Renal artery calcification and mortality among clinically asymptomatic adults.

OBJECTIVES

The goal of this study was to assess the associations between renal artery calcification (RAC) and mortality in a healthy outpatient cohort with no known cardiovascular disease (CVD).

BACKGROUND

Studies in individuals with known diabetes and kidney disease have suggested that RAC confers additional mortality risk independent of coronary artery calcification, but this hypothesis has not been explored in healthier populations.

METHODS

RAC was assessed by using computed tomography scan in healthy outpatients with no known CVD. Cox proportional hazards models were used to examine the association of RAC with mortality.

RESULTS

The mean age of participants was 57 years; 42.6% were women. RAC was present in 622 (14%) of 4,450 participants. Over a median follow-up of 8.2 years, there were 178 deaths. After adjustment for age, sex, diabetes, smoking, cholesterol, and family history of CVD, the presence of RAC conferred a >60% increased hazard for all-cause mortality (hazard ratio [HR]: 1.63 [95% confidence interval (CI): 1.17 to 2.29]). Adjustment for calcification in other vascular beds attenuated this association (HR: 1.40 [95% CI: 0.99 to 1.97]). Adjustment for hypertension, a potential mediator of the association, did not substantially change the results (HR: 1.44 [95% CI: 1.02 to 2.03]). Adding RAC to a model including Framingham risk and coronary artery calcification improved the predictive ability of the model, from 0.73 to 0.77 (p = 0.0002); the net reclassification index was 14.4% for the addition of RAC. Results for cardiovascular mortality were not significant and were limited by the small number of cardiovascular deaths.

CONCLUSIONS

RAC was associated with an increased risk of subsequent all-cause mortality in healthy outpatient individuals, independent of traditional cardiac risk factors. The risk was modestly attenuated by adjustment for vascular calcification in other vascular beds, suggesting partial confounding by systemic calcified atherosclerosis. The effect did not seem to be mediated by hypertension.