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Bariatric Surgery in Patients with Chronic Kidney Disease: Comparison
Please note this is a comparison between Version 2 by Sirius Huang and Version 1 by Sylwia Czaja-Stolc.

Morbid obesity is considered a civilization disease of the 21st century. Not only does obesity increase mortality, but it is also the most important cause of the shortening life expectancy in the modern world. Obesity is associated with many metabolic abnormalities: dyslipidemia, hyperglycemia, cardiovascular diseases, and others. An increasing number of patients diagnosed with chronic kidney disease (CKD) are obese. Numerous additional disorders associated with impaired kidney function make it difficult to conduct slimming therapy and may also be associated with a greater number of complications than in people with normal kidney function.

  • obesity
  • bariatric surgery
  • chronic kidney disease

1. Obesity and Chronic Kidney Disease

There is an increase in the incidence of chronic kidney disease (CKD), which is usually diagnosed relatively late when nephroprotective actions bring little benefit. For this reason, the number of people requiring renal replacement therapy (RRT), including dialysis and kidney transplantation, is also increasing [11][1]. CKD is divided into five stages according to the glomerular filtration rate (GFR). RRT is usually started when the GFR is lower than 15 mL/min/1.73 m2 or earlier when it is accompanied by, among others, malnutrition, overhydration, and severe uremia [12][2].
Overweight and obesity are factors contributing to the increased incidence of CKD. It is estimated that excessive body weight may contribute to up to 30% of CKD cases [13][3]. Obesity leads to functional and structural changes in the kidneys. Hyperfiltration and proteinuria, which are caused by glomerulosclerosis and tubulointerstitial fibrosis, are observed. These disorders are called obesity-related glomerulopathy (ORG) [14][4]. Excess body weight leads to chronic inflammation, oxidative stress, lipotoxicity, and impaired adipokine secretion, which also adversely affects kidney function [7][5].
Despite the existence of the so-called obesity paradox (reverse epidemiology), i.e., a positive correlation between excess body weight and the higher survival rate of patients undergoing dialysis, obesity may be an obstacle in qualifying for kidney transplantation [15][6]. Both donors and transplant recipients may be disqualified due to excess body weight. The body weight cut-offs that qualify for transplantation depend on the principles of the treatment center and the individual state of health of the patient. In most centers, body mass index (BMI) over 40 kg/m2 is a contraindication to the procedure, and over 35 kg/m2 is a relative contraindication [16][7]. The number of kidney transplant recipients (KTRs) with a BMI over 30 kg/m2 doubles every 15 years [17][8]. Obesity during transplantation is associated with poorer perioperative outcomes in terms of length of surgery and hospitalization, wound infections, delayed graft function, incisional hernia, and other complications [18,19][9][10].
According to data from 2013, over 25% of all living kidney donors are obese at the time of surgery [20][11]. Obesity increases the risk of ESRD among living kidney donors. Locke et al. observed that obese kidney donors had a 1.9-fold higher risk of post-donation ESRD when compared with non-obese donors. An increase in BMI of more than 27 kg/m2 before organ donation was associated with a 7% increase in ESRD risk after kidney donation [21][12].

2. Bariatric Surgery (BS)

Regarding the treatment of obesity, Capehorn et al. suggested a 4-tier framework to treat overweight and obesity systematically. The treatment starts with primary activity in tier 1—the general physician usually coordinates this phase. Tier 2 is a tighter regiment of lifestyle changes in preferably a group setting. The last conservative treatment step is tier 3—a step based on a multidisciplinary team with obesity specialists (mostly physiotherapists, psychologists, and nutritionists). The fourth tier is designed for individuals with a very severe and complex form of obesity, mostly for patients with BMI > 40 kg/m2 or BMI > 35 kg/m2 with obesity-related comorbidities and constitutes the surgical treatment of obesity [22][13].
These guidelines are still widely used. However, there is increasing evidence that bariatric procedures should also be considered for patients with DM2 and a BMI of 30 to 35 kg/m2 if hyperglycemia is inadequately controlled despite optimal medical treatment for DM2. Substantial evidence indicates that surgery results in greater improvements in weight loss and DM2 outcomes compared with nonsurgical interventions, regardless of the type of procedures used [23][14].
