Endocrine Abstracts

Background: Obesity can damage kidney via directly, through the production of pro-inflammatory adipocytokines, and indirectly due to systemic complications. Several strategies are available for weight loss (lifestyle, anti-obesity drugs and surgery therapy), but there are no guidelines to manage subjects with obesity and chronic kidney disease. Very low-calorie ketogenic diet (VLCKD) is an increasingly used tool for weight loss in subjects with obesity. Thus, we aimed to investigate the effects of VLCKD on subjects with obesity and mild kidney failure (MKF).

Methods: A cross-sectional study was conducted on 92 subjects with obesity (35.85 ± 4.61 kg/m²; 27M/65F aged 52.03 ± 11.41 years) that underwent to a VLCKD. Anthropometric parameters and biochemistry data were collected before and at the end of active phase of VLCKD. Glomerular Filtration Rate (GFR) was calculated with the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. Forty-nine subjects had MKF (GFR 60-89 ml/min/1.73m²) and 43 had normal kidney function (NKF) (GFR≥90 ml/min/1.73m²) and were therefore designated as control.

Results: In the entire study population, the average weight loss was -10.67 ± 4.29 % of initial weight, with significant reductions in BMI (from 35.85 ± 4.61 to 32.50 ± 4.35 kg/m², P<0.001) and waist circumference (from 107.01 ± 11.32 to 99.98 ± 11.42 cm, P<0.001) at the end of the active phase of VLCKD. We also reported an improvement of several metabolic parameters: fasting blood glucose, insulin, HOMA-IR, total cholesterol, LDL and triglycerides (P<0.001 for all). No clinically relevant variation regarding liver and kidney function were detected. Of note, at the end of the active phase of VLCKD we found out significant reduction of GFR in subjects with NKF (from 104.53 ± 7.30 to 100.76 ± 11.39 ml/min/1.73m²; P=0.031) while a significant increase in subjects with MKF (from 79.33 ± 7.82 to 84.61 ± 11.65 ml/min/1.73m²; P=0.001). Finally, 30.6% of patients with MKF reported normalization of glomerular filtrate after the VLCKD.

Conclusion: Obesity can damage the kidney through alterations in the hemodynamics resulting in glomerular hyperfiltration, proteinuria and, finally, impairment of the GFR. VLCKD on the one hand reduced glomerular hyperfiltration in subjects with obesity with still NKF, and on the other hand improved filtration in those subjects who have already suffered a reduction in GFR. Consequently, VLCKD is a safe and effective tool for obesity-related kidney complications.