Hypertension and diabetes, but not leptin and adiponectin, mediate the relationship between body fat and chronic kidney disease.

Adiponectin Diabetes Hypertension Kidney Leptin Obesity

Journal

Endocrine
ISSN: 1559-0100
Titre abrégé: Endocrine
Pays: United States
ID NLM: 9434444

Informations de publication

Date de publication:
16 Apr 2024
Historique:
received: 14 12 2023
accepted: 28 03 2024
medline: 17 4 2024
pubmed: 17 4 2024
entrez: 16 4 2024
Statut: aheadofprint

Résumé

Obesity may promote kidney damage through hemodynamic and hormonal effects. We investigated the association between body mass index (BMI), total body fat (TBF) and chronic kidney disease (CKD) and whether hypertension, diabetes, leptin and adiponectin mediated these associations. In this cross-sectional analysis of the Netherlands Epidemiology of Obesity study, 6671 participants (45-65 y) were included. We defined CKD as eGFR <60 ml/min/1.73 m At baseline mean (SD) age was 56 (6), BMI 26.3 (4.4), 44% men, and 4% had CKD. Higher BMI and TBF were associated with 1.08 (95%CI 1.05; 1.11) and 1.05-fold (95%CI 1.02; 1.08) increased odds of CKD, respectively. As adiponectin was not associated with any of the outcomes, it was not studied further as a mediating factor. The association between BMI and CKD was 8.5% (95%CI 0.5; 16.5) mediated by diabetes and 22.3% (95%CI 7.5; 37.2) by hypertension. In addition, the association between TBF and CKD was 9.6% (95%CI -0.4; 19.6) mediated by diabetes and 22.4% (95%CI 4.2; 40.6) by hypertension. We could not confirm mediation by leptin in the association between BMI and CKD (35.6% [95%CI -18.8; 90.3]), nor between TBF and CKD (59.7% [95%CI -7.1; 126.6]). Our results suggest that the relations between BMI, TBF and CKD are in part mediated by diabetes and hypertension.

Identifiants

pubmed: 38627329
doi: 10.1007/s12020-024-03811-6
pii: 10.1007/s12020-024-03811-6
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s).

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Auteurs

Robin Lengton (R)

Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands. r.lengton@lumc.nl.
Department of Internal Medicine, Division of Endocrinology, Erasmus University Medical Center Rotterdam, Rotterdam, The Netherlands. r.lengton@lumc.nl.

Friedo W Dekker (FW)

Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.

Elisabeth F C van Rossum (EFC)

Department of Internal Medicine, Division of Endocrinology, Erasmus University Medical Center Rotterdam, Rotterdam, The Netherlands.

Johan W de Fijter (JW)

Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.

Frits R Rosendaal (FR)

Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.

Ko Willems van Dijk (KW)

Department of Human Genetics and Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands.

Ton J Rabelink (TJ)

Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.

Saskia Le Cessie (S)

Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.
Department of Biomedical Data Sciences, Leiden University Medical Center, Leiden, The Netherlands.

Renée de Mutsert (R)

Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.

Ellen K Hoogeveen (EK)

Department of Clinical Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.
Department of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Department of Nephrology, Jeroen Bosch Hospital, Den Bosch, The Netherlands.

Classifications MeSH