ESPE Abstracts (2022) 95 RFC11.3

ESPE2022 Rapid Free Communications Late Breaking (6 abstracts)

Predictors of kidney damage development in children with metabolically healthy and metabolically unhealthy obese phenotypes

Anna Di Sessa , Antonio Paride Passaro , Alberto Maria Colasante , Serena Ferrara , Giuseppina Rosaria Umano , Pierluigi Marzuillo & Emanuele Miraglia del Giudice


University of Campania "Luigi Vanvitelli", Naples, Italy

Background: A close association has been reported between obesity and renal damage in adults, but evidence in childhood is still limited.

Methods: We retrospectively studied 396 children and adolescents with obesity. Clinical, biochemical, and instrumental evaluations were performed. Patients were stratified according to the metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO) phenotypes. Kidney damage was defined as the presence of reduced eGFR and/or proteinuria and/or hypertension.

Results: Children with kidney damage had higher BMI-SDS values and an increased prevalence of Non Alcoholic fatty liver disease (NAFLD) than those without kidney damage (2.30±0.51 vs. 2.14±0.63 and 62.4% vs. 35.5%, P=0.012 and P<0.0001, respectively). As markers of inflammation, they also showed higher levels of platelets, white blood cells, and neutrophils than those without kidney damage (P=0.038, P=0.017, and P=0.037, respectively). More, higher Homeostasis model assessment of insulin resistance (HOMA-IR) values were found in subjects with kidney damage compared to those without kidney damage (4.58±3.47 vs. 3.38±1.96, P<0.0001). As expected, patients with MUO phenotype showed a worse cardiometabolic profile than those with MHO phenotype (all P<0.0001). MUO patients also showed a higher prevalence of NAFLD compared to MHO subjects (80% vs. 59.5%, P=0.003). They also had an OR to show kidney damage of of 1.92 (CI 1.22-3.01, P=0.005) after adjustment for age, sex, BMI-SDS, and HOMA-IR. Patients with MUO having kidney damage showed higher prevalence of NAFLD and increased HOMA-IR values than those without kidney damage (65.2% vs. 34.8%, P<0.0001; 5.33±3.19 vs. 4.09±2.02, P=0.015, respectively). Inflammation markers such as platelets, white blood cells, and neutrophils were also found to be higher in these patients compared to those without kidney damage (P=0.015, P=0.039, and P=0.04, respectively). More, significant differences were reported for uric acid, fasting glucose, fasting insulin, HOMA-IR, total cholesterol, and LDL cholesterol levels in MHO children with kidney damage compared to peers without kidney damage (all P<0.05). Children with MHO phenotype showed an OR of 1.05 (CI 1.00-1.09, P=0.028) to show kidney damage after adjustments for confounders.

Conclusion: Children with obesity showed an increased risk of early kidney damage. Although this risk has been found to be higher in subjects with MUO phenotype, it should be not underestimated in children with MHO profile because of their adverse cardiometabolic risk profile predisposing to obesity-related comorbidities development over time.

Volume 95

60th Annual ESPE (ESPE 2022)

Rome, Italy
15 Sep 2022 - 17 Sep 2022

European Society for Paediatric Endocrinology 

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