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Review
. 2015 Aug 15;309(4):F273-9.
doi: 10.1152/ajprenal.00547.2014. Epub 2015 Jun 3.

Obesity and renovascular disease

Xin Zhang  1 , Lilach O Lerman  2
Affiliations
Review

Obesity and renovascular disease

Xin Zhang et al. Am J Physiol Renal Physiol. .

Abstract

Obesity remains a prominent public health concern. Obesity not only contributes greatly to cardiovascular events but has also been identified to initiate and affect the progression of preexisting chronic kidney disease. The prevalence of renal artery stenosis is growing world-wide, especially in the elderly population and in individuals with atherosclerotic risk factors such as obesity. Prolonged renovascular disease causes inflammation and microvascular remodeling within the post-stenotic kidney, which promote tissue scarring and may account for irreversible renal damage. Obesity has been shown to aggravate kidney damage via several pathways, including exacerbation of microvascular regression and renal cell injury mediated by adipocytes and insulin resistance, thereby worsening the structural and functional outcomes of the kidney in renovascular disease. Dietary modification and inhibition of the renin-angiotensin-aldosterone system have been shown to alleviate obesity-induced tissue injury and remodeling. Possibly, angiogenic factors may boost microvascular repair in the ischemic kidney in the obesity milieu. Novel therapeutic interventions targeting deleterious pathways that are activated by obesity and responsible for kidney damage need to be explored in future studies.

Keywords: adipocyte; insulin resistance; microvasculature; obesity; renal artery stenosis; renin-angiotensin-aldosterone system.

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Figures

Fig. 1.
Fig. 1.
Representative microcomputed tomography images showing the intrarenal microvasculature in lean, obese, renal artery stenosis (RAS), and obese+RAS pigs. Microvascular density is markedly decreased in Obese+RAS kidneys compared with RAS alone, suggesting aggravated microvascular loss.
Fig. 2.
Fig. 2.
Potential mechanisms by which obesity promotes kidney injury in the post-stenotic kidney. Renal artery stenosis activates the renin-angiotensin-aldosterone and the sympathetic nervous systems, which lead to vasoconstriction and hypertension. Oxidative stress, inflammation, and decreased angiogenic signaling elicit microvascular rarefaction and glomerulosclerosis in the stenotic kidney. Expanded adipose tissue not only enhances systemic hypertension but also magnifies inflammatory and oxidative injury by secreting cytokines, elicits podocyte injury, and aggravates microvascular rarefaction.
See this image and copyright information in PMC

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