Bariatric procedures are divided into three types: restrictive, malabsorptive, and combination procedures (with a restrictive and malabsorptive component).
Restrictive surgical procedures lead to the decreased size of the stomach and reduced feeling of hunger or cause early satiety with smaller volumes of food [24,25][15][16]. Surgical procedures in this category include gastric banding (GB), vertical-banded gastroplasty (VBG), and sleeve gastrectomy (SG), where GB and VBG are methods, which are performed more and more rarely. SG is the most popular procedure, nowadays number one worldwide [26,27][17][18].
Malabsorptive procedures decrease the absorption of nutrients by excluding food from segments of the alimentary tract by either shortening the length of the tract or by bypassing anatomical segments or inter-transposing various segments of the bowel [28][19]. The first of these procedures were done in the fifties and the sixties, namely the jejunal–ileal bypass [29][20], the duodenojejunal bypass (DJB) [30][21], and later the biliopancreatic diversion (BPD) either with or without the duodenal switch [28,31][19][22].
The combination of both types of surgery aims to benefit from the restrictive and malabsorptive procedure. The Roux en-Y Gastric Bypass (RYGB) or One Anastomosis Gastric Bypass (OAGB) are the most well-known examples. While performing this procedure, a small pouch is created by performing a partial gastrectomy followed by creating an anastomosis of the small pouch to the jejunum (gastro-jejunostomy). Then, a bypass is achieved by identifying the transected stomach remnant and its attached segment of the duodenum and proximal jejunum, which is then mobilized at the jejunal end (the Roux en-Y limb), to be anastomosed to a distal segment of the jejunum to form a jejuno-jejunostomy [32][23].
The OAGB consists of a long conduit from below the crow’s foot extending up to the left of the angle of His. The stomach is divided, and a small, long tube is created, which becomes the pouch, similar in shape to the pouch of SG. OAGB has a 2–3 cm gastro-jejunal anastomosis to an anti-colic loop of jejunum 150–200 cm distal to the ligament of Treitz. The power of OAGB comes from the fact that it is both a “non-obstructive” restrictive procedure and has a significant fatty food intolerance component with minimal malabsorption [33][24].
According to the 2016 International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO) survey data from 58/62 IFSO Societies, the total number of bariatric/metabolic procedures performed in 2016 was 685,874. The most common primary surgical bariatric/metabolic procedure was laparoscopic sleeve gastrectomy (LSG) (340,550; 53.6%), followed by LRYGB (191,326; 30.1%), and OAGB (30,563; 4.8%) [26,27][17][18].
BS results in durable excess weight loss (EWL). It reduces or at least improves comorbidities, improves the quality of life (QoL), and increases lifespan [34][25]. In addition to weight loss, BS impacts the resolution of DM2, metabolic syndrome, and cardiovascular diseases [35][26].
There is an increasing interest in metabolic improvements, which are observed even before any significant weight loss [36][27]. Walter Pories was the first to show this in 1992. He suggested that the beneficial effects of bariatric surgery go beyond weight loss [37][28]. It is known that BS can also improve the outcomes of patients suffering from many respiratory, cardiovascular, and metabolic diseases [38,39,40,41,42][29][30][31][32][33].
It is a well-known fact that some of the gut hormones modified by BS have anorectic actions and can significantly affect postoperative weight loss [43][34]. It is also recognized that macronutrient as well as micronutrient malabsorption is a complication of BS and it is not a desired mechanism of action for its long-term efficacy. Lower absorption of food and some metabolites leads to their deficiencies [44][35].
