Impact of Obesity in Kidney Diseases

Abstract

The clinical consequences of obesity on the kidneys, with or without metabolic abnormalities, involve both renal function and structures. The mechanisms linking obesity and renal damage are well understood, including several effector mechanisms with interconnected pathways. Higher prevalence of urinary albumin excretion, sub-nephrotic syndrome, nephrolithiasis, increased risk of developing CKD, and progression to ESKD have been identified as being associated with obesity and having a relevant clinical impact. Moreover, renal replacement therapy and kidney transplantation are also influenced by obesity. Losing weight is key in limiting the impact that obesity produces on the kidneys by reducing albuminuria/proteinuria, declining rate of eGFR deterioration, delaying the development of CKD and ESKD, and improving the outcome of a renal transplant. Weight reduction may also contribute to appropriate control of cardiometabolic risk factors such as hypertension, metabolic syndrome, diabetes, and dyslipidemia which may be protective not only in renal damage but also cardiovascular disease. Lifestyle changes, some drugs, and bariatric surgery have demonstrated the benefits.

Interactive effect of obesity and cognitive function decline on the risk of chronic kidney disease progression in patients with type 2 diabetes mellitus: a 9.1-year cohort study

“…The interaction of moderate and severe obesity with cognitive decline on CKD risk progression may be explained by biological and behavioral pathways. There are several common mechanisms in the associations between obesity, cognitive decline and CKD risk progression, including inflammation, metabolic disorders, and endothelial dysfunction [35][36][37][38][39][40]. With regards to inflammation [35,36], obesity can be mediated by downstream comorbid conditions such as hypertension or DM.…”

“…Microvascular endothelial dysfunction has also been reported to be a significant risk factor for cognitive impairment [40], and it may be a mechanism for an increased risk of CKD progression [47]. Three possible mechanisms have been proposed to explain the impact of the interaction between obesity and cognitive decline on CKD risk progression [35][36][37][38][39][40]. However, further studies are needed to verify these mechanisms.…”

Obesity and Cancer: Potential Mediation by Dysregulated Dietary Phosphate

“…Additionally, conditions comorbid with obesity could contribute to renal damage, thereby increasing the risk of dysregulated phosphate, phosphate toxicity, and associated tumorigenesis discussed in the present paper. Comorbid conditions such as atherogenic dyslipidemia, hypertension, insulin resistance, and type 2 diabetes cause renal damage in obesity through oxidative stress, inflammation, upregulation of the renin-angiotensinaldosterone system, increased activity of the sympathetic nervous system, and endothelial dysfunction [87]. Future research should investigate the biological pathways between obesity-related cancers and comorbid conditions involving impaired kidney function and dysregulation of phosphate metabolism.…”

Resistencia a La Insulina E Hiperinsulinemia en Escolares Con Exceso De Peso.

“…Estas diferencias entre niñas y niños han sido atribuidas a diferencias en el estadio puberal y al grado de adiposidad (37). Sin embargo, Wilkin y cols (38) y Peplies y cols (30) han mostrado en niñas prepúberes valores de insulina e Índice HOMA-IR más altos que en niños, sugiriendo que las niñas poseen una predisposición intrínseca asociada al género de desarrollar resistencia a la insulina, la cual es independiente del estadio puberal y del estado nutricional (39).…”