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(Hypertension. 2009;53:749.)
© 2009 American Heart Association, Inc.
Editorial Commentaries |
From the Division of Nephrology, Virginia Commonwealth University Health System, Richmond.
Correspondence to Domenic A. Sica, MD, Professor of Medicine and Pharmacology, Chairman, Clinical Pharmacology and Hypertension, Virginia Commonwealth University Health System, 1101 E Marshall St, Sanger Hall-Room 8-062, Richmond, VA 23298-0160. E-mail dsica@mcvh-vcu.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Chronic kidney disease (CKD), with or without associated comorbidities, has emerged as a global health care problem, with >1.75 million people currently being kept alive by means of dialysis or transplantation.1 This number is projected to double within the next decade. The cumulative global cost for dialysis and transplantation is predicted to exceed $1 trillion over the next decade. Preventing the development of end-stage renal disease would obviously have a significant positive impact on global health care costs, which would be of particular import for developing countries where dialysis is largely unaffordable. This economic plight is being addressed with implementation of early screening for the presence of CKD. Such screening, including measuring blood pressure (BP), serum creatinine, and urine protein excretion, carries minimal cost and is readily available.2 Once a patient is screened, cost-effective treatment measures exist that can target BP, protein excretion, smoking status, body weight, glycemic control, as well as management of hyperlipidemia.
BP reduction in CKD patients can prove particularly challenging, not uncommonly requiring
3 antihypertensive medications, and even then, BP is often still not at goal. Reducing urine protein excretion is another modifiable risk factor for renal failure progression that is best managed with multidrug therapy. During the past 2 decades, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and, most recently, direct renin inhibitors have emerged as preferred therapies for both the BP and proteinuria treatment aspects of CKD. Each of these drug classes, whether given individually or when combined, has a finite capacity to
Related Article:
Hypertension 2009 53: 754-760.
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