obesity has become a heavy public health problem in the united states , with a prevalence among adults increasing to 32% from 13% between the 1960s and 2004 .
currently , 66% of adults and 16% of children and adolescents are overweight or obese .
although obesity has long been recognized as an independent risk factor for cardiovascular diseases and diabetes mellitus , newer research points to obesity as an important risk factor for chronic kidney diseases ( ckds ) [ 24 ] . in 1974 , weisinger et al .  
subsequent studies confirmed that obesity could induce renal injury , namely , obesity - related glomerulopathy ( org ) [ 68 ] . a large - scale clinicopathologic study including 6818 renal biopsies from 1986 to 2000 revealed a progressive increase in biopsy incidence of org from 0.2% in 19861990 to 2.0% in 19962000 . the tenfold increase in incidence of org over 15 years suggests a newly emerging epidemic .
the clinical characteristics of subjects with org typically manifest with nephrotic or subnephrotic proteinuria , accompanied by renal insufficiency [ 810 ] .
histologically , org presents as focal segmental glomerulosclerosis ( fsgs ) and glomerular hypertrophy or glomerular hypertrophy alone and relatively decreased podocyte density and number and mild foot process fusion [ 8 , 11 , 12 ] .
clinically , it is distinguished from idiopathic fsgs ( i - fsgs ) by its lower incidence of nephrotic syndrome , more benign course , and slower progression of proteinuria and renal failure [ 8 , 11 ] .
potential mechanisms by which obesity affects renal physiology include altered renal hemodynamics , insulin resistance , hyperlipidemia , activation of renin - angiotensin - aldosterone system ( raas ) , inflammation , and oxidative stress .
increases in both glomerular filtration rate ( gfr ) and renal plasma flow ( rpf ) were observed in obese subjects and animals [ 13 , 14 ] .
this likely occurs because of afferent arteriolar dilation as a result of proximal salt reabsorption , coupled with efferent renal arteriolar vasoconstriction as a result of elevated angiotensin ii ( angii ) .
these effects may contribute to hyperfiltration , glomerulomegaly , and later focal glomerulosclerosis [ 8 , 9 ] .
insulin resistance can raise the transcapillary pressure gradient and cause hydrostatic pressure and hyperfiltration by reducing norepinephrine - induced efferent arteriolar constriction , leading to glomerular hypertrophy and sclerosis .
hyperinsulinemia also has been shown to stimulate the synthesis of growth factors such as insulin - like growth factor- ( igf- ) 1 and igf-2 and transforming growth factor-1 ( tgf-1 ) , which accelerate production of extracellular matrix and promote glomerular hypertrophy and sclerosis [ 17 , 18 ] .
hyperlipidemia may promote glomerulosclerosis through mechanisms that involve engagement of low - density lipoprotein receptors on mesangial cells , direct podocyte toxicity , oxidative cellular injury , macrophage chemotaxis , and increase renal expression of sterol regulatory element - binding proteins ( srebp-1 and srebp-2 ) , resulting in the renal accumulation of cholesterol and triglycerides and together with significant renal increase of fibrogenic cytokines [ 19 , 20 ] .
obese subjects usually have increases in plasma renin activity , angiotensinogen , angiotensin - converting enzyme activity , and circulating angii , which trigger or promote renal damage by renal hemodynamic changes and nonhemodynamic pathways such as hyperinsulinemia , oxidative stress , and inflammation [ 2123 ] .
inflammatory abnormalities and oxidative stress are characteristic findings of obesity and play important roles in the renal damage associated with obesity , which will be discussed in detail in the following .
recent studies have demonstrated that obesity causes chronic low - grade systemic inflammation and thus contributes to the development of systemic metabolic dysfunction that is associated with obesity - related disorders and renal disease [ 2427 ] .
levels of some inflammatory markers and cytokines such as c - reactive protein ( crp ) , tumor necrosis factor- ( tnf- ) , interleukin-6 ( il-6 ) , and macrophage migration inhibitory factor ( mif ) are elevated , whereas concentrations of adiponectin , a protein hormone that exerts anti - inflammatory activities , are reduced in obesity [ 2834 ] .
leptin is a 16-kda - peptide hormone encoded by obese ( ob ) gene that is mainly produced by adipose tissue .
leptin serves as a regulator of energy balance by binding to the full - length leptin receptors  obese receptor b ( ob - rb ) in the hypothalamus , leading to reduction in food intake and elevation in temperature and energy expenditure .
