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Review
. 2022 Jul 19;9(2):61-74.
doi: 10.1002/osp4.629. eCollection 2023 Apr.

Obesity and chronic kidney disease: A current review

Affiliations
Review

Obesity and chronic kidney disease: A current review

Saira Nawaz et al. Obes Sci Pract. .

Abstract

Background: Obesity poses significant challenges to healthcare globally, particularly through its bi-directional relationship with co-morbid metabolic conditions such as type 2 diabetes and hypertension. There is also emerging evidence of an association between obesity and chronic kidney disease (CKD) which is less well characterized.

Methods: A literature search of electronic libraries was conducted to identify and present a narrative review of the interplay between obesity and CKD.

Findings: Obesity may predispose to CKD directly as it is linked to the histopathological finding of obesity-related glomerulopathy and indirectly through its widely recognized complications such as atherosclerosis, hypertension, and type 2 diabetes. The biochemical and endocrine products of adipose tissue contribute to pathophysiological processes such as inflammation, oxidative stress, endothelial dysfunction, and proteinuria. The prevention and management of obesity may prove critical in counteracting both the development and advancement of CKD. Moreover, measures of abdominal adiposity such as waist circumference, are generally associated with worse morbidity and mortality in individuals receiving maintenance hemodialysis.

Conclusion: Obesity is a risk factor for the onset and progression of CKD and should be recognized as a potential target for a preventative public health approach to reduce CKD rates within the general population. Future research should focus on the use of glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter 2 inhibitors in patients with CKD and obesity due to their multi-faceted actions on major outcomes.

Keywords: chronic kidney disease; dialysis; obesity; transplantation.

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Conflict of interest statement

Smeeta Sinha reports receiving research funding from Amgen, Ethicon, and AstraZeneca and receiving honoraria from Astra Zeneca, Napp Pharmaceuticals, Vifor Pharma, Novartis, Bayer, and Sanofi‐Genzyme. Philip A. Kalra reports grants from Vifor and receiving Honoria from Astra Zeneca, Astellas, Pharmacosmos, Boehringer Ingelheim, Napp, and Vifor. The other authors have nothing to disclose.

Figures

FIGURE 1
FIGURE 1
Direct and indirect mechanisms by which adiposity can perturb renal function and lead to kidney disease. HDL, high‐density lipoprotein; IL‐6, interleukin‐6; LDL, low‐density lipoprotein; MCP‐1, monocyte chemo‐attractant protein 1; PAI, plasminogen‐activator inhibitor; TG, triglycerides; TNF‐α, tumor necrosis factor alpha

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