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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
REVIEW ARTICLE  
Year : 2016  |  Volume : 27  |  Issue : 5  |  Page : 875-884
The triad of kidney, obesity, and bariatric surgery


1 Department of Nephrology, Southern California Permanente Medical Group, Fontana, CA, USA
2 Department of Research and Evaluation, Kaiser Permanente Southern California, Pasadena, CA, USA

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Date of Web Publication22-Sep-2016
 

   Abstract 

There is an epidemic of obesity in the USA. Obesity significantly increases the risk of developing chronic kidney disease. Multiple studies have shown overall health and mortalityrelated benefits of medical and surgical weight loss. Renal benefits of bariatric surgery include decrease in proteinuria and hyperfiltration. There have only been a few small studies in patients with abnormally low glomerular filtration rate (GFR) that have shown improvements in GFR postsurgery over a short term. Long-term and larger scale studies are needed to see if renal benefits of weight loss are sustained in post-bariatric surgery patients.

How to cite this article:
Imam TH, Coleman KJ. The triad of kidney, obesity, and bariatric surgery. Saudi J Kidney Dis Transpl 2016;27:875-84

How to cite this URL:
Imam TH, Coleman KJ. The triad of kidney, obesity, and bariatric surgery. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2020 Oct 28];27:875-84. Available from: https://www.sjkdt.org/text.asp?2016/27/5/875/190772

   Emerging Epidemic of Obesity Top


In adults, according to the World Health Organization (WHO), a body mass index (BMI) of ≥30 kg/m 2 is considered obese. There are approximately two billion adults who are either overweight or obese. [1] This number is expected to increase by 40% in upcoming decades. [2] In 2008, the annual medical costs related to the management of obesity in the USA were estimated at $147 billion, up from $78.5 billion in 1998. [3] The WHO Global Health Risks Report of 2009 estimated that increased BMI and physical inactivity combined accounted for six million deaths, surpassing the excess mortality associated with tobacco. [4] All grades of obesity are associated significantly with higher all-cause mortality in the general population. [5],[6]

However, contrary to what is established in the general population, an elevated BMI has been shown to have a favorable influence on survival in the hemodialysis (HD) population, a concept known as reverse epidemiology or the obesity paradox. In a national sample of 3607 HD patients from the United States Renal Data System (USRDS), no evidence of increased mortality risk was found even for higher values of BMI over five years. [7] In the Dialysis Outcomes and Practice Patterns Study, the lowest mortality risk in patients on HD was a BMI of 25-39.9 kg/m 2 . [8] The explanations for marked differences in mortality risk patterns based on BMI ranges in the HD patients are neither precise nor clear. The potential explanations for this apparent phenomena include misclassification due to estimates of obesity based solely on height and weight, increased energy reserves in the form of higher body fat, a "survivor bias" in the years leading up to endstage renal disease (ESRD), and a diminished or paradoxical effect of obesity and its metabolites in uremia. [9] In addition, accelerated atherosclerosis, characteristic of uremic milieu, is the driving force for vascular disease in all HD patients which renders obesity a less important risk factor for the disease. [8] Despite this apparent paradox, it is not without controversy. Kaizu et al observed an increased mortality among HD patients at extreme BMI producing a "U"-shaped mortality curve. [10]


   Controversy of Body Mass Index Top


Although measurement of BMI is simple and is useful for population studies, it has its limitations. BMI cannot differentiate weight change due to an increase in muscle mass, fat mass, or that due to increase in body water. The measure was developed as a practical measure of body fat; however, it does not directly measure body fat. [11] Some research communities have suggested that waist circumference (WC) is a better measure of body fat that is more often related to disease etiology; central adiposity. Even after adjusting for total body fat and BMI, a higher level of abdominal fat has shown strong association with mortality, [12] hypertension (HTN), and diabetes mellitus (DM). [13] However, WC risk cutoff points lose their incremental predictive value when BMI is ≥35 kg/m 2 . [14]


   The Burden of Chronic Kidney Disease Top


The burden of chronic kidney disease (CKD) has been on the rise, and most patients remain undiagnosed in early stages of CKD. More than 10% of adults in the USA have CKD. [15] According to the USRDS, between 1988 and 1994 and 2005 and 2010, the overall prevalence of CKD, defined either by the estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m 2 , or a urine albumin/creatinine (Cr) ratio (ACR) of ≥30 mg/g, rose from 12.3% to 14%. For only eGFR <60 mL/min/1.73m 2 , prevalence rose from 4.9% to 6.7%; for ACR ≥30 mg/g, the prevalence rose from 8.8% to 9.4%. BMI ≥30 kg/m 2 was associated with 7.4% prevalence rate of eGFR <60 mL/min/1.73 m 2 (up from 6.2% in the period 1988- 1994). [16]