There is also a considerable number of publications describing the BS procedures among patients with a BMI lower than 35 kg/m2 and assessing the relationship between the gut hormone profiles and DM2 remission. The study by Celik et al. presents glycemic control. It was assessed in a prospective cohort of patients who had a Diverted Sleeve Gastrectomy with Ileal Transposition (DSIT), OAGB compared with SG in the first 30 days after BS. This study proved that the DSIT and OAGB were superior to SG in achieving glycemic control, defined as fasting glucose lower than 126 mg/dL [45][36]. These improvements in glycemic control after DSIT/OAGB are based on the Foregut–Hindgut hypothesis [46][37]. Transfer of the distal part of the ileum just below the pylorus that digested food stimulates producing hormones such as glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and oxyntomodulin—hormones known for their anti-diabetogenic action. The increased blood levels of these hormones are found after other BS, such as RYGB, LSG, or BPD-DS. Despite the increasing interest in the metabolic aspect of BS, many issues of comorbidities resolution still need to be explained [47][38].
Surgical interference with the anatomy of the gastrointestinal tract can cause significant changes in the composition of the gut microbiome, which may affect the composition and number of various metabolites produced by intestinal bacteria. Research on this phenomenon has developed significantly over the past decade and suggests an association between microbiome changes after bariatric BS and patient health, especially in the context of metabolic disturbances [48,49][39][40].

3. Bariatric Surgery in Patients with Chronic Kidney Disease

BS is performed on CKD patients treated conservatively, on dialysis, before and after kidney transplantation. Weight loss in the above-mentioned groups of patients brings positive effects. Rapid and sustained weight loss due to BS enables patients with ESRD to stop dialysis treatment and receive a transplant. Additionally, pre-transplant metabolic surgery may reduce the risk of mortality and graft failure. On the other hand, it increases the pool of people who can donate an organ [19][10]. Weight loss slows disease progression in non-dialysis patients [50][41].
In 2022, a clinical practice guideline by the DESCARTES Working Group of ERA was published on the management of obesity in kidney transplant candidates and recipients. According to the guidelines, BS should be considered in kidney transplant candidates and recipients with a BMI ≥ 40 kg/m2 or a BMI ≥ 35 kg/m2 and at least one serious obesity-related condition that can be mitigated by weight loss. The suggested surgical method is LSG [9][42]. The 2020 Kidney Disease Improving Global Outcomes (KDIGO) recommendations suggest that obesity should not be a contraindication to kidney transplantation, but suggest weight loss interventions for obese candidates before transplantation [51][43].
Among the complications of DM2 is diabetic kidney disease (DKD). Its pathophysiology is associated with the metabolic disorders accompanying both DM2 and obesity, namely hyperglycemia, dyslipidemia, and arterial hypertension. DKD develops in approximately 40% of diabetic patients and significantly increases all-cause and cardiovascular mortality in this patient group [52][44]. Madsen et al. investigated the effect of RYGB on the remission of DM2 and its vascular complications. Due to the BS, 74% of the operated patients achieved remission of DM2 after one year after the surgery. Additionally, RYGB reduced the risk of vascular complications and reduced the development of DKD [53][45]. Bariatric procedures not only reduce the risk of developing DKD but also improve the results of patients suffering from it. Heneghan et al. reported that in obese patients with moderate and severe albuminuria, BS caused, in 58,3% of patients, remission of albuminuria at a 5-year follow-up [54][46]. Similar conclusions were drawn by Canney et al., who in their study achieved, at 13-months follow-up, diabetic albuminuria remission in 78% of patients undergoing RYGB [55][47].
Additionally, BS improves kidney function independently of improvements in glycemia. In a study where DM2 was not an inclusion criterion, metabolic surgery reduced the risk of eGFR decline by more than 30% by 58% and decreased serum creatinine by 57% [56][48]. In a long follow-up study, BS reduced the incidence of ESRD by over 70% approx. 18 years after surgery [57][49].
It appears that the improvement in the parameters of CKD is independent of postoperative weight loss, glycemic control, and blood pressure [52][44]. Table 1 shows the results of the studies of patients with CKD undergoing BS.
Table 1.
Literature review on the effect of BS on patients with CKD.
Studies show many benefits of BS among CKD patients. On the other hand, the results of the meta-analysis show that patients on chronic dialysis have a significantly higher risk of postoperative mortality and myocardial infarction after bariatric surgery compared to patients without renal failure [64][56]. However, it is known that obesity also increases cardiovascular risk, so it is necessary to compare the risks associated with BS and those of long-term obesity.

