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Patients with chronic renal disease are at increased risk for the development of cardiovascular disease, which is the main cause of death in this growing population. Among the risk factors involved, hypertension and proteinuria are major contributors to kidney damage and, if not controlled, may eventually lead to the progression of renal failure and end-stage renal disease. Both proteinuria and hypertension can be primary pathologic events or can appear as complications of other disease processes. Initially, these two factors may operate separately but, as progression ensues, both processes generally combine, potentiating their effects and hastening renal damage. Therefore, strategies to reduce blood pressure and proteinuria are essential in order to slow the worsening of many nephropathies. Therapies that target the renin-angiotensin system offer particular benefit, as hypertension and proteinuria can be precisely reduced with angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers. However, with this intervention, plasma renin activity remains high, and although primary endpoints may be controlled, elevated renin concentration can contribute to cardiovascular damage. Aliskiren, a direct renin inhibitor, is the first example of a novel class of antihypertensive drugs with potent antiproteinuric effects, which, alone or combined, can contribute to delaying the progression of kidney disease.

Role of aliskiren in blood pressure control and renoprotection