   Obesity in End-stage Renal Disease Top


Obesity has been shown as an independent predictor for ESRD even after adjustments for blood pressure (BP) and DM. A review of >300,000 members of Kaiser Permanente health plan was performed. During 8,347,955 person-years of follow-up, 1476 new cases of ESRD were noted. Compared to those patients who had BMI <25 kg/m 2 , those with BMI 25-29.9 kg/m 2 , had the adjusted relative risk (RR) of 1.87 for ESRD. The RR went as high as 7.07 for those with BMI ≥40 kg/m 2 . [17]

Using the 2000 US Centers for Disease Control and Prevention, BMI for age and sex classification of children and adolescents (85- 94 th percentile for overweight and ≥95 percentile for obese), adolescent overweight was associated with hazard ratio (HR) of 3 and obesity with HR of 6.89, for all-cause treated ESRD during a 25-year period. For the same period, overweight and obesity had HR of 5.96 and 19.37, respectively, as independent risks for developing diabetic ESRD. [18]

Temporal trends in BMI and obesity were examined among incident patients with ESRD between 1995 and 2002. Mean BMI increased from 25.7 to 27.5 kg/m 2 , and obesity with BMI ≥30 and ≥35 kg/m 2 , increased by 33% and 63%, respectively. The rate of change in BMI during this time was about twice in the incident ESRD population compared to the overall USA population [Figure 1]. [19]
Figure 1: Temporal trends of body mass index among the incident adult end-stage renal disease patients by the year of initial start of dialysis in the total adult USA population (Behavioral Risk Factor Surveillance System) for the corresponding year. Data are age adjusted for the 2000 USA census (with permission from American Society of Nephrology).

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There is limited data in the USRDS, which shows that among incident ESRD patients, the mean BMI was 29.14 kg/m 2 in 2008-2010 (up from 27.6 kg/m 2 in 2002-2004). [16] It rose to 31.6 kg/m 2 in 2010-2012. [20]


   Chronic Kidney Disease as an Outcome of Obesity Top


Obesity can be considered the number one preventable risk factor for CKD. For the period of 2005-2010, the odds ratio (OR) for developing CKD with a BMI of ≥30 kg/m 2 was 1.41. In comparison, the highest OR for developing CKD was 3.38 for DM. [16] Even after adjustment for confounding variables, obesity with central fat distribution has a 70% increased risk for microalbuminuria. [21]

In the Framingham Offspring cohort, BMI per standard deviation unit had an OR of 1.28 for developing CKD after a mean follow-up of close to 2500 subjects for 18.5 years. BMI was positively related to the odds of having glomerular filtration rate (GFR) in the fifth or lower percentile after long-term follow-up. [22],[23]

In one of the first large scale studies, population-based studies of its kind from Sweden, overweight (BMI >25 kg/m 2 ) and obese (BMI >30 kg/m 2 ), men and women without self-reported DM or HTN, at age of 20 years, had a three-fold risk of developing CKD compared with normal weight (BMI <25 kg/m 2 ) adults of the same age. [23] In a five-year follow-up of more more than 5000 patients, hypertensive adults without any baseline kidney disease, the incidence of CKD at year five was 34% in obese adults compared to 28% in patients of normal weight. After adjustment for all covariates including DM, mean baseline diastolic BP, and slope of diastolic BP, both baseline overweight (OR: 1.21) and obesity (OR: 1.40) were associated with increased odds of incident CKD. [24]

A meta-analysis of three cross-sectional and 19 case-control studies confirmed that compared with normal weight individuals, pooled RR of kidney disease was 1.4 for overweight and 1.8 for obese individuals. It was estimated that 24.2% of kidney disease cases among men and 33.9% among women in the USA could be prevented if overweight and obesity were eliminated. [25]


   Pathology Top


Physiological studies in obese non-diabetic human subjects have shown increased renal plasma flow and increased GFR, resulting in increased filtration fraction. [26] This glomerular HTN and hyperfiltration cause proteinuria and deterioration of renal function over time, leading to CKD. Further on, weight loss was shown to decrease hyperfiltration, and also albumin excretion rate. [27]