leptin receptors can be classified as secreted - forms ( ob - re ) , short - forms ( ob - ra , c , d , and f ) mainly expressed in peripheral tissue , and long - forms ( ob - rb ) predominantly expressed in hypothalamus .
the kidney expresses abundant concentrations of the truncated isoform of the leptin receptor ob - ra , but only a small amount of the full - length receptor ob - rb .
leptin production is associated with increased size of adipocytes and is positively correlated with the body mass index ( bmi ) . increased circulating leptin , a marker of leptin resistance , is common in obesity .
obesity - induced leptin resistance injures numerous peripheral tissues including kidney , liver , myocardium , and vasculature [ 36 , 38 ] .
leptin results in the development of renal disease by binding to its specific receptors in renal endothelial cells and mesangial cells . in glomerular endothelial cells ,
leptin stimulates cellular proliferation , tgf-1 synthesis , and type iv collagen production [ 36 , 39 ] . in mesangial cells , leptin upregulates synthesis of the tgf- type ii receptor , but not tgf-1 , and stimulates glucose transport and type i collagen production through signal transduction pathways involving phosphatidylinositol-3-kinase .
however , both those cell types increase their expression of extracellular matrix in response to leptin .
transgenic mice with leptin overexpression demonstrated an increase in collagen type iv and fibronectin mrna in the kidney .
leptin is involved in the development of glomerulosclerosis through a paracrine tgf- pathway ( between glomerular endothelial and mesangial cells ) that promotes the deposition of extracellular matrix , proteinuria , and , eventually , glomerulosclerosis .
infusion of leptin into normal rats for 3 weeks fosters the development of focal glomerulosclerosis and proteinuria .  
leptin also has proinflammatory actions through its interaction with mediators of innate and adaptive immunity and crp .
leptin regulates components of innate and adaptive immunity , including t lymphocytes and monocytes / macrophages [ 42 , 43 ] .
central leptin administration in ob / ob mice accelerates renal macrophage infiltration through the melanocortin system .
leptin stimulates central t - cell production and a peripheral shift in favor of t helper ( th ) 1 adaptive immune responses ( proinflammatory ) as opposed to th2 responses ( anti - inflammatory ) .
leptin has been shown to modulate adaptive immunity by enhancing t - cell survival and stimulating production of proinflammatory cytokines such as ifn- and il-2 .
leptin also has structural and functional resemblance to proinflammatory cytokines , such as il-6 , and may modulate crp , a leptin - interacting protein . therefore , these direct and indirect effects of leptin on the kidney , including stimulating cellular proliferation and hypertrophy , increasing extracellular matrix expression , and exhibiting proinflammatory activities , may partially explain obesity - related kidney disease .
adiponectin is a 30 kda adipocyte - derived protein hormone encoded by the adipose most abundant gene transcript 1 ( apm1 ) ,   which plays a role in the suppression of inflammation - associated metabolic disorders .
adiponectin is highly abundant in human serum , but its level is decreased in most obese animal and human subjects , particularly in those with visceral obesity [ 4951 ] .
recent clinical studies show a negative association of adiponectin in obese patients , [ 52 , 53 ] suggesting that adiponectin may play a key role in the development of obesity - related albuminuria and alteration of renal function .
studies with the adiponectin knockout mouse provide evidence that adiponectin can regulate podocyte function and thus contribute to the initial development of albuminuria [ 37 , 53 ] .
sharma et al . showed that knockout of adiponectin in mice increased albuminuria and caused fusion of podocyte foot processes . in cell culture studies with podocytes ,
( zo-1 ) to the plasma membrane , and reduced the renal predominant nadph oxidase nox 4 , largely via a 5-amp - activated - protein kinase- ( ampk- ) dependent pathway .
treatment of the adiponectin knockout mice with exogenous adiponectin was able to decrease albuminuria and improve podocyte morphology .
chronic hyperadiponectinemia significantly alleviated the progression of proteinuria in early - stage diabetic nephropathy by several mechanisms .
it led to an increase in nephrin expression , improvement of the endothelial dysfunction due to decreases in endothelin 1 ( et-1 ) and plasminogen activator inhibitor 1 ( pai-1 ) , and an increase in endothelial nitric oxide synthase ( enos ) expression in the renal cortex .
