Body mass index and the risk of progression of chronic kidney disease.

OBJECTIVE

To examine the independent relationship between obesity, as estimated by body mass index (BMI), and progression of chronic kidney disease. We hypothesized that BMI would be associated with decline in estimated glomerular filtration rate (eGFR), independent of diabetes mellitus, hypertension, and other risk factors for progression of chronic kidney disease.

DESIGN

A retrospective cohort study was carried out.

SETTING

The study was carried out at Nephrology ambulatory clinics of the London Health Sciences Centre, Canada.

PATIENTS

The study included incident and prevalent patients with eGFR <60 mL/min/1.73 m(2). Eligible patients were observed between the calendar years 2005 and 2007. Subjects were excluded on the basis of <12 months of follow-up, age <18 years, or past kidney transplantation.

INTERVENTION

Least-squares regression was used to estimate change of eGFR over time. Baseline clinical and demographic factors, including BMI and diabetes, were examined in univariate and multivariate analyses.

MAIN OUTCOME MEASURE

Change in eGFR over time was assessed in this study.

RESULTS

A total of 214 subjects were observed for a mean of 4.48 ± 1.84 years. In univariate analysis, BMI was not statistically associated with eGFR change as either a continuous or a categorical variable. Using a BMI cut-off of 30 kg/m(2), no statistical difference in slope of eGFR was found, with a decline of 2.2 mL/min/1.73 m(2) per year in the nonobese group, and 2.69 mL/min/1.73 m(2) per year in the obese group (P = .13). Multivariate analysis demonstrated high baseline eGFR, proteinuria, and diabetic nephropathy to be associated with a faster decline in eGFR. Use of renin-angiotensin-aldosterone blockade was associated with an improved slope of eGFR over time.

CONCLUSION

Our results do not support the hypothesis that obesity is independently associated with a decline in kidney function.