Obesity-related glomerulopathy (ORG) is now a clear entity involving obese patients and a new evolving epidemic. [28] ORG can develop into full-blown focal and segmental glomerulosclerosis (FSGS). Clinically, such patients have a lesser incidence of edema compared to other patients with FSGS. Biopsy findings reveal lesser segmental sclerosis, less podocyte effacement, and more glomerulopathy. A study compared 15 obese patients with biopsy-proven FSGS with 15 non-obese patients with biopsy proven idiopathic FSGS. Those with obese FSGS had lower proteinuria, and none had hypoalbuminemia or edema. Comparatively, nonobese FSGS had a higher burden of proteinuria, hypoalbuminemia, and edema. Glomerulopathy was observed in all renal biopsies in obese patients. Mean glomerular diameter was 356 ± 24 μm in obese versus 199 ± 26 μm in nonobese individuals. The Kaplan-Meier estimated probabilities of renal survival after five and 10 years were 77% and 51%, respectively, in obese patients, and 52% and 30%, respectively in non-obese patients. [29] [Figure 2] summarizes various factors that play a role in the development of ORG. [30]
Figure 2: Major pathogenic steps involved in the development of renal dysfunction in obesity (with permission from Elsevier).

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Obesity-related inflammation is now considered a major pathological event in inducing kidney damage. Visceral adipose tissue elaborates renin-angiotensin-aldosterone system, plasminogen activator inhibitor, adipocytespecific metabolites such as free fatty acids, leptin, and adiponectin which then directly stimulate renal damage from increased vasoconstriction, decreased vasodilation, podocyte injury, endothelial dysfunction, and glomerular basement membrane thickening [Figure 3]. [31] Significant decrease in urinary and serum inflammatory markers that correlate directly with weight loss has been shown. These were also associated with improvement in renal functions. [32]
Figure 3: Influence of adiposity on renal damage (with permission from Wolters Kluwer Health, Inc.).

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   Health Benefits of Surgical Weight Loss Top


Bariatric surgery has effectively shown a mean percent excess weight loss of 61.2% in a meta-analysis of 136 studies involving 22,094 patients who underwent gastric banding, gastric bypass, gastroplasty, biliopancreatic diversion, or duodenal switch. Resolution of DM and HTN was 76.8% and 61.7%, respectively. [33] Another study of 2500 veterans who underwent bariatric surgery was matched to 7462 control patients and found, on Kaplan-Meier analysis, estimated mortality rates of 13.8% at 10 years for surgical patients and 23.9% for matched control patients. [34]

A systemic review performed in 2013 by Puzziferri et al [35] examined weight and health outcomes for gastric bypass, gastric band, or sleeve gastrectomy (SG) with at least two years of follow-up measures for at least 80% of the initial cohort. They found that at least 50% excess weight loss occurred in 31% of gastric band studies, in 65.7% for gastric bypass, and in 64.5% for SG studies. Remission of DM (defined as glycated hemoglobin <6.5% without medications) was 66.7% after gastric banding, and for HTN (defined as <140/90 mm Hg without medications), it was 17.4%. Very few studies reviewed have reported long-term results with sufficient follow-up to minimize biased results. This conclusion has been found in other reviews of the evidence for bariatric surgery on health and weight outcome. [36]


   Renal Benefits of Medical Weight Loss Top


Despite showing that healthy lifestyle lowers all-cause mortality in CKD, very few studies overall have followed kidney function with healthy lifestyle and diet on a long-term basis. [37] The first major study to examine combinations of healthy lifestyle factors in relation to allcause mortality, specifically in CKD, was published in 2013 with 2288 patients having eGFR<60 mL/min/1.73 m 2 and a median followup of 13 years. It showed that compared to patients who were non-adherent, adherence to a healthy lifestyle was associated with lower allcause mortality risk in CKD. [38] In a small study, 22 obese patients with diabetic nephropathy were given a low-calorie, normal protein diet for four weeks. There was a decrease in subcutaneous fat along with a drop of 6.2 ± 3 kg in total body weight. There was notably a significant decrease in serum Cr and urinary protein (mean decrease 1.8 ± 1.7 g/day). [39] In another study, six obese patients with diabetic nephropathy were followed up for 12 weeks. Their GFR was <40 mL/min/1.73 m 2 . These patients received a very low-calorie ketogenic diet and exercise encouragement. Median weight went down to 104.3 kg from 118.5 kg. There was 36% reduction in 24 h albuminuria, but it did not reach statistical significance. However, a significant reduction in serum Cr was noted (3.54 mg/dL vs. 3.13 mg/dL, P <0.05). [40] Another group of 30 overweight/obese patients (BMI >27 kg/m 2 ) with diabetic and nondiabetic nephropathies were randomized to follow either a low-calorie normal protein diet or maintain their usual diet for five months. Mean weight loss in the diet group was 4.1 ± 3%, whereas there was weight gain in the usual diet group. Diet group saw a drop of proteinuria from 2.8 ± 1.4 g/day to 1.9 ± 1.4 g/day, whereas a rising trend was noted in the control group. Overall renal function remained stable in the diet group but worsened in the other group. [41]