References

  1. Yamada, Y.; Ikenoue, T.; Saito, Y.; Fukuma, S. Undiagnosed and untreated chronic kidney disease and its impact on renal outcomes in the Japanese middle-aged general population. J. Epidemiol. Commun. Health 2019, 73, 1122–1127.
  2. National Kidney Foundation. KDOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification and Stratification. Am. J. Kidney Dis. 2002, 39, 1–266.
  3. Rhee, C.M.; Ahmadi, S.F.; Kalantar-Zadeh, K. The dual roles of obesity in chronic kidney disease: A review of the current literature. Curr. Opin. Nephrol. Hypertens. 2016, 25, 208–216.
  4. D’Agati, V.D.; Chagnac, A.; de Vries, A.P.; Levi, M.; Porrini, E.; Herman-Edelstein, M.; Praga, M. Obesity-related glomerulopathy: Clinical and pathologic characteristics and pathogenesis. Nat. Rev. Nephrol. 2016, 12, 453–471.
  5. Martin-Taboada, M.; Vila-Bedmar, R.; Medina-Gómez, G. From Obesity to Chronic Kidney Disease: How Can Adipose Tissue Affect Renal Function? Nephron 2021, 145, 609–613.
  6. Kittiskulnam, P.; Johansen, K.L. The obesity paradox: A further consideration in dialysis patients. Semin. Dial. 2019, 32, 485–489.
  7. Potluri, K.; Hou, S. Obesity in kidney transplant recipients and candidates. Am. J. Kidney Dis. 2010, 56, 143–156.
  8. Friedman, A.N.; Miskulin, D.C.; Rosenberg, I.H.; Levey, A.S. Demographics and trends in overweight and obesity in patients at time of kidney transplantation. Am. J. Kidney Dis. 2003, 41, 480–487.
  9. Jarrar, F.; Tennankore, K.K.; Vinson, A.J. Combined Donor-Recipient Obesity and the Risk of Graft Loss After Kidney Transplantation. Transpl. Int. 2022, 35, 10656.
  10. Bellini, M.I.; Paoletti, F.; Herbert, P.E. Obesity and bariatric intervention in patients with chronic renal disease. J. Int. Med. Res. 2019, 47, 2326–2341.
  11. Taler, S.J.; Messersmith, E.E.; Leichtman, A.B.; Gillespie, B.W.; Kew, C.E.; Stegall, M.D.; Merion, R.M.; Matas, A.J.; Ibrahim, H.N.; RELIVE Study Group. Demographic, metabolic, and blood pressure characteristics of living kidney donors spanning five decades. Am. J. Transpl. 2013, 13, 390–398.
  12. Locke, J.E.; Reed, R.D.; Massie, A.; MacLennan, P.A.; Sawinski, D.; Kumar, V.; Mehta, S.; Mannon, R.B.; Gaston, R.; Lewis, C.E.; et al. Obesity increases the risk of end-stage renal disease among living kidney donors. Kidney Int. 2017, 91, 699–703.
  13. Capehorn, M.S.; Haslam, D.W.; Welbourn, R. Obesity Treatment in the UK Health System. Curr. Obes. Rep. 2016, 5, 320–326.
  14. Lebovitz, H.E. Metabolic surgery for type 2 diabetes with BMI < 35 kg/m2: An endocrinologist’s perspective. Obes. Surg. 2013, 23, 800–808.
  15. Buchwald, H.; Avidor, Y.; Braunwald, E.; Jensen, M.D.; Pories, W.; Fahrbach, K.; Schoelles, K. Bariatric surgery: A systematic review and meta-analysis. JAMA 2004, 292, 1724–1737.
  16. Pories, W.J. Bariatric surgery: Risks and rewards. J. Clin. Endocrinol. Metab. 2008, 93 (Suppl. 1), S89–S96.
  17. Angrisani, L.; Santonicola, A.; Iovino, P.; Vitiello, A.; Zundel, N.; Buchwald, H.; Scopinaro, N. Bariatric Surgery and Endoluminal Procedures: IFSO Worldwide Survey 2014. Obes. Surg. 2017, 27, 2279–2289.
