Abstract
Abstract Background and Aims Obesity is a strong risk factor for the development of chronic kidney disease (CKD) through its close association with hypertension and diabetes. As metabolic demands increase with higher body mass indices, a compensatory glomerular hyperfiltration occurs to meet the increasing burden, consequently increasing intraglomerular pressure that can lead to the development of CKD and may influence the progression of already established kidney damage. The aim of our study was to determine whether there was an association between body mass index (BMI) and kidney disease progression in patients with primary glomerulonephritides (GN). Method We performed a single-centre retrospective cohort study in patients with biopsy-proven primary glomerular disease [minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous nephropathy (MN) and IgA nephropathy (IgAN)] diagnosed between July 1998 and December 2018. We excluded patients with no available data on weight at presentation or height, and those lost to follow-up. Patients were stratified into three groups according to BMI to <25 kg/m2, between 25-30 kg/m2 and >30 kg/m2. Baseline characteristics were compared between the groups, serum creatinine, proteinuria and microscopic hematuria were recorded at presentation, and yearly afterwards until the end of follow-up. We compared among BMI groups the mean yearly change in eGFR, and yearly increase in proteinuria. Renal adverse outcomes were: time to doubling serum creatinine and initiation of renal replacement therapy (RRT). We performed a multivariate survival analysis to evaluate the risk factors associated with a renal composite outcome that included doubling serum creatinine and initiation of RRT. Results We included 178 patients that presented with a biopsy-proven primary glomerular disease (18 patients with MCD, 38 had FSGS, 38 MN and 84 IgAN), with a mean age of 50.6±18.0 years, 71.3% were males, mean BMI of 28.2±5.4 kg/m2. There were no differences in age at presentation, sex or BMI between the four groups of GN. 24.2% of patients had BMI <25 kg/m2 (Non-obese group), 43.8% had a BMI between 25-30 kg/m2 (Overweight group) and 32% had BMI >30 kg/m2 (obese group). Non-obese group had lower baseline systolic and diastolic blood pressure than the overweight group (p=0.021 and p=0.015) and the obese group (p=0.001 and p<0.001), but there were no differences in blood pressure between the latter two groups. Patients in the non-obese group were younger (p=0.001) than in the other two groups. There were no differences in baseline serum creatinine (p=0.60), proteinuria (p=0.98) or microscopic hematuria (p=0.46) across the three BMI groups. Survival analysis revealed no relation between BMI and the renal composite outcome (log-rank=2.18, p=0.337) or death (log-rank=0.117, p=0.943). Multivariate survival analysis revealed that the risk factors associated with the renal composite outcome were baseline creatinine (χ2=6.61, p=0.010) and urine albumin-creatinine ratio (χ2=6.48, p=0.011), but there was no association with BMI (p=0.427). Conclusion BMI at presentation was associated with higher blood pressure, but not with baseline serum creatinine or proteinuria, and was not associated with an increased risk of progression of kidney disease in primary glomerular diseases.
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