   Renal Benefits of Surgical Weight Loss Top


The term "bariatric" comes from the Greek words "baros," meaning "weight" and "iatrikos," meaning medicine. Since the 1991 NIH consensus statement regarding obesity, bariatric surgery procedure has bloomed. [42] A 2010 report showed that the incidence of bariatric surgery has plateaued at approximately 113,000 cases per year. Complication rates have fallen from 10.5% in 1993 to 7.6% of all cases in 2006. It costs the health economy at least $1.5 billion annually. [43] Presently, the three most common procedures are gastric banding, gastric bypass, and SG. The Roux-en-Y gastric bypass (RYGB) combines both restrictive and bypass methods.

Higher risk has been shown in patients with CKD undergoing bariatric surgery. Multivariable logistic regression demonstrated that the CKD stage predicts higher complication rates (OR for each higher CKD stage was 1.30) after adjustment for DM and HTN. However, the absolute incidence rate of complications was <10%. [44] Although earlier data had shown increased morbidity, but those were open procedures. Laparoscopic methods have shown less morbidity. [45] Among ESRD patients, after adjusting for confounding factors, dependence on dialysis was not found to be an independent predictor of major morbidity post bariatric surgery. [46]

Various studies involving a relatively small number of patients and relatively short duration of follow-up have been published regarding the renal-related outcomes of bariatric surgery, primarily proteinuria, and hyperfiltration. Mostly, these initial studies did not include patients with low GFR. One of the earliest prospective studies published in 2006, comprised 61 extremely obese (BMI ≥40 kg/m 2 ) patients with baseline high Cr clearance (CrCl). The control group had 24 patients with normal BMI. The obese group had higher baseline CrCl and 24 h proteinuria. After 24 months of bariatric surgery, there was statistically significant decrease not only in proteinuria but also in CrCl, down from hyperfiltration stage. [47] Another 140 patients who had RYGB were reviewed after eight months of surgery. GFR, as measured by 24 h samples, went from 148.7 ± 35.2 mL/min to 113.8 ± 31.7 mL/min. [48] A systemic review published in 2009, showed significant decrease in GFR (by 23.7 mL/min) in patients with hyperfiltration (average GFR 140 mL/min) after weight loss from bariatric surgery, while nonsurgical interventions had mixed results. [49]

Among the first retrospective analysis of patients with low GFR (GFR 30-59 mL/min/ 1.73m 2 ) was a study that included 25 patients who underwent bariatric surgery. After 12 months, they showed a rise in mean GFR from 47.9 ± 10.2 to 61.6 ± 16.7 mL/min/1.73 m 2 . [50] Another 233 patients with different CKD stages were followed for one year post-surgery. The weight loss was similar in different groups. The GFR increased from 76.8 ± 16.7 mL/min to 93.3 ± 20.4 mL/min in CKD stage 2 group and from 49.5 ± 6.6 mL/min to 66.8 ± 19.3 mL/min in CKD stage 3 group. [51]

Significant improvement in proteinuria has also been shown in various studies. For example, 52 patients with DM for a mean duration of 8.6 years and BMI of 49 ± 8.7 kg/m 2 were followed for at least five years after bariatric surgery. Of those, patients with diabetic nephropathy (37.6%), defined as micro or macroalbuminuria, (58.3%) experienced a resolution of these conditions. [52] A meta-analysis showed that every kilogram of intentional weight loss reduced urine protein by an average of 110 mg, irrespective of decline in mean arterial BP. [49] A 24-month observational prospective study was carried out in 255 patients who had either SG or RYGB. At 12 months, the urine albumin-to-Cr ratio went down to 42.2 ± 142.8 mg/g from 85.7 ± 171 mg/g (P <0.005). Change in BMI from baseline was the only independent predictor of reduction or normalization of proteinuria at 12 months. [53]