  18. Angrisani, L.; Santonicola, A.; Iovino, P.; Vitiello, A.; Higa, K.; Himpens, J.; Buchwald, H.; Scopinaro, N. IFSO Worldwide Survey 2016: Primary, Endoluminal, and Revisional Procedures. Obes. Surg. 2018, 28, 3783–3794.
  19. Scopinaro, N.; Gianetta, E.; Civalleri, D.; Bonalumi, U.; Bachi, V. Bilio-pancreatic bypass for obesity: II. Initial experience in man. Br. J. Surg. 1979, 66, 618–620.
  20. Kremen, A.J.; Linner, J.H.; Nelson, C.H. An experimental evaluation of the nutritional importance of proximal and distal small intestine. Ann. Surg. 1954, 140, 439–448.
  21. Cohen, R.V.; Schiavon, C.A.; Pinheiro, J.S.; Correa, J.L.; Rubino, F. Duodenal-jejunal bypass for the treatment of type 2 diabetes in patients with body mass index of 22–34 kg/m2: A report of 2 cases. Surg. Obes. Relat. Dis. 2007, 3, 195–197.
  22. Gagner, M. Hypoabsorption Not Malabsorption, Hypoabsorptive Surgery and Not Malabsorptive Surgery. Obes. Surg. 2016, 26, 2783–2784.
  23. Fobi, M.A.; Lee, H.; Holness, R.; Cabinda, D. Gastric bypass operation for obesity. World J. Surg. 1998, 22, 925–935.
  24. Rutledge, R.; Kular, K.; Manchanda, N. The Mini-Gastric Bypass original technique. Int. J. Surg. 2019, 61, 38–41.
  25. Picot, J.; Jones, J.; Colquitt, J.L.; Gospodarevskaya, E.; Loveman, E.; Baxter, L.; Clegg, A.J. The clinical effectiveness and cost-effectiveness of bariatric (weight loss) surgery for obesity: A systematic review and economic evaluation. Health Technol. Assess 2009, 13, 215–357.
  26. Ashrafian, H.; le Roux, C.W.; Darzi, A.; Athanasiou, T. Effects of bariatric surgery on cardiovascular function. Circulation 2008, 118, 2091–2102.
  27. Cummings, D.E.; Cohen, R.V. Beyond BMI: The need for new guidelines governing the use of bariatric and metabolic surgery. Lancet Diabetes Endocrinol. 2014, 2, 175–181.
  28. Pories, W.J.; MacDonald, K.G.; Flickinger, E.G.; Dohm, G.L.; Sinha, M.K.; Barakat, H.A.; May, H.J.; Khazanie, P.; Swanson, M.S.; Morgan, E.; et al. Is type II diabetes mellitus (NIDDM) a surgical disease? Ann. Surg. 1992, 215, 633–642.
  29. Buchwald, H.; Estok, R.; Fahrbach, K.; Banel, D.; Jensen, M.D.; Pories, W.J.; Bantle, J.P.; Sledge, I. Weight and type 2 diabetes after bariatric surgery: Systematic review and meta-analysis. Am. J. Med. 2009, 122, 248–256.e5.
  30. Van Huisstede, A.; Rudolphus, A.; Castro Cabezas, M.; Biter, L.U.; van de Geijn, G.J.; Taube, C.; Hiemstra, P.S.; Braunstahl, G.J. Effect of bariatric surgery on asthma control, lung function and bronchial and systemic inflammation in morbidly obese subjects with asthma. Thorax 2015, 70, 659–667.
  31. Van Huisstede, A.; Rudolphus, A.; van Schadewijk, A.; Cabezas, M.C.; Mannaerts, G.H.; Taube, C.; Hiemstra, P.S.; Braunstahl, G.J. Bronchial and systemic inflammation in morbidly obese subjects with asthma: A biopsy study. Am. J. Respir. Crit. Care Med. 2014, 190, 951–954.
  32. Jeng, E.I.; Aranda, J.M.; Ahmed, M.; Klodell, C.T. Left Ventricular Assist Device and Bariatric Surgery: A Bridge to Heart Transplant by Weight and Waiting Time Reduction. J. Card Surg. 2016, 31, 120–122.