recent studies suggest that adiponectin exerts anti - inflammatory effects by suppressing tnf--induced activation of nuclear factor-b ( nf-b ) in human aortic endothelial cells and aortic smooth muscle cells through inhibition of ib phosphorylation [ 55 , 56 ] and inhibition of vascular cell adhesion molecule 1 ( vcam-1 ) and intercellular adhesion molecule 1 ( icam-1 ) expression , thereby reducing monocyte adhesion and macrophage - induced cytokine production   and crp expression in human adipose tissue .
human adipose tissue expressed crp , which was negatively correlated with adiponectin expression in adipose tissue .
low levels of adiponectin are associated with higher levels of highly - sensitive c - reactive protein ( hs - crp ) and il-6 , two inflammatory mediators that are involved in the initiation and progression of atherosclerosis and renal disease .
therefore , hypoadiponectinemia contributes to development of a low - grade systemic chronic inflammation state , suggesting that hypoadiponectinemia may play a causative role in the systemic and vascular inflammation commonly found in obesity and obesity - related disorders , including renal injury , through its proinflammatory effects .
resistin , also known as adipocyte - specific secretory factor ( adsf ) or as found in inflammatory zone ( fizz ) , is a cysteine - rich 12.5-kda polypeptide that belongs to a small family called resistin - like molecules ( relms ) [ 60 , 61 ] . in rodents
, resistin is secreted from white adipocytes [ 62 , 63 ] . in human , it is produced largely by macrophages and expressed in adipose tissue predominantly by nonadipocyte resident inflammatory cells [ 6466 ] .
current evidence suggests that resistin has been variably associated with obesity , insulin resistance , inflammation , and renal dysfunction .
resistin levels are elevated in both genetic and diet - induced animal models of obesity [ 62 , 67 ] . studies of obese subjects have frequently noted higher serum levels of resistin as well as direct correlations between resistin level and adiposity as measured by bmi [ 68 , 69 ] .
there has been a link between circulating resistin and low - grade inflammation that accompany obesity .
resistin is associated with elevated crp and white blood cells , suggesting that the role of resistin may be a component of obesity - related inflammation .
it has recently been found that resistin involves in the regulation of proinflammatory cytokine expression .
resistin strongly upregulates il-6 and tnf- in human peripheral blood mononuclear cells ( pbmcs ) via nf-b pathway .
human resistin enhanced secretion of proinflammatory cytokines , tnf- and il-12 in macrophages by nf-b - dependent pathway . studies also show that increased levels of resistin in patients with ckd are associated with declined renal function and inflammation [ 73 , 74 ] .
this suggests that resistin may play an important role in obesity and obesity - associated disease by triggering the release of other proinflammatory cytokines .
a growing body of evidence indicates that obesity - related glomerulopathy is associated with upregulation of inflammatory mediators .
obesity leads to adipose tissue macrophage infiltration in white adipose tissue and increased levels in proinflammatory cytokines .
several inflammatory mediators released from adipocytes and macrophages , such as tnf- , il-6 , il-1 , crp , monocyte chemoattractant protein 1 ( mcp-1 ) , pai-1 , and mif , contribute to a low level of chronic inflammatory state in obesity and may be responsible for renal injury in obesity - associated glomerulopathy .
an emerging pattern of gene expression was observed in adipose tissue in mice fed high fat - fed diets , indicating a shift toward global upregulation of inflammatory genes , including tnf- , il-6 , and mcp-1 .
tnf- , a proinflammatory cytokine , is predominantly produced by macrophages infiltrating adipose tissue [ 77 , 78 ] and can also be produced by the kidney .
this cytokine is involved in the genesis of inflammation and contributes to obesity - associated insulin resistance [ 8082 ] . within the kidney , angii , advanced glycation end - products ( ages ) , and oxidized low - density lipoprotein ( ldl )
a recent study demonstrates that tnf- reduces the expression of klotho , a protein expressed by renal cells , through an nf-b - dependent mechanism , which contribute to renal injury .
tnf- enhances the expression of pai-1 in human adipose tissue and plasma pai-1 levels in obesity subjects and is responsible for reduced fibrinolysis and also a component of extracellular matrix , leading to renal fibrosis and terminal renal failure [ 8890 ] .
tnf- also has been shown to induce the expression of mcp-1 via p38 mitogen - activated protein kinase ( mapk ) signaling pathway in renal mesangial cells .
mcp-1 , a key regulator in recruiting monocytes to the glomeruli , may also contribute to renal damage at a later stage of kidney disease in obesity .
il-6 is another important proinflammatory mediator systemically secreted from adipose tissue and locally produced in the kidney .