Despite the "obesity paradox" in the ESRD population, some indirect benefits of surgical weight loss have also been shown in patients on HD. [54] Although no studies have yet been done that have looked at survival in post bariatric HD patients, improved chances of successful renal transplantation have been shown in ESRD patients following bariatric surgery. [55],[56],[57]

A large meta-analysis on the renal effects of weight loss concluded that most of the studies had limitations. Subgroup analysis according to CKD staging was not performed in most studies. There was considerable heterogeneity in the number of patients, severity of obesity, level of renal impairment, comorbidities, and irregular follow-up making generalized conclusions about the impact of bariatric surgery on CKD difficult. All this limits data pooling, and only a systematic narrative approach can be taken for review. [58]


   Conclusion Top


The burden of obesity-related renal damage will increase significantly over the coming decades. This emerging epidemic may turn out to be among the most important preventable risks for the development of CKD. Early recognition of obesity is vital so that timely weight loss programs can be initiated. Obesity treatment will turn out to be the number one therapy for reversing the trend of increasing CKD. Within this framework, bariatric surgical treatment options should play a pivotal role in setting public health policies. Even after implementation of all policies and processes for obesity control, it may take decades to reverse the rates of obesity to what were present 30-40 years ago. [59] Despite limited studies, it has now become crucial for nephrologists to manage and treat obesity in their patients with CKD. Bariatric surgery should be considered in individuals if medical management and lifestyle changes do not show results. It has shown potential for preventing further decline of GFR and thus ESRD. Long-term and large-scale studies need to be done in obese patients with CKD and ESRD who undergo bariatric surgery. Whether the benefits are sustained and whether any unforeseen harms emerge over decades, are yet to be shown.


   Clinical Significance Top


  • There is an epidemic of obesity
  • Obesity has been shown to lead to CKD
  • Based on present data, obesity is the number one preventable risk factor for developing CKD
  • Intentional weight loss has shown, in short term, improvement in renal function and proteinuria
  • Large-scale and long-term studies are needed to see if renal benefits from surgical weight are sustained or not and if any potential harms may mitigate the benefits.



   Acknowledgments Top


The authors would like to thank Grace Johnston, for library support and Portia Summers, for editing assistance.

Conflict of interest: None declared.

 
   References Top

1.
World Obesity Federation. About Obesity. England World Obesity Federation; 2015. Available from: http://www.worldobesity.org/resources/aboutobesity/. [Last cited on 2015 Oct 20.  Back to cited text no. 1
    
2.
Kelly T, Yang W, Chen CS, Reynolds K, He J. Global burden of obesity in 2005 and projections to 2030. Int J Obes (Lond) 2008;32:14317.  Back to cited text no. 2
    
3.
Centers for Disease Control and Prevention (CDC). Division of Nutrition, Physical Activity, and Obesity. Adult Obesity Facts. Atlanta, GA; 2015. Available from: http://www.cdc.gov/obesity/data/adult.html. [Last cited on 2015 Jan 10].  Back to cited text no. 3
    
4.
World Health Organization. Global Health Risks: Mortality and Burden of Disease Attributable to Selected Major Risks. Geneva, WHO Press; 2009. Available from: http://www.who.int/healthinfo/global_burden_disease/GlobalHealthRisks_report_part2.pdf. [Last cited on 2015 Jan 11].  Back to cited text no. 4
    
5.
Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010. JAMA 2012;307:491-7.  Back to cited text no. 5
    
6.
Flegal KM, Kit BK, Orpana H, Graubard BI. Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and metaanalysis. JAMA 2013;309:71-82.  Back to cited text no. 6
    
7.
Leavey SF, Strawderman RL, Jones CA, Port FK, Held PJ. Simple nutritional indicators as independent predictors of mortality in hemodialysis patients. Am J Kidney Dis 1998;31: 997-1006.  Back to cited text no. 7
    
8.
Leavey SF, McCullough K, Hecking E, Goodkin D, Port FK, Young EW. Body mass index and mortality in "healthier" as compared with "sicker" haemodialysis patients: results from the Dialysis Outcomes and Practice Patterns Study (DOPPS). Nephrol Dial Transplant 2001;16: 2386-94.  Back to cited text no. 8
    