  33. Lim, C.P.; Fisher, O.M.; Falkenback, D. Bariatric surgery provides a “bridge to transplant” for morbidly obese patients with advanced heart failure and may obviate the need for transplantation. Obes. Surg. 2016, 26, 486–493.
  34. Iacobellis, G.; Singh, N.; Wharton, S.; Sharma, A.M. Substantial changes in epicardial fat thickness after weight loss in severely obese subjects. Obesity 2008, 16, 1693–1697.
  35. Pakiet, A.; Haliński, Ł.P.; Rostkowska, O.; Kaska, Ł.; Proczko-Stepaniak, M.; Śledziński, T.; Mika, A. The Effects of One-Anastomosis Gastric Bypass on Fatty Acids in the Serum of Patients with Morbid Obesity. Obes. Surg. 2021, 31, 4264–4271.
  36. Celik, A.; Pouwels, S.; Karaca, F.C.; Çağıltay, E.; Ugale, S.; Etikan, İ.; Büyükbozkırlı, D.; Kılıç, Y.E. Time to Glycemic Control—an Observational Study of 3 Different Operations. Obes. Surg. 2017, 27, 694–702.
  37. Celik, A.; Ugale, S.; Ofluoglu, H.; Asci, M.; Celik, B.O.; Vural, E.; Aydin, M. Technical feasibility and safety profile of laparoscopic diverted sleeve gastrectomy with ileal transposition (DSIT). Obes. Surg. 2015, 25, 1184–1190.
  38. Celik, A.; Ugale, S.; Ofluoglu, H.; Vural, E.; Cagiltay, E.; Cat, H.; Asci, M.; Celik, B.O. Metabolic Outcomes of Laparoscopic Diverted Sleeve Gastrectomy with Ileal Transposition (DSIT) in Obese Type 2 Diabetic Patients. Obes. Surg. 2015, 25, 2018–2022.
  39. Koulas, S.G.; Stefanou, C.K.; Stefanou, S.K.; Tepelenis, K.; Zikos, N.; Tepetes, K.; Kapsoritakis, A. Gut Microbiota in Patients with Morbid Obesity Before and After Bariatric Surgery: A Ten-Year Review Study (2009–2019). Obes. Surg. 2021, 31, 317–326.
  40. Scheithauer, T.P.M.; Davids, M.; Winkelmeijer, M.; Verdoes, X.; Aydin, Ö.; de Brauw, M.; van de Laar, A.; Meijnikman, A.S.; Gerdes, V.E.A.; van Raalte, D.; et al. Compensatory intestinal antibody response against pro-inflammatory microbiota after bariatric surgery. Gut Microbes. 2022, 14, 2031696.
  41. Kassam, A.F.; Mirza, A.; Kim, Y.; Hanseman, D.; Woodle, E.S.; Quillin, R.C.; Johnson, B.L.; Govil, A.; Cardi, M.; Schauer, D.P.; et al. Long-term outcomes in patients with obesity and renal disease after sleeve gastrectomy. Am. J. Transpl. 2020, 20, 422–429.
  42. Oniscu, G.C.; Abramowicz, D.; Bolignano, D.; Gandolfini, I.; Hellemans, R.; Maggiore, U.; Nistor, I.; O’Neill, S.; Sever, M.S.; Koobasi, M.; et al. Management of obesity in kidney transplant candidates and recipients: A clinical practice guideline by the DESCARTES Working Group of ERA. Nephrol. Dial. Transpl. 2021, 37 (Suppl. 1), i1–i15.
  43. Chadban, S.J.; Ahn, C.; Axelrod, D.A.; Foster, B.J.; Kasiske, B.L.; Kher, V.; Kumar, D.; Oberbauer, R.; Pascual, J.; Pilmore, H.L.; et al. KDIGO Clinical Practice Guideline on the Evaluation and Management of Candidates for Kidney Transplantation. Transplantation 2020, 104 (Suppl. 1), S11–S103.