studies have demonstrated the positive relationship between bmi and plasma il-6 concentrations [ 9294 ] .
studies also suggest that il-6 plays a key role in the development of renal disease .
endogenous il-6 enhances the degree of renal injury , dysfunction , and inflammation caused by ischemia / reperfusion by promoting the expression of adhesion molecules and subsequent oxidative stress .
transgenic knockout of il-6 ameliorates renal injury as measured by serum creatinine and histology . blocking the il-6
receptor prevents progression of proteinuria and renal lipid deposit as well as the mesangial cell proliferation associated with severe hyperlipoproteinemia .
il-6 also stimulates the synthesis of crp , which is well known as both a marker and important risk factor of atherosclerosis in the general population and ckd patients .
mif was initially described as an immunomodulatory factor isolated from the supernatants of t lymphocytes and was found to inhibit the random migration of macrophages .
subsequent studies have indicated that mif acts as a proinflammatory cytokine and pituitary - derived hormone that potentiates endotoxemia .
immunologically induced crescentic antiglomerular basement membrane glomerulonephritis , treatment with anti - mif antibody reduced proteinuria , prevented the loss of renal function , attenuated histological damage including glomerular crescent formation , inhibited renal leukocytic infiltration and activation , and reduced il-1 expression by both intrinsic kidney cells and macrophages .
thus , mif is a key mediator of the inflammatory and immune response and plays a pathological role in immune - mediated renal injury .
oxidative stress is caused by an imbalance between increased production of reactive oxygen species ( ros ) and/or reduced antioxidant activity , leading to oxidative damage to cells or tissue including lipids , proteins and dna .
it is known that oxidative stress is involved in pathological processes of various diseases , such as cancer , diabetes mellitus , hypertension , and cardiovascular disease .
studies have suggested that obesity is associated with increased oxidative stress [ 103 , 104 ] .
analysis of oxidative markers in obesity subjects indicates that oxidative damage is associated with increased bmi and percentage of body fat [ 105 , 106 ] .
conversely , parameters of antioxidant capacity are inversely related to the amount of body fat and central obesity [ 107 , 108 ] . the possible mechanisms of obesity - related oxidative stress include increased oxygen consumption and subsequent production of free radicals derived from the increase in mitochondrial respiration , diminished antioxidant capacity , fatty acid oxidation , lipid oxidizability , and cell injury causing increased rates of free radical formation [ 104 , 109 , 110 ] .
it is also reported that the increase in obesity - associated oxidative stress is due to the presence of excessive adipose tissue accumulation .
accumulated adipose tissue generates an immune response leading to the secretion of proinflammatory cytokines , including tnf- , il-1 , and il-6 , which lead to increased generation of ros .
excessive fat accumulation also stimulates nicotinamide adenine dinucleotide phosphate ( nadph ) oxidase activity , which contributes to ros production .
ros , in return , augmented the expressions of nadph oxidase ( nox ) subunits , including nox4 and pu.1 in adipocytes , establishing a vicious cycle that augments oxidative stress in white adipose tissue and blood .
oxidative stress in adipocyte seems to be responsible for the low - grade proinflammatory state commonly observed in obesity [ 113 , 114 ] .
oxidative stress is increasingly viewed as a major upstream component in cell - signaling cascades involved in inflammatory responses , stimulating the expression of proinflammatory cytokines .
ros activate redox - sensitive transcription factors , particularly nf-b , inducing the release of proinflammatory cytokines and the expression of adhesion molecules and growth factors , including tnf- , il-6 , il-1 , tgf-1 , connective tissue growth factor , igf-1 , platelet - derived growth factor , and vcam-1 [ 115 , 116 ] .
h2o2 stimulates il-4 and il-6 gene expression and cytokine secretion by an apurinic / apyrimidinic - endonuclease / redox - factor-1- ( ape / ref-1- ) dependent pathway .
ros increased the expression levels of pai-1 , il-6 , and mcp-1 through nadph oxidase pathway . oxidized high - density lipoprotein ( hdl )
enhances proinflammatory properties such as tnf- and mcp-1 in renal mesangial cells partly via cd36 and ldl receptor-1 and via mapk and nf-b pathways .
oxidized ldl can stimulate tnf- synthesis from renal cells and initiate local effects of renal damage .
