MO412: Impact of Body Mass Index on Mortality and End–Stage Kidney Disease in Patients With Non-Dialysis Dependent Chronic Kidney Disease

Abstract

Abstract BACKGROUND AND AIMS Obesity is a major global problem affecting more than 1.9 billion adults [1]. The aetiological factors of obesity are complex and consist of genetic, social and environmental elements. Obesity can lead to chronic kidney disease (CKD) via both direct and indirect pathways. However, the effect of obesity on the progression of CKD remains unclear. This study aimed to investigate the impact of higher body mass index (BMI) on clinical outcomes in a large UK cohort of patients with non-dialysis dependent (NDD)-CKD. METHOD The Salford Kidney Study is a longitudinal prospective cohort of more than 3000 patients with NDD-CKD. All patients with available BMI at baseline from October 2002 to December 2016 were included in this study. Patients were grouped according to their BMI into underweight [(BMI < 18.5 kg/m2), n = 35], healthy weight [(BMI 18.5–24.9 kg/m2), n = 628], overweight [(BMI 25–29.9 kg/m2), n = 860] and obese [(BMI > 30 kg/m2), n = 897]. Cox-regression analysis was performed to study the strength of association between BMI groups and major clinical outcomes [all-cause mortality, end-stage kidney disease (ESKD) and annual rate of progression of CKD (delta eGFR)] by using the healthy weight BMI group as a reference. The outcomes were also analysed in a 1:1 propensity score-matched analysis between patients in the healthy weight and obese groups (414 in each). RESULTS A total of 2420 patients with a median follow-up of 44.3 months were available for analysis. The median age of the cohort was 67 years and 58% were male. The prevalence of hypertension and diabetes increased with a higher BMI (84.0% and 18.8% in healthy weight, 91.7% and 31.0% in overweight and 94.2% and 46.8% in the obese groups, respectively). There was no significant difference in the baseline eGFR between the groups with a median of 29.3 mL/min/1.73 m2. There was an inverse association between a higher BMI and all-cause mortality [obese versus healthy weight: hazard ratio (HR): 0.88; 95% confidence interval (CI): 0.81–0.96; P = 0.004] but there was no association observed with ESKD (HR 0.96; 95% CI: 0.87–1.06; P = 0.422). The delta eGFR was not significantly different between the different BMI groups (Table 1). A similar observation with all-cause mortality being better in the obese group was noted in the propensity-matched analysis (HR:0.88; CI:0.81–0.96; P = 0.004) (Table 2). CONCLUSION In our large cohort of patients, a higher BMI was seen to be protective against all-cause mortality. Furthermore, the annual rate of decline in eGFR was similar among the BMI groups. Patients with normal BMI had significantly higher all-cause mortality compared with the obese group.