Treatment for obesity in patients with CKD englobes a wide range of options, from lifestyle modification to bariatric surgery. Weight loss improves metabolic parameters and stimulates changes in renal function that lead to improvement of glomerular hyperfiltration. The most common clinical presentation is a slowly increasing non-nephrotic proteinuria that is followed by a progressive decline of kidney function. The use of multitarget therapies, with appropriate dietary education, emerging diets, the use of new RAAS blocking agents, the combination of iSGLT2 or GLP-1 agonists, as well as bariatric surgery, may play a key role in finally achieving the desired nephroprotection in this CKD population. New therapeutic agents and novel biomarkers, such as adipocyte cytokines, are needed to monitor and mitigate progression to end-stage renal disease. The emerging “lipidomics” and the role of nonalcoholic fatty liver are relevant research lines.

Obesity has been widely reported as an important risk factor for all major cardiovascular events, and the onset and progression of chronic kidney disease (CKD) are not the exception [1]. The world-wide prevalence of obesity is rapidly increasing, especially after the COVID-19 pandemic where the number of subjects with weight-gain experienced an alarming increase due to lock-down in several countries [2]. The renal effects of obesity have been extensively described both clinically and histologically, with a wide range of injuries that include the onset of albuminuria, obesity-related glomerulopathy, podocyte injury, and hyperfiltration [3].

Therapeutic strategies to manage patients with obesity and CKD include lifestyle interventions, blockage of the renin-angiotensin-aldosterone system (RAAS), antidiabetic agents, and even bariatric surgery, with generally positive results in terms of improving blood-pressure levels, reduction of albuminuria and stabilization of glomerular filtration rate (GFR) [4, 5]. New therapeutic alternatives have been the objective of the study to slow the progression of CKD in patients with obesity, emerging plant-based diets, new RAAS blocking agents, as well as bariatric surgery in combination with the emerging “lipidomics” for those who fail to achieve weight loss through lifestyle modification, on the basis that bariatric surgery has shown reductions in risk for estimated GFR (eGFR) decline and kidney failure with very encouraging results [5].

There is little information in the literature on the effect of different nephroprotective measures in obese patients with CKD. For this reason, the aim of this review was to analyze the new therapeutic options available for renal damage associated with obesity, with special emphasis in the role of bariatric surgery and its effects across several clinical and molecular parameters in CKD population.

Lifestyle Modification

Conservative management of obesity primarily consists in reduced calorie diet and increased exercise, although this approach has failed to show a long-term benefit on halting CKD progression, with high rates of weight gain after rapid initial weight loss [6]. In most lifestyle intervention randomized controlled trials (RCTs), lifestyle modification was generally effective at reducing weight and lowering blood pressure and proteinuria, although follow-up was short and conclusions on long-term effects on eGFR could not be drawn. As for diet regimes, no convincing data exist supporting the superiority of a specific dietary pattern to promote weight loss in the general population or in subjects with CKD. Recent studies found no differences in eGFR change and albuminuria decrease in patients with CKD comparing different diet regimes (low fat, Mediterranean, or low carbohydrate) after 2-year follow-up [7].

As for intermittent fasting (exposure to fasting periods), it has been shown that this regime can increase insulin sensitivity, improves lipid metabolism, and reduces abdominal fat and inflammation, among other metabolic benefits [8]. Periods of energy restriction, long enough to deplete liver glycogen stores, activate a metabolic switch toward use of fatty acids and ketones. Cells adaptation consists of a reduction in insulin signaling and overall protein synthesis. During the recovery phase, glucose plasma levels increase, ketone levels drop, and cells increase protein synthesis [8]. All these benefits are yet to be confirmed in CKD population.

Diet intervention may have a deeper impact if it is complemented with other non-pharmacological interventions in patients with CKD. Wend et al. [9] retrospectively analyzed 17 patients with CKD from a nonsurgical multimodality obesity treatment program (a combination of cognitive-behavioral therapy, physical exercise training, and nutritional therapy offered in small groups) over 12 months. Average eGFR increased by 14.8 ± 18.0 mL/min to a 12-month value of 68.2 ± 19.3 mL/min; all subjects experienced significant weight loss and reduced the need for hypertension medication. These findings are supported by a recent review by Yamamoto et al. [10] who analyzed a total of 15 trials including 622 patients with CKD and evaluated the efficacy of aerobic exercise of 3–12 months’ duration showing marked improvement in reducing obesity, high blood pressure, and low exercise capacity in overweight/obese patients, but without any significant effect on eGFR and proteinuria.