9.
U.S. Renal Data System, USRDS 2011 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. Bethedsda, MD; 2011. Available from: http://www.usrds.org/2011/pdf/v2_ch09_11.pdf. [Last cited on 2016 Mar 12].  Back to cited text no. 9
    
10.
Kaizu Y, Tsunega Y, Yoneyama T, et al. Overweight as another nutritional risk factor for the long-term survival of non-diabetic hemodialysis patients. Clin Nephrol 1998;50:44-50.  Back to cited text no. 10
    
11.
Agarwal R, Bills JE, Light RP. Diagnosing obesity by body mass index in chronic kidney disease: an explanation for the "obesity paradox?" Hypertension 2010;56:893-900.  Back to cited text no. 11
    
12.
Kramer H, Shoham D, McClure LA, et al. Association of waist circumference and body mass index with all-cause mortality in CKD: The REGARDS (Reasons for Geographic and Racial Differences in Stroke) Study. Am J Kidney Dis 2011;58:177-85.  Back to cited text no. 12
    
13.
Balkau B, Deanfield JE, Després JP, , et al. International Day for the Evaluation of Abdominal Obesity (IDEA): a study of waist circumference, cardiovascular disease, and diabetes mellitus in 168,000 primary care patients in 63 countries. Circulation 2007;116: 1942-51.  Back to cited text no. 13
    
14.
NHLBI Obesity Education Initiative Expert Panel on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults (US). Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report. Bethesda, MD: National Heart, Lung, and Blood Institute. NIH Publication No. 98-4083; 1998. Available from: http://www.ncbi.nlm.nih.gov/books/NBK2003/pdf/TOC.pdf. [Last cited on 2015 Jan 11].  Back to cited text no. 14
    
15.
Centers for Disease Control and Prevention (CDC). Chronic Kidney Disease InitiativeProtecting Kidney Health. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention; 2015. Available from: http://www.cdc.gov/diabetes/projects/pdfs/ckd_summary.pdf. [Last cited on 2015 Jan 11].  Back to cited text no. 15
    
16.
U.S. Renal Data System, USRDS 2012 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. Bethedsda, MD; 2012. Available from: http://www.usrds.org/2012/pdf/v1_ch_1_12.pdf. [Last cited on 2015 Jan 12].  Back to cited text no. 16
    
17.
Hsu CY, McCulloch CE, Iribarren C, Darbinian J, Go AS. Body mass index and risk for endstage renal disease. Ann Intern Med 2006; 144:21-8.  Back to cited text no. 17
    
18.
Vivante A, Golan E, Tzur D, et al. Body mass index in 1.2 million adolescents and risk for end-stage renal disease. Arch Intern Med 2012;172:1644-50.  Back to cited text no. 18
    
19.
Kramer HJ, Saranathan A, Luke A, et al. Increasing body mass index and obesity in the incident ESRD population. J Am Soc Nephrol 2006;17:1453-9.  Back to cited text no. 19
    
20.
U.S. Renal Data System, USRDS 2014 Annual Data Report: Epidemiology of Kidney Disease in the United States. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. Bethedsda, MD; 2014. Available from: http://www.usrds.org/2014/ref/C_PatientChars_14.xls. [Last cited on 2015 Jul 4].  Back to cited text no. 20
    
21.
Pinto-Sietsma SJ, Navis G, Janssen WM, de Zeeuw D, Gans RO, de Jong PE; PREVEND Study Group. A central body fat distribution is related to renal function impairment, even in lean subjects. Am J Kidney Dis 2003;41:73341.  Back to cited text no. 21
    
22.
Fox CS, Larson MG, Leip EP, Culleton B, Wilson PW, Levy D. Predictors of new-onset kidney disease in a community-based population. JAMA 2004;291:844-50.  Back to cited text no. 22
    
23.
Ejerblad E, Fored CM, Lindblad P, Fryzek J, McLaughlin JK, Nyrén O. Obesity and risk for chronic renal failure. J Am Soc Nephrol 2006; 17:1695-702.  Back to cited text no. 23
    
24.
Kramer H, Luke A, Bidani A, Cao G, Cooper R, McGee D. Obesity and prevalent and incident CKD: the hypertension detection and follow-up program. Am J Kidney Dis 2005;46:587-94.  Back to cited text no. 24
    
