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Chronic Kidney Disease
Author(s) -
Peter A. McCullough
Publication year - 2006
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.106.636662
Subject(s) - medicine , kidney disease , disease , pathology
Inhibition of the renin-angiotensin-aldosterone system (RAAS) is a cornerstone of treatment in patients with chronic kidney disease (CKD).1 Treatment with ACE inhibitors (ACEIs) and angiotensin receptor blockers has been shown to lower blood pressure, reduce proteinuria, and slow the progression of CKD caused by diabetes and other diseases.1 Approximately 50% of patients with CKD will incur cardiovascular disease (CVD); conversely, 20% of those with CVD meet a definition of CKD, most commonly an estimated glomerular filtration rate of <60 mL/min per 1.73 m2, with no other signs of kidney damage (Figure). Clinical trials of patients with CVD often attempt to exclude patients with CKD, given their higher rates of study medication discontinuation, difficulty in clinical and experimental treatment, and potentially unique form(s) of CVD, which may add to variation in trial outcomes. We have learned in recent years that the serum creatinine alone is an insensitive indicator of reduced renal filtration, and the estimated glomerular filtration rate (eGFR) is best obtained from a calculation based on the creatinine, age, gender, and race.2 In the Prevention of Events with an ACE Inhibitor (PEACE) trial discussed in …

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