New diet regimes in countries where obesity is endemic, are rapidly gaining popularity. Low carbohydrate, high-protein diets are widely promoted as an effective mean for rapid weight loss and better glycemic control. However, Ko et al. [11] analyzed the evidence available on high-protein diets on patients with CKD, suggesting that glomerular hyperfiltration caused by a high-protein diet may lead to an increase in albuminuria and an initial rise and subsequent decline in eGFR. Furthermore, growing evidence suggests that high-protein diets may be associated with a number of metabolic complications that may be detrimental to kidney health.

Another interesting possibility is the potential of plant-based diets: regimes that emphasize on the consumption of plant foods (fruit, vegetables, nuts, seeds, oils, whole grains, legumes, and beans) with or without small or moderate amounts of meat, fish, seafood, eggs, and dairy. Being plants the only dietary source of fiber, the gut microbiota profile is shifted toward increased production of anti-inflammatory compounds and reduced production of uremic toxins, in fact, some microbial species are able to utilize specific substrates from dietary protein or fiber to expand their populations. Some symbiotic bacteria such as Saccharolytic bacteria ferment dietary fiber, releasing short-chain fatty acids that enhance gut barrier integrity and have anti-inflammatory and immunomodulatory effects, on the other hand proteolytic bacteria ferment dietary protein, which leads to the production of several uremic toxins that are absorbed into the bloodstream and may accumulate in people with low GFR [12].

In addition, low net endogenous acid load may mitigate metabolic acidosis and potentially slow the progression of kidney disease and reduction in the ratio of hyperkalemia as well as lower phosphorus intake [12]. Proper RCTs are needed to give suitable evidence on this matter.

New Pharmacological Options

Finerenone

Finerenone is a novel, selective, nonsteroidal mineralocorticoid receptor (MR) antagonist that blocks MR-mediated sodium reabsorption and MR overactivation and has demonstrated anti-inflammatory and anti-fibrotic effects. Recent data from pooled analysis of the FIDELIO and FIGARO trials, which aimed to perform an efficacy and safety analysis across a broad spectrum of CKD and type 2 diabetic patients on finerenone compared with placebo, found reductions both in cardiovascular events and kidney failure outcomes with finerenone [13]. The mean body mass index (BMI) of the patients included in both trials was 31.3 ± 6.0 kg/m2. Hence, we can extrapolate that the shown benefits of finerenone in terms of cardiovascular events and kidney protection in diabetic CKD population are also present in patients with concomitant obesity. Experiments on murine models have demonstrated that finerenone elicits direct effects on the activation of interscapular brown adipose tissue, representing a promising pharmacologic tool to treat human metabolic diseases associated with adipose tissue dysfunctions such as obesity in the setting of CKD [14].

Glucagon-Like Peptide 1 Receptor Agonists and Sodium-Glucose Co-Transporter Type 2 Inhibitors

Glucagon-like peptide 1 receptor agonists (GLP-1RA) is a class B G protein-coupled receptor not only expressed in the pancreas and central nervous system but also detected in lower levels in the gut, kidneys, lungs, liver, heart, muscle, peripheral nervous system, and other tissues. GLP-1 increases insulin secretion in response to nutrients, particularly glucose, and suppresses glucagon secretion from pancreatic islet cells, with a reduction in postprandial glucose levels as the net result [15].

The use of GLP-1 RAs is widely supported on very strong data in terms of cardiovascular outcomes, with multiple systematic reviews and meta-analyses demonstrating improvement in both weight and glycemia [16]. A RCT comparing liraglutide, 3.0 mg, daily versus placebo in 2,254 adults with prediabetes demonstrated efficacy in reducing weight and risk for diabetes [17]. The evidence in the CKD group has also been established in several trials, but none of them were designed to measure weight loss as a primary outcome. Liraglutide, a GLP-1 RA FDA approved for weight loss indication [7], has shown benefits in terms of glycemic control, blood pressure, lipid levels. The dose of 1.8 mg has been related to a decreased risk of death from cardiovascular disease, nonfatal myocardial infarction, and nonfatal cerebral infarction in diabetic patients with and without CKD [18]. Recently, the use of semaglutide, 2.4 mg, also has been FDA approved in people with overweight or obesity, based on findings from the STEP 8 RCT, where semaglutide proved non-inferior to liraglutide in terms of weight reduction and safety profile [19].

