Renal dysfunction predicts attenuation of ischemic heart disease mortality risk from elevated glucose among treated hypertensive patients.
Academic Article
Overview
abstract
BACKGROUND: Impaired fasting glucose (IFG) and renal dysfunction are recognized as independent risk factors for adverse heart outcomes. This study examines the interaction of renal dysfunction and IFG (>or=110 mg/dL) upon the risk of ischemic heart disease (IHD) mortality among treated hypertensive subjects. METHODS: Subjects were 9918 participants in a worksite-based antihypertensive treatment program in New York City (1981 to 1999) with baseline estimated glomerular filtration rate (GFR) >30 mL/min/1.73 m2 (estimated by Cockcroft and Gault formula) observed for a mean follow-up of 9.6 +/- 5.0 years (range 0.5-20.0 years). Outcome events were IHD deaths (n = 337) ascertained from the National Death Index. Cox proportional hazard models were constructed for the entire cohort to assess the interaction and then stratified by moderate renal dysfunction (MRD; GFR 60-30 mL/min/1.73 m2). Age and sex adjusted rates were calculated within MRD and NKF-defined categories. Hazard ratios for IFG were calculated within MRD strata. RESULTS: The interaction product term of MRD and IFG significantly improved (P = .001) a Cox proportional hazard model after adjusting for known cardiovascular risk factors. Among participants with GFR >or=60 mL/min/1.73 m2 the IHD mortality hazard ratio for IFG was 1.47 (95% CI = 1.09-1.99; P = .012). Conversely, among participants with MRD, the IHD mortality hazard ratio for IFG was 0.44 (95% CI = 0.21-0.94; P = .034). CONCLUSIONS: These results suggest an attenuating effect modification of GFR on IHD mortality risk associated with IFG among treated hypertensive subjects. Whether the observed qualitative interaction is simply statistical or reflects a biological counter-regulatory mechanism requires additional study.