increased ros production and mcp-1 secretion from accumulated fat may cause infiltration of macrophages and inflammation in adipose tissue of obesity . moreover , enhanced macrophage migration induces the release of proinflammatory cytokines , which further stimulates the generation of ros [ 119 , 120 ] .
therefore , oxidative stress - induced cytokine production is likely to further increase oxidative stress levels , setting a vicious cycle   that may promote the progression of kidney damage in obesity .
oxidative stress has been commonly identified in obesity - related renal diseases and may be the mechanism underlying the initiation or progression of renal injury in obesity [ 122 , 123 ] .
previous studies suggest that oxidative stress triggers , at an early age , the onset of kidney lesions and functional impairment in zucker obese ( zo ) fa / fa rats , a good model of obesity - related renal disease , in absence of hyperglycaemia , hypertension , and inflammation .
ros are highly reactive molecules that oxidize lipids and proteins , cause cellular injury , and promote glomerular and renal tubule injury and associated proteinuria .
ros are produced by various cells , such as vascular cells , inflammatory cells , and renal cells , and have distinct function on different types of cells , such as endothelial dysfunction , inflammatory gene expression , and renal tubule ion transport .
a major source for vascular and renal ros is a nox family of nonphagocytic nad(p)h oxidases , including the prototypic nox2 homolog - based nad(p)h oxidase , as well as other nad(p)h oxidases , such as nox1 and nox4 .
numerous reports indicate that within the kidney , nad(p)h oxidase , an enzyme that produces superoxide ( o2  ) by transferring electrons from nadh / nadph to molecular oxygen and thereby forming o2  , h , and nad / nadp , is capable of modulating renal epithelial ion transport [ 130 , 131 ] .
nap(d)h oxidase - derived ros can alter renal pressure natriuresis and blood pressure regulation through its effects on renal hemodynamics and renal tubular sodium transport .
recent data suggest that nadph oxidase - mediated oxidative injury to the proximal tubule , like that seen in the glomerulus , contributes to proteinuria in insulin - resistant states .
oxidative stress also plays an important role in the pathogenesis of renal damage through its effects on vascular biology .
ros are generated by all types of vascular cells , including endothelial , smooth muscle , and adventitial cells .
ros influence vascular cell growth , migration , proliferation , and activation [ 132 , 133 ] .
physiologically , ros can mediate cellular function , receptor signals , and immune responses on vascular cells . in pathophysiological condition ,
ros contribute to progressive vascular dysfunction and remodeling through oxidative damage caused by decreased nitric oxide ( no ) bioavailability , impaired endothelium - dependent vasodilatation and endothelial cell growth , apoptosis or anoikis , endothelial cell migration , and activation of adhesion molecules and inflammatory reactions [ 134 , 135 ] .
obesity accelerates the progression of renal injury , associated with augmented inflammation in adipose and kidney tissues .
studies in il-6 transgenic mice suggested that high concentrations of il-6 contribute to development of renal injury .
treatment with anti - il-6 receptor antibody mr16 - 1 prevented progression of proteinuria , renal lipid deposit , and the mesangial cell proliferation in hypercholesterolemia - induced renal injury .
inhibition of tnf- by etanercept , a tnf- antagonist , also decreased blood pressure and protected the kidney through reduction of renal nf-b , oxidative stress , and inflammation .
tnf- blockade increases renal cyp2c23 expression and slows the progression of renal damage in salt - sensitive hypertension .
tnf- inhibition also reduces renal injury in deoxycorticosterone - acetate- ( doca- ) salt hypertensive rats via suppression of renal cortical nf-b activity .
treatment of adiponectin - knockout mice with adenovirus - mediated adiponectin results in amelioration of albuminuria , glomerular hypertrophy , and tubulointerstitial fibrosis and reduces the elevated levels of vcam-1 , mcp-1 , tnf- , tgf-1 , collagen type i / iii , and nadph oxidase components .
excessive fat accumulation contributes to macrophage infiltration in adipose tissue and increased production of proinflammatory cytokines , such as tnf- , il-8 , and il-6 [ 142145 ] .
consequently , it is possible that weight loss may be a potential method to reduce inflammation .
evidence indicates that weight loss induced by nutritional intervention or gastric surgery markedly improves the systemic and adipose tissue inflammatory states linked to obesity [ 143 , 146 , 147 ] .
studies by gene profiling analysis have shown that caloric restriction - induced weight reduction leads to the regulation of a wide variety of inflammation - related molecules in human adipose tissue .
