Abstract
Diabetes and hypertension are the leading causes of end-stage renal disease in the Western world. Inadequate control of both systemic and glomerular capillary pressure in diabetics results in increasing hydraulic force and mechanical stretch on the glomeruli, with a subsequent increase in proteinuria and ultimately glomerulosclerosis. Therapeutic strategies that combine systemic and glomerular capillary pressure reduction result in reduced proteinuria and are ideal for preventing renal injury. Both experimental and clinical studies have demonstrated the importance of intensive control of blood pressure, preferably to systolic blood pressure (SBP) < or =130 mm Hg to delay progression of renal disease. In particular, drugs that block the renin-angiotensin system (RAS) offer the advantage of consistently reducing glomerular capillary pressure and proteinuria relative to changes in systemic blood pressure. This combination of events is ideal for delaying progression of renal disease. However, the use of drugs that block the RAS is not a surrogate for maintaining tight control of blood pressure.

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