The continuous growth in the prevalence of overweight, aggravated by the COVID pandemic (1), is causing metabolic, orthopedic, psychological, and cardiovascular consequences and revealing other relevant damages with clinical significance (2).

The prevalence of obesity, age-standardized, among adults aged 18 and older, defined as a body mass index (BMI) of >30 kg/m², has been rising over the past few decades, reaching a worrying figure of 650 million obese adults in the world in 2016 (3). Obesity is prevalent, especially in first-world countries where it continues to increase (4). Between 2005 and 2015, the obesity rate was approximately 32% in the United States and 24% in the United Kingdom (5). Data from the Framingham cohort show that not only the degree of obesity but also the period of exposure is important (6). Obesity is not only associated with increased mortality but also is a main risk factor for many diseases including chronic kidney disease (CKD) (7), nephrolithiasis, and renal cell cancer (8) (Table 1).

In addition, approximately 15% of United States adults (37 million people) are estimated to have CKD, with diabetes and hypertension being the most common causes. Other risk factors such as cardiac disease, family history of CKD, inherited kidney disorders, previous renal injuries, older age, and obesity are now recognized (9). In the National Health and Nutrition Examination Survey, 44% of patients with CKD in the United States were obese (22% with class 1 obesity, 11% with class 2, and 11% with class 3), with an overall percentage increasing through the following years. This prevalence is higher than that in the general population (36%) (10). In addition, CKD is the second leading cause of death-and disability-adjusted life years (11), and data show that more than two-thirds of deaths related to obesity are due to cardiovascular disease (CVD) in the world (12).

Efforts to reduce the systemic, particularly the renal, effects of the overweight pandemic must be adopted seriously, using the best available tools, especially if the knowledge about the effects of obesity on the kidney and the benefits of its reversal is growing. Bariatric surgery techniques are emerging as the most successful weight loss strategies for adults with extreme obesity, and their application in patients with chronic kidney disease deserves to be validated.

A definitive link between obesity and renal damage was established in 1923 by Preble (13), increasing in a stepwise fashion as BMI rises, even adjusted by the existence of hypertension, diabetes, history of smoking, and CVD (14). Indeed, obese individuals had a 3-fold higher risk of CKD than normal-weight healthy subjects (14, 15), regardless of their metabolic status and even in the absence of remarkable metabolic abnormalities (16). The most recognized link between obesity and CKD is centered on the insulin resistance associated with glucose intolerance, dyslipidemia, and hypertension that frequently progresses to overt type 2 diabetes mellitus (T2DM) (17). The relationship between diabetes and obesity is so close that it has led to the coining of the term “diabesity” (18). The relevance of obesity and its impact on the incidence and progression of CKD deserves attention because of its high prevalence, broad impact on health outcomes, and its modifiable nature (19).

A big meta-analysis of cohort studies, including 600,000 cases, assessed the effect of obesity on the CKD risk beyond its association with T2DM: obesity could be associated with a 51% increase in the risk of new-onset albuminuria and 18% in the risk of new onset of CKD stage 3 at 5 years (20). Furthermore, an Israeli army study reported hazard ratios for kidney failure of 3 and 6.9 for individuals with overweight and obesity, respectively, compared to normal BMI subjects. It is interesting to observe that having overweight (BMI between 25 and 29.9 kg/m²) could increase or not the risk (6, 14), suggesting a weight threshold.

Although diabetes and hypertension alone explain most obesity-associated renal risk, in many observational studies, obesity is independently associated with the development of proteinuria, acute kidney injury, CKD, and end-stage kidney disease, both in otherwise healthy and in higher-risk groups like prehypertensive individuals (21–24). In addition, obesity may accelerate the loss of function in a variety of renal diseases such as polycystic disease, IgA nephropathy, renal transplant, and diabetic renal disease (25–27). Furthermore, low birth weight, low renal endowment, or any cause of reduced renal mass display an increased risk of progression to CKD and end-stage kidney disease (ESKD) when associated with obesity (28).

There are many BS modalities, which are described later. The most frequently used has been the gastric bypass, but there is a trend to adopt the sleeve gastrectomy (SG) as the first choice (17) owing to its reduced complexity and comparable results with Roux-en-Y gastric bypass (RYGB) (71). All commonly performed procedures are done laparoscopically with a short hospital stay and each surgical technique has its own risks and complications.

A meta-analysis of eight studies (six retrospective studies) including 766 patients with CKD of ≥3 described eGFR and/or creatinine improvement in 63% of the cases, independent of the surgery technique used, blood pressure, BMI, or presence of diabetes (84). Only one study revealed creatinine increase at a follow-up of 2 years.

Although it has been reported that individuals with a lower preoperative eGFR experience less weight loss after BS, others have found that preoperative renal function may not have an independent impact on postoperative weight loss in patients with eGFR of ≥30 mL/min (103). On the contrary, severe CKD (stages 4 and 5) may have the worst results in terms of weight loss, and some authors propose to perform the surgery at the earliest possible (104) because long-term studies suggest that surgical intervention might be the most beneficial at earlier stages of kidney disease (94).

More advanced stages of CKD do not appear to be statistically associated with an increased risk of early postoperative complications (105). Studies in the strict pre-dialysis phase are lacking, but it is possible that the post-surgery reduction of hyperfiltration and the post-operatory rapid catabolic state might accelerate the need for dialysis (106).

