The role of calcium antagonists in chronic kidney disease.

Curr Opin Nephrol Hypertens

Rush University Hypertension/Clinical Research Centre, Department of Preventive Medicine, Rush Presbyterian/St Luke's Medical Centre, Chicago, Illinois 60612, USA.

Published: March 2004

Purpose Of Review: To review goals of antihypertensive treatment in chronic kidney disease in the context of what role calcium antagonists play toward reducing progression of kidney disease.

Recent Findings: All recently published guidelines recommend a blood pressure goal of less than 130/80 mmHg in patients with chronic kidney disease. Use of calcium antagonists is not recommended as part of the initial armamentarium. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, when used in concert with diuretics reduce blood pressure as well as both proteinuria and the rate of decline in the glomerular filtration rate. The evidence for calcium antagonists in this regard is more divergent. Dihydropyridine calcium antagonists, e.g. amlodipine, felodipine, help achieve blood pressure goals and reduce stroke risk. When used with a renin-angiotensin system blocker they do not detract from the benefits of this blockade on slowing progression of kidney disease. Non-dihydropyridine calcium antagonists, e.g. verpamil or diltiazem, decrease proteinuria and in studies with 5 to 6 years follow-up preserve kidney function similarly to angiotensin-converting enzyme inhibitors. The reason for this outcome difference between calcium antagonists is partial preservation of renal autoregulation compared to its obliteration by the dihydropyridine subclass.

Summary: Use of calcium antagonists is safe and necessary to achieve blood pressure goals in people with chronic kidney disease. While both subclasses are safe and necessary to achieve blood pressure goals, dihydropyridine calcium antagonists fail to significantly slow the progression of kidney disease among patients with established nephropathy and macroalbuminuria when compared to agents that block the renin-angiotensin system.

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Source
http://dx.doi.org/10.1097/00041552-200403000-00003DOI Listing

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