BACKGROUND: Diabetic nephropathy (DN) is a potentially fatal complication of diabetes mellitus. While lifestyle changes can reduce diabetes risk, it is unclear whether improved lifestyle can slow or reverse DN progression. This study evaluated whether an intensive lifestyle intervention (IL-I) targeting weight loss and inflammation through increased physical activity and reduced caloric intake can delay DN progression.

MATERIAL AND METHODS: Patients were randomly divided into 2 groups. Both groups received diet and exercise guidelines, but one (IL-I) received more frequent external support than the other (control). We compared markers of metabolic and cardiovascular health, redox status, inflammation, and renal function between groups at 3 and 6 months. Metabolic and cardiovascular metrics included BMI, blood pressure, blood glycosylated hemoglobin (HbA1c), and serum HDL-cholesterol. Redox status was evaluated by serum superoxide dismutase (SOD) and the lipid oxidation product malondialdehyde (MDA), while inflammation was assessed by serum concentrations of IL-6 and TNF-α. Renal function was assessed by urine/serum 8-OHdG, albumin: creatinine ratio (ACR), and the renal fibrosis marker TGF-β1.

RESULTS: Both groups demonstrated initial BMI reduction, lower HbA1c, and higher HDL-cholesterol, but changes were significantly larger in the IL-I group at 6 months. Blood pressure at 6 months was reduced only in the IL-I group. The IL-I group also achieved a greater sustained SOD increase and MDA reduction. Finally, only the IL-I group demonstrated significant reductions in urine ACR, serum/urine 8-OHdG, and plasma TGF-β1. These indicators deteriorated after IL-I was stopped.

CONCLUSIONS: Lifestyle changes including exercise and diet can delay renal damage and promote improvement from DN.

Keywords: Caloric Restriction, Fibrosis, Life Style, Blood Glucose, Body Mass Index, Case-Control Studies, Cholesterol, HDL, Diabetes Mellitus, Glycated Hemoglobin A, RNA-Binding Proteins, Risk Reduction Behavior, Transforming Growth Factor beta1