  44. Martin, W.P.; White, J.; López-Hernández, F.J.; Docherty, N.G.; le Roux, C.W. Metabolic Surgery to Treat Obesity in Diabetic Kidney Disease, Chronic Kidney Disease, and End-Stage Kidney Disease; What Are the Unanswered Questions? Front. Endocrinol. 2020, 11, 289.
  45. Madsen, L.R.; Baggesen, L.M.; Richelsen, B.; Thomsen, R.W. Effect of Roux-en-Y gastric bypass surgery on diabetes remission and complications in individuals with type 2 diabetes: A Danish population-based matched cohort study. Diabetologia 2019, 62, 611–620.
  46. Heneghan, H.M.; Cetin, D.; Navaneethan, S.D.; Orzech, N.; Brethauer, S.A.; Schauer, P.R. Effects of bariatric surgery on diabetic nephropathy after 5 years of follow-up. Surg. Obes. Relat. Dis. 2013, 9, 7–14.
  47. Canney, A.L.; Cohen, R.V.; Elliott, J.A.; Aboud, C.; Martin, W.P.; Docherty, N.G.; le Roux, C.W. Improvements in diabetic albuminuria and podocyte differentiation following Roux-en-Y gastric bypass surgery. Diab. Vasc. Dis. Res. 2020, 17, 1479164119879039.
  48. Chang, A.R.; Chen, Y.; Still, C.; Wood, G.C.; Kirchner, H.L.; Lewis, M.; Kramer, H.; Hartle, J.E.; Carey, D.; Appel, L.J.; et al. Bariatric surgery is associated with improvement in kidney outcomes. Kidney Int. 2016, 90, 164–171.
  49. Shulman, A.; Peltonen, M.; Sjöström, C.D.; Andersson-Assarsson, J.C.; Taube, M.; Sjöholm, K.; le Roux, C.W.; Carlsson, L.M.S.; Svensson, P.A. Incidence of end-stage renal disease following bariatric surgery in the Swedish Obese Subjects Study. Int. J. Obes. 2018, 42, 964–973.
  50. Navaneethan, S.D.; Yehnert, H. Bariatric surgery and progression of chronic kidney disease. Surg. Obes. Relat. Dis. 2009, 5, 662–665.
  51. Imam, T.H.; Fischer, H.; Jing, B.; Burchette, R.; Henry, S.; DeRose, S.F.; Coleman, K.J. Estimated GFR before and after Bariatric Surgery in CKD. Am. J. Kidney Dis. 2017, 69, 380–388.
  52. Prasad, P.; Khullar, D.; Grover, R.; Chhabra, G.; Gupta, N.; Sinha, A.; Sharma, A.; Ahluwalia, V.; Chowbey, P. The Effect of Bariatric Surgery on Patients with Chronic Kidney Disease. Obes. Surg. 2020, 30, 4665–4668.
  53. Sheetz, K.H.; Gerhardinger, L.; Dimick, J.B.; Waits, S.A. Bariatric Surgery and Long-term Survival in Patients with Obesity and End-stage Kidney Disease. JAMA Surg. 2020, 155, 581–588.
  54. Cohen, J.B.; Lim, M.A.; Tewksbury, C.M.; Torres-Landa, S.; Trofe-Clark, J.; Abt, P.L.; Williams, N.N.; Dumon, K.R.; Goral, S. Bariatric surgery before and after kidney transplantation: Long-term weight loss and allograft outcomes. Surg. Obes. Relat. Dis. 2019, 15, 935–941.
  55. Schindel, H.; Winkler, J.; Yemini, R.; Carmeli, I.; Nesher, E.; Keidar, A. Survival benefit in bariatric surgery kidney recipients may be mediated through effects on kidney graft function and improvement of co-morbidities: A case-control study. Surg. Obes. Relat. Dis. 2019, 15, 621–627.
  56. Palamuthusingam, D.; Singh, A.; Palamuthusingam, P.; Hawley, C.M.; Pascoe, E.M.; Johnson, D.W.; Fahim, M. Postoperative outcomes after bariatric surgery in patients on chronic dialysis: A systematic review and meta-analysis. Obes. Res. Clin. Pract. 2021, 15, 473–484.
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