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


CONCLUSIONS
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.
Shlipak
Michael G
MG
San Francisco VA Medical Center, San Francisco, CA 94121, USA. michael.shlipak@ucsf.edu
Katz
Ronit
R
Kestenbaum
Bryan
B
Fried
Linda F
LF
Siscovick
David
D
Sarnak
Mark J
MJ
D000367:Age Factors; D000368:Aged; D050197:Atherosclerosis / Q000150:complications / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D003404:Creatinine / Q000097:blood; D055316:Cystatin C / Q000097:blood; D005260:Female; D005919:Glomerular Filtration Rate; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007674:Kidney Diseases / Q000209:etiology* / Q000503:physiopathology; D016014:Linear Models; D008137:Longitudinal Studies; D008297:Male; D016017:Odds Ratio; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D014481:United States
C525030:CST3 protein, human; D055316:Cystatin C; D003404:Creatinine