Paradoxically, in patients in dialysis, morbid obesity is protective if it is accompanied by muscle mass gain (107, 108). However, weight loss, if intentional, has not been demonstrated to be deleterious (109), and BS may be a good bridge to obtain a transplant (110) since the risk of surgical and post-surgical complications is increased in patients with obesity when transplanted, including retarded wound healing and infection, lymphocele, and CVD (111, 112). In patients in dialysis, before transplant, BS reduced mortality (regardless of developing ESRD) (113) incidence of diabetes and approximately 60% of cardiac disease (114).

Better selection criteria to submit patients to BS, which include the severity of obesity, goals (metabolic, effects on progression or regression of CKD), patients preferences, and tolerance to the risk, are also necessary (19).

Obesity may impede access to kidney transplantation (19, 109, 115). In fact, it affects kidney transplant candidates, recipients, and potential living kidney donors deserving to be faced (116).

Meta-analysis has shown that patients with obesity after renal transplants have a higher risk of delayed graft function, risk of death, biopsy-proven acute rejection, and allograft loss (117). Patients who gained >15% of their initial weight during the first year showed higher mortality 10 years after, with a functioning kidney (118).

Some authors suggest that surgery should be considered 6–12 months after transplantation for patients with a BMI of >35 kg/m² with cardiovascular and metabolic comorbidities and without previous bariatric procedures (116).

The intervention, whether performed before or after the transplant, is effective and safe, and the time to do so must be individualized for each patient (119).

The pharmacological effect of BS on immunosuppressive regimens must be tailored because potential changes in drug disposition after the anatomical and functional changes in the gastrointestinal tract (120) need to be faced with closer surveillance of drug blood levels.

Perisurgical complications are higher in patients having both obesity and renal disease (73, 121), and creatinine levels of >2 mg/dL have a higher risk of re-intervention, readmission, and acute kidney injury (122, 123). With a low incidence (<15% at 30 days), patients with CKD experience more frequent complications and readmissions after BS than patients without CKD, and it should not be a contraindication for the procedure (124) because the absolute risk is low and mortality does not increase (103, 125). Indeed, safety has improved substantially after the 2000s (73). Post-op acute kidney injury, if it occurs in a context without sepsis or in subjects who do not have previous CKD 4 or 5, has a good prognosis (126).

Long-term problems vary with the surgical technique used (127). Mechanical, stenotic problems may be observed after GS or RYGB. Gastroesophageal reflux is more typical of GS (128). RYGB has its own specific complications such as cholelithiasis (40% of the cases), incisional or internal hernias, dumping syndrome after ingestion of a high quantity of simple carbohydrates, and oxalate nephropathy. Reduced oral intake as well as altered stomach and small bowel absorption reduce the availability of various micronutrients, particularly iron, calcium, vitamin B12, thiamine, and folate (128) (Table 3).

An important matter is that 1/3 of the patients submitted to BS may experience suboptimal results or significant weight regain in the first few postoperative years (129). Psychological aspects may be involved in the failure, since a high prevalence of pathologies, mainly eating and impulse control disorders can be found in patients requiring BS (129) that are not modified by the surgery (130), including the suicide risk (131). With any technique, failures are described, making lifelong follow-up necessary (128) to detect it and any potential complication at the earliest, performed by the best multidisciplinary BS team (132) available that should include at least a nutritionist, a psychologist, a gastroenterologist, and a nephrologist.

An important issue in the therapy of obesity and its consequences is the persistence and duration of its effects. Although there is little doubt about the superiority of surgery over non-invasive therapies in terms of effectiveness, RCTs are expected to compare surgery treatment in addition to pharmacotherapy versus lifestyle changes and pharmacotherapy alone to help in deciding rationally the best recommendation in CKD, established or at risk of it. A synergic effect between surgery and medical therapies exists (17).

The most important point is an eventual change in the CV risk. Here, the best studies have been done using RYGB showing, at 7 years of follow-up, a reduction in adjusted mortality of 40%, mainly attributed to a reduction in diabetes-associated cardiovascular events (133). But these data must be analyzed with caution because patients who received surgery are probably healthier and more motivated than their severely obese controls. In addition, it must be highlighted that an increase in non-disease-related death (accidents or suicide) has been described after BS (133).

Then, the targeted use of metabolic surgery to improve the cardiovascular and renal risks must be balanced against the undesirable short and long-term risks and sequelae of the procedure, which can be of particular concern to patients with CKD (17).

The lack of randomized clinical trials, low follow-up rates, and poorly reported data regarding co-morbidities and quality of life in many of the studies indicate that these findings should be interpreted with caution.

The use of multitarget therapies with appropriate education and combinations of SGLT2 or GLP-1 agonists with RAS blockade and BS could obtain more integrated management of the inflammatory state and modulate adipocyte cytokines, in order to obtain the best renal protection (123).

Taking all of the above into account, if an increment in urinary albumin excretion is found in a patient with obesity, it is mandatory to intervene to reduce overweight, control hypertension, diabetes, and dyslipidemia with all the available tools to prevent future chronic renal damage (2).

The author confirms being the sole contributor of this work and has approved it for publication.

This work was supported by the Programa de Especialización en Medicina Interna, Facultad de Medicina, Universidad Austral de Chile.

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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