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Renal, Electrolyte and Hypertension Division, University of Pennsylvania, Philadelphia, Pennsylvania
Correspondence: Dr. Debbie L. Cohen, Renal, Electrolyte and Hypertension Division, Department of Medicine, University of Pennsylvania, 1 Founders Building, 3400 Spruce Street, Philadelphia, PA 19104. Phone: 215-615-0794; Fax: 215-615-0349; E-mail: debbie.cohen{at}uphs.upenn.edu
Antagonism of the rennin-angiotensin-aldosterone-system (RAAS) decreases BP and reduces proteinuria in chronic kidney disease. BP is decreased approximately 5 mmHg when angiotensin II blockers are added to angiotensin-converting enzyme (ACE) inhibitors and is less than typically seen when other agents are added to existing ACE inhibitor regimens. Dual RAAS blockade results in additional reduction in proteinuria. Clinically insignificant increases in hyperkalemia and modest decreases in GFR occur. Data regarding long-term preservation of renal function are lacking. We suggest dual RAAS blockade be used in patients with chronic kidney disease with residual proteinuria on maximal ACE inhibitor or angiotensin II blocker therapy, anticipating additional data with ongoing trials.
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