The current state of RAAS blockade in the treatment of hypertension and proteinuria.

Hypertension is a well-established risk factor for cardiovascular disease (CVD) and chronic kidney disease (CKD). Patients with CKD have significant morbidity (ie, increased risk of CVD) and progression to end-stage renal disease. Increase in albuminuria over time to levels greater than 300 mg/d, in spite of blood pressure being at goal, is an independent predictor for nephropathy progression. Data provide support, however, for reducing proteinuria by at least 30% after treatment is initiated in patients with proteinuria. Pharmacologic blockade of the renin-angiotensin-aldosterone system (RAAS) slows progression of advanced proteinuric CKD more effectively than other antihypertensive agents. In post hoc analyses, this slowed progression has been correlated to reductions in proteinuria of 30% or more after blood pressure-lowering therapy is initiated. Increases in proteinuria, in spite of blood pressure reduction, are associated with faster declines in kidney function regardless of whether RAAS blockers are used.