There is a clear, inverse association between the level of blood pressure and the progression of renal disease. This association appears to extend well within the "normotensive" blood pressure range. Currently, there are no absolutely incontrovertible data from prospective, randomized trials in humans documenting that high blood pressure is the cause of an accelerated loss of GFR, or that the loss in renal function can be prevented by lowering blood pressure below 140/90 mmHg. Nevertheless, an aggressive lowering of blood pressure in patients with hypertension and renal disease seems reasonable and desirable. First, the control of blood pressure lowers the "all causes" risk of cardiovascular morbidity and mortality in all patients with elevated blood pressure. Second, any detrimental effects on GFR are uncommon or transient in these patients. Third, the beneficial effects on GFR are firmly supported in animal studies and in humans with malignant hypertension. Fourth, a growing body of evidence from human trials supports the inverse correlation between blood pressure and decrease in GFR, even below a level of 140/90 mmHg. The evidence for these conclusions is reviewed.