25.
Wang Y, Chen X, Song Y, Caballero B, Cheskin LJ. Association between obesity and kidney disease: a systematic review and metaanalysis. Kidney Int 2008;73:19-33.  Back to cited text no. 25
    
26.
Chagnac A, Weinstein T, Korzets A, Ramadan E, Hirsch J, Gafter U. Glomerular hemodynamics in severe obesity. Am J Physiol Renal Physiol 2000;278:F817-22.  Back to cited text no. 26
    
27.
Chagnac A, Weinstein T, Herman M, Hirsh J, Gafter U, Ori Y. The effects of weight loss on renal function in patients with severe obesity. J Am Soc Nephrol 2003;14:1480-6.  Back to cited text no. 27
    
28.
Kambham N, Markowitz GS, Valeri AM, Lin J, D′Agati VD. Obesity-related glomerulopathy: an emerging epidemic. Kidney Int 2001;59: 1498-509.  Back to cited text no. 28
    
29.
Praga M, Hernández E, Morales E, et al. Clinical features and long-term outcome of obesityassociated focal segmental glomerulosclerosis. Nephrol Dial Transplant 2001;16:1790-8.  Back to cited text no. 29
    
30.
Cignarelli M, Lamacchia O. Obesity and kidney disease. Nutr Metab Cardiovasc Dis 2007;17: 757-62.  Back to cited text no. 30
    
31.
Hunley TE, Ma LJ, Kon V. Scope and mechanisms of obesity-related renal disease. Curr Opin Nephrol Hypertens 2010;19:227-34.  Back to cited text no. 31
    
32.
Fenske WK, Dubb S, Bueter M, et al. Effect of bariatric surgery-induced weight loss on renal and systemic inflammation and blood pressure: a 12-month prospective study. Surg Obes Relat Dis 2013;9:559-68.  Back to cited text no. 32
    
33.
Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and metaanalysis. JAMA 2004;292:1724-37.  Back to cited text no. 33
    
34.
Arterburn DE, Olsen MK, Smith VA, et al. Association between bariatric surgery and longterm survival. JAMA 2015;313:62-70.  Back to cited text no. 34
    
35.
Puzziferri N, Roshek TB 3rd, Mayo HG, Gallagher R, Belle SH, Livingston EH. Longterm follow-up after bariatric surgery: a systematic review. JAMA 2014;312:934-42.  Back to cited text no. 35
    
36.
Gloy VL, Briel M, Bhatt DL, et al. Bariatric surgery versus non-surgical treatment for obesity: a systematic review and meta-analysis of randomised controlled trials. BMJ 2013;347: f5934.  Back to cited text no. 36
    
37.
Kiortsis DN, Christou MA. Management of obesity-induced kidney disease: a critical review of the literature. Obes Facts 2012;5:82132.  Back to cited text no. 37
    
38.
Ricardo AC, Madero M, Yang W, et al. Adherence to a healthy lifestyle and all-cause mortality in CKD. Clin J Am Soc Nephrol 2013;8:602-9.  Back to cited text no. 38
    
39.
Saiki A, Nagayama D, Ohhira M, et al. Effect of weight loss using formula diet on renal function in obese patients with diabetic nephropathy. Int J Obes (Lond) 2005;29:1115-20.  Back to cited text no. 39
    
40.
Friedman AN, Chambers M, Kamendulis LM, Temmerman J. Short-term changes after a weight reduction intervention in advanced diabetic nephropathy. Clin J Am Soc Nephrol 2013;8:1892-8.  Back to cited text no. 40
    
41.
Morales E, Valero MA, León M, Hernández E, Praga M. Beneficial effects of weight loss in overweight patients with chronic proteinuric nephropathies. Am J Kidney Dis 2003;41:31927.  Back to cited text no. 41
    
42.
Gastrointestinal surgery for severe obesity. NIH consensus statement 1991. Vol. 9 (1);.1-20.  Back to cited text no. 42
    
43.
Livingston EH. The incidence of bariatric surgery has plateaued in the U.S. Am J Surg 2010;200:378-85.  Back to cited text no. 43
    
44.
Turgeon NA, Perez S, Mondestin M, et al. The impact of renal function on outcomes of bariatric surgery. J Am Soc Nephrol 2012;23: 885-94.  Back to cited text no. 44
    
