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Clinical and subclinical cardiovascular disease and kidney function decline in the elderly.

Shlipak MG, Katz R, Kestenbaum B, Fried LF, Siscovick D, Sarnak MJ. Clinical and subclinical cardiovascular disease and kidney function decline in the elderly. Atherosclerosis. 2009 May 1; 204(1):298-303.

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OBJECTIVE: Kidney function decline in elderly persons may be the result of microvascular atherosclerosis. As a proxy for the renovascular system, we evaluated the association of clinical and subclinical cardiovascular disease (CVD) with kidney function decline. METHODS: This study included 4380 subjects from the Cardiovascular Health Study, a longitudinal, community-based cohort of persons aged > or = 65 from 4 U.S. communities. Creatinine and cystatin C were measured at baseline, year 3, and year 7; eligible subjects had at least two measures. Creatinine-based estimated glomerular filtration rate (eGFR(creat)) was calculated using the MDRD equation. Rapid kidney function decline was defined as an annual eGFR loss > 3 mL/min/1.73 m(2). Predictors of rapid kidney decline included prevalent and subclinical measures of CVD. RESULTS: Mean decline in eGFR(creat) was 0.4+/-2.6/year; 714 (16%) had rapid progression. In multivariate models adjusted for demographics, cardiovascular risk factors, and inflammation, prevalent stroke (OR, 95% CI: 1.55, 1.16-2.08) and heart failure (OR, 95% CI: 1.80, 1.40-2.31) were independent predictors of rapid kidney decline. Among persons without clinical CV, the subclinical disease measures ankle-arm index < 0.9 (OR, 95% CI: 1.67, 1.25-2.24), common carotid intima-media thickness ( > or = 1.14 mm) (OR, 95% CI: 1.52, 1.12-2.06) and internal carotid intima-media thickness ( > 1.82 mm) (OR, 95% CI: 1.50, 1.12-2.02) had independent associations with rapid kidney function decline. Results were similar using cystatin C. CONCLUSION: Clinical atherosclerosis and heart failure and subclinical measures of CVD have independent associations with kidney function decline progression in the elderly, suggesting an underlying role of renal atherosclerosis.

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