weight loss globally improves the inflammatory profile of obese subjects through a decrease of proinflammatory factors and an increase of anti - inflammatory molecules in white adipose tissue .
roux - en - y - gastric - bypass- ( rygb- ) induced weight loss has been shown to reduce mcp-1 , il-18 , il-6 , and tnf- concentrations [ 149 , 150 ] .
a longer - term weight reduction induced by rygb in corpulence also prevails in regulating circulating cytokine concentrations .
weight loss also ameliorates the low - grade inflammation state that leads to glomerular dysfunction in obesity . in morbidly obese individuals with glomerular hyperfiltration ,
weight loss by surgical interventions normalizes glomerular filtration rate ( gfr ) and reduces blood pressure and microalbuminuria .
weight loss improves renal function as shown by reduced levels of serum creatinine and improved creatinine clearance .
since ros play a key role in the pathogenesis of renal injury such as glomerulosclerosis and tubulointerstitial fibrosis , approaches to reduce oxidative stress by antioxidants supplementation , nutritional and surgical interventions may have renoprotective effects .
garcinia protects against obesity - induced nephropathy by attenuating oxidative stress through reduced lipid peroxidation and levels of oxidized ldl .
the obese zucker rat is a good model for studying obesity - related kidney disease because it develops proteinuria , glomerular hypertrophy , and focal segmental glomerulosclerosis [ 155157 ] . using these rats
, it has been demonstrated that nephropathy is associated with oxidative stress , and supplementation with an antioxidant ebselen improved kidney damage by ameliorating proteinuria and renal focal and segmental sclerosis .
chronic ebselen therapy also improved vasculopathy with lipid deposits , tubulointerstitial scarring , and inflammation .
for example , administration of grape seed proanthocyanidin extract ( gspe ) , an efficient phytochemical antioxidant , can protect against the nephrotoxicity effects induced by cisplatin and gentamicin [ 159 , 160 ] and reverse experimental myoglobinuric acute renal failure .
quercetin , a flavonoid that exhibits antioxidant properties in many diseases , could also protect the rat kidney against lead - induced injury and improve renal function .
thus , antioxidants may be a potential therapeutic to prevent the renal damage in org .
nutritional and surgical interventions are additional approaches to reduce oxidative stress and prevent kidney injury in obesity .
caloric restriction and protein restriction reduce free radicals and ros formation and inhibit accumulation of oxidative biomarkers in animal models . in genetically obese animals ,
diet restriction can prevent or greatly delay the onset of specific degenerative lesions , in particular glomerulonephritis associated with obesity .
since adipose tissue mass in obesity contributes to oxidative stress , bariatric surgery - induced weight loss also results in decreasing systemic oxidative stress in adiposity . weight loss induced by diet restriction or bariatric surgery not only improves inflammation state but also reduces oxidative stress state in obesity , which may protect renal function in obesity - related glomerulopathy .
obesity causes chronic low - grade inflammation and systemic and local oxidative stress , which may play a pivotal role in the initiation or progression of obesity - associated glomerulopathy .
elevated inflammation in obesity is the result of the production of adipokines and increased inflammatory cytokines and decreased anti - inflammatory factors .
oxidative stress is triggered by an imbalance between increased production of ros and/or reduced antioxidant activity .
both inflammation and oxidative stress induce damage to renal tubule and glomerulus and result in endothelial dysfunction in the kidney
. therefore , anti - inflammation and antioxidant interventions may be the potential therapies to prevent and treat obesity - related renal diseases .
 obesity - related glomerulopathy is an increasing cause of end - stage renal disease . 
 obesity has been considered a state of chronic low - grade systemic inflammation and chronic oxidative stress . 
 augmented inflammation in adipose and kidney tissues promotes the progression of kidney damage in obesity . 
 adipose tissue , which is accumulated in obesity , is a key endocrine organ that produces multiple biologically active molecules , including leptin , adiponectin , resistin , that affect inflammation , and subsequent deregulation of cell function in renal glomeruli that leads to pathological changes . 
 oxidative stress is also associated with obesity - related renal diseases and may trigger the initiation or progression of renal damage in obesity . in this paper , we focus on inflammation and oxidative stress in the progression of obesity - related glomerulopathy and possible interventions to prevent kidney injury in obesity . 
1. Introduction
2. Inflammation in Obesity-Related Glomerulopathy
3. Oxidative Stress in Obesity-Related Glomerulopathy
4. Potential Interventions to Prevent Renal Injury
5. Conclusion