45.
Neff KJ, Frankel AH, Tam FW, Sadlier DM, Godson C, le Roux CW. The effect of bariatric surgery on renal function and disease: a focus on outcomes and inflammation. Nephrol Dial Transplant 2013;28 Suppl 4:iv73-82.  Back to cited text no. 45
    
46.
Andalib A, Aminian A, Khorgami Z, Navaneethan SD, Schauer PR, Brethauer SA. Safety analysis of primary bariatric surgery in patients on chronic dialysis. Surg Endosc 2016;30:2583-91.  Back to cited text no. 46
    
47.
Navarro-Díaz M, Serra A, Romero R, et al. Effect of drastic weight loss after bariatric surgery on renal parameters in extremely obese patients: long-term follow-up. J Am Soc Nephrol 2006;17 12 Suppl 3:S213-7.  Back to cited text no. 47
    
48.
Serpa Neto A, Bianco Rossi FM, Dal Moro Amarante R, Alves Buriti N, Cunha Barbosa Saheb G, Rossi M. Effect of weight loss after Roux-en-Y gastric bypass, on renal function and blood pressure in morbidly obese patients. J Nephrol 2009;22:637-46.  Back to cited text no. 48
    
49.
Afshinnia F, Wilt TJ, Duval S, Esmaeili A, Ibrahim HN. Weight loss and proteinuria: systematic review of clinical trials and comparative cohorts. Nephrol Dial Transplant 2010;25:1173-83.  Back to cited text no. 49
    
50.
Navaneethan SD, Yehnert H. Bariatric surgery and progression of chronic kidney disease. Surg Obes Relat Dis 2009;5:662-5.  Back to cited text no. 50
    
51.
Hou CC, Shyu RS, Lee WJ, Ser KH, Lee YC, Chen SC. Improved renal function 12 months after bariatric surgery. Surg Obes Relat Dis 2013;9:202-6.  Back to cited text no. 51
    
52.
Heneghan HM, Cetin D, Navaneethan SD, Orzech N, Brethauer SA, Schauer PR. Effects of bariatric surgery on diabetic nephropathy after 5 years of follow-up. Surg Obes Relat Dis 2013; 9:7-14.  Back to cited text no. 52
    
53.
Amor A, Jiménez A, Moizé V, et al. Weight loss independently predicts urinary albumin excretion normalization in morbidly obese type 2 diabetic patients undergoing bariatric surgery. Surg Endosc 2013;27:2046-51.  Back to cited text no. 53
    
54.
Zalesin KC, McCullough PA. Bariatric surgery for morbid obesity: risks and benefits in chronic kidney disease patients. Adv Chronic Kidney Dis 2006;13:403-17.  Back to cited text no. 54
    
55.
Newcombe V, Blanch A, Slater GH, Szold A, Fielding GA. Laparoscopic adjustable gastric banding prior to renal transplantation. Obes Surg 2005;15:567-70.  Back to cited text no. 55
    
56.
Koshy AN, Coombes JS, Wilkinson S, Fassett RG. Laparoscopic gastric banding surgery performed in obese dialysis patients prior to kidney transplantation. Am J Kidney Dis 2008;52:e15-7.  Back to cited text no. 56
    
57.
Weiss H, Nehoda H, Labeck B, Oberwalder M, Konigsrainer A, Margreiter R. Organ transplantation and obesity: evaluation, risks and benefits of therapeutic strategies. Obes Surg 2000;10:465-9.  Back to cited text no. 57
    
58.
Bolignano D, Zoccali C. Effects of weight loss on renal function in obese CKD patients: a systematic review. Nephrol Dial Transplant 2013;28 Suppl 4:iv82-98.  Back to cited text no. 58
    
59.
Stenvinkel P, Zoccali C, Ikizler TA. Obesity in CKD - what should nephrologists know? J Am Soc Nephrol 2013;24:1727-36.  Back to cited text no. 59
    

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Correspondence Address:
Talha H Imam
Department of Nephrology, Southern California Permanente Medical Group, Fontana, CA
USA
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DOI: 10.4103/1319-2442.190772

PMID: 27751993

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    Abstract
    Emerging Epidemi...
    Controversy of B...
    The Burden of Ch...
    Obesity in End-s...
    Chronic Kidney D...
   Pathology
    Health Benefits ...
    Renal Benefits o...
    Renal Benefits o...
   Conclusion
    Clinical Signifi...
   Acknowledgments
    References
    Article Figures
 

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