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Review
. 2021 Apr 13:8:655871.
doi: 10.3389/fmed.2021.655871. eCollection 2021.

A Nephrologist Perspective on Obesity: From Kidney Injury to Clinical Management

Clara García-Carro  1 , Ander Vergara  2   3 , Sheila Bermejo  2   3 , María A Azancot  2   3 , Joana Sellarés  2   3 , Maria José Soler  2   3
Affiliations
Review

A Nephrologist Perspective on Obesity: From Kidney Injury to Clinical Management

Clara García-Carro et al. Front Med (Lausanne). .

Abstract

Obesity is one of the epidemics of our era. Its prevalence is higher than 30% in the U.S. and it is estimated to increase by 50% in 2030. Obesity is associated with a higher risk of all-cause mortality and it is known to be a cause of chronic kidney disease (CKD). Typically, obesity-related glomerulopathy (ORG) is ascribed to renal hemodynamic changes that lead to hyperfiltration, albuminuria and, finally, impairment in glomerular filtration rate due to glomerulosclerosis. Though not only hemodynamics are responsible for ORG: adipokines could cause local effects on mesangial and tubular cells and podocytes promoting maladaptive responses to hyperfiltration. Furthermore, hypertension and type 2 diabetes mellitus, two conditions generally associated with obesity, are both amplifiers of obesity injury in the renal parenchyma, as well as complications of overweight. As in the native kidney, obesity is also related to worse outcomes in kidney transplantation. Despite its impact in CKD and cardiovascular morbility and mortality, therapeutic strategies to fight against obesity-related CKD were limited for decades to renin-angiotensin blockade and bariatric surgery for patients who accomplished very restrictive criteria. Last years, different drugs have been approved or are under study for the treatment of obesity. Glucagon-like peptide-1 receptor agonists are promising in obesity-related CKD since they have shown benefits in terms of losing weight in obese patients, as well as preventing the onset of macroalbuminuria and slowing the decline of eGFR in type 2 diabetes. These new families of glucose-lowering drugs are a new frontier to be crossed by nephrologists to stop obesity-related CKD progression.

Keywords: adiposity; chronic kidney disease; insulin resistance; kidney transplantation; obesity.

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Conflict of interest statement

AV reports non-financial support from Mundipharma, outside the submitted work. MS reports personal fees from NovoNordisk, Janssen, AstraZeneca, Fresenius, Mundipharma, Pfizer, Bayer and Vifor, grants and non-financial support from Boehringer, and non-financial support from Eli Lilly and Esteve outside of the submitted work. CG-C has received travel and congress fees support from Astra-Zeneca, Esteve, NovoNordisk, Boehringer-Ingelheim Lilly, Astellas, Otsuka, Novartis and Baxter. CG-C has given scientific lectures and participated in advisory boards organized by Astra-Zeneca, Boehringer-Ingelheim Lilly, Mundipharma and NovoNordisk. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Pathways involved in obesity-related kidney disease. Three main pathways involved (hemodynamic, adipose tissue related and insulin resistance—hyperinsulinemia pathways) have been highlighted in different colors. It can be observed how three pathways interact simultaneously to produce kidney injury. TNF-α, tumor necrosis factor α; MCP-1, monocyte chemoattractant protein 1; IL-6, interleukine 6; RAS, renin-angiotensin system; GFB, glomerular filtration barrier; SNS, sympathetic nervous system; Na+, sodium.
Figure 2
Figure 2
Connection between obesity and diabetes. Pathways involved in insulin resistance and insulin deficiency that lead to diabetes in obese patients. FFA, free fatty acids; TG, triglycerides.
See this image and copyright information in PMC

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