Influence of obesity on progression of non-diabetic chronic kidney disease: a retrospective cohort study.Nephron Clin Pract. 2009; 113(1):c16-23.NC
BACKGROUND
There is increasing awareness of the impact of obesity on chronic diseases including chronic kidney disease (CKD). Until recently, a limited number of epidemiologic studies have examined the association between obesity and CKD. We conducted a retrospective cohort study to evaluate whether obesity impacts on the rate of non-diabetic CKD progression.
METHODS
The medical records of 125 non-diabetic CKD patients in the Sheffield Kidney Institute, Sheffield, UK, who have been followed-up for around 10 years, were reviewed. Various socio-demographic, clinical and biochemical parameters were retrospectively collected from the patients' database. Participants were categorized into normal weight, overweight and obese groups. Multivariate regression analysis was used for modelling with estimated glomerular filtration rate (eGFR) reduction per year as the dependent variable to evaluate the impact of obesity (BMI) on CKD progression.
RESULTS
Patients studied were mostly CKD stage 3 with a mean GFR of 36.2 ml/min/1.73 m(2) for the control group and 44.3 ml/min/1.73 m(2) for those who were overweight or obese. Baseline diastolic and mean arterial blood pressure were significantly higher in overweight than normal weight CKD patients (p = 0.009 and p = 0.014 respectively). On follow-up, systolic, diastolic and mean arterial blood pressure were significantly higher in overweight (p = 0.03, p = 0.005 and p = 0.003, respectively) and obese (p = 0.008, p = 0.022 and p = 0.003, respectively) compared to normal weight CKD patients. Mean follow-up triglycerides level was significantly higher in obese than normal weight patients (p = 0.042). The frequency of CKD progression based on eGFR fall per year (>1 ml/min/1.73 m(2)/year) was 62.5% in overweight and 79.5% in obese compared to 44.7% in normal weight CKD patients (p = 0.007). However, no significant difference in the rate of progression (fall of eGFR ml/min/1.73 m(2)/year) was observed between the three groups. On multivariate regression analysis, adjusted for other covariates (age, BP and proteinuria), baseline BMI was an independent predictor of CKD progression (fall in eGFR, ml/min/1.73 m(2)/year) (R(2) = 0.122 and p < 0.001). Percentage changes in BMI over the observation period did not affect the rate of eGFR decline. Young age also predicted a faster CKD progression.
CONCLUSIONS
Baseline BMI and young age are strongly and independently associated with faster CKD progression based on the annual rate of eGFR fall. Prospective studies to investigate the relationship between BMI and CKD and its complications are warranted.
