraorgan hypertension. Accelerated vascular and glomerular damage and functional deterioration result. Treatment of systemic hypertension with agents that reduce glomerular capillary pressure has been shown to ameliorate the manifestations of experimental glomerular disease. The importance of preventing hemodynamic injury to the arterioles and glomerular capillaries in the management of human renal disease is stressed.
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