Adverse effects of liraglutide and other GLP-1 RAs include higher rates of gastrointestinal events leading to discontinuation, but interestingly, there is no increased risk for acute kidney injury. Other studies suggest that GLP-1 RAs may have beneficial effects on kidney outcomes, although this finding has largely been driven by improvements in albuminuria in most trials [20]. A recent European consensus supported the preferred use of GLP-1 RAs and SGLT2 inhibitors (SGLT2i) in the treatment of patients with type 2 diabetes mellitus (T2DM) and CKD. Sodium-dependent glucose co-transporter proteins 1 and 2 (SGLT1/2) regulate renal glucose reabsorption in the proximal renal tubule of the kidney [21]. Although no SGLT2i is FDA approved specifically for weight loss, modest weight loss (about 1–3 kg) has been observed with the use of these drugs [7].

These promising treatments are capable to prevent cardiovascular events and kidney failure on diabetic patients with already high cardiovascular and renal risk. In particular, SGLT2i showed outstanding effects to slow the decline of eGFR and reduce the progression to end-stage renal disease in patients with diabetes that were already taking RAS inhibitors. The renoprotective effect of SGLT2i is of great interest in clinical practice, in diabetic patients who combine a high cardiovascular risk and kidney disease: SGLT2i reduced the risk of dialysis, transplantation or death due to kidney disease and remarkably, renoprotection was achieved across different levels of kidney function, even for the subgroup with baseline eGFR between 30 and 45 mL/min [21, 22].

A systematic review and meta-analysis of RCTs of SGLT2i that reported effects on kidney outcomes analyzed empagliflozin (EMPA-REG OUTCOME), canagliflozin (CANVAS Program and CREDENCE), and dapagliflozin (DECLARE–TIMI 58) trials. SGLT2i reduced the risk of dialysis, transplantation, or death due to kidney disease (RR 0.67, 95% CI: 0.52–0.86, p = 0.0019). End-stage kidney disease was also reduced (0.65, 0.53–0.81, p < 0.0001). Renoprotection was present irrespective of baseline albuminuria and use of RAS blockade [22].

Heymsfield and collaborators examined the effects of ertugliflozin during 26 weeks in patients with overweight and obesity with T2DM. Greater reductions from baseline in HbA1, body weight, and SBP compared with placebo were noted. More patients receiving ertugliflozin achieved the metabolic goal of weight loss ≥5%, compared with placebo. For ertugliflozin 5 mg and 15 mg, mean changes in absolute body weight were −1.4 kg and −1.2 kg for BMI 25 to <30, −1.8 kg and −1.9 kg for BMI 30 to <35, and −2.5 kg and −2.9 kg for BMI ≥35. Percent body weight changes were similar across BMI subgroups [23].

As for nondiabetic population, the DAPA-CKD trial revealed that for patients with CKD, regardless of the presence or absence of diabetes, the risk of a composite of a sustained decline in the eGFR of at least 50%, end-stage kidney disease, or death from renal or cardiovascular causes was significantly lower with dapagliflozin than with placebo after a 2-year follow-up. Patients in the dapagliflozin group had a mean BMI of 29.4 ± 6.0 [24], demonstrating that SGLTi2 may play a role in preventing or hampering kidney disease progression in nondiabetic patients with obesity.

A careful patient selection by a risk assessment algorithm will mitigate adverse effects and facilitate the acceptance of SGLT2i and GLP-1 RA for heart and kidney protection. When a patient has concomitant heart failure and CKD, SGLT2i is preferred. However, for patients with high metabolic risks or when eGFR is lower than 30 mL/min per 1.73 m2 GLP-1 RA is a better option [25].

Others

Phentermine-topiramate has shown to be very effective for achieving weight loss, but RCTs with short follow-up and trial exclusion criteria including creatinine clearance <60 mL/min preclude the recommendation of this agent in obese patients with CKD [7]. As for Bupropion-Naltrexone, given its effect on increasing blood pressure and uncertain effects on kidney function, it is not recommended in CKD [7]. Trials on patients with advanced CKD treated with orlistat showed significant weight loss and no serious adverse events, although the evidence is still scarce, and orlistat should be used with caution [18].

Bariatric Surgery

Short- and Long-Term CKD Reducing Effects

Bariatric surgery is much more effective in weight loss than low-calorie diets and is an accepted treatment option for severe obesity. This therapeutic approach has beneficial effects on long-term obesity-related comorbidities, including renal disease (Table 1). A recent study proposes that the impact of bariatric surgery on type 2 diabetic patients may depend on age and found that adolescents showed faster resolution of elevated urine albumin-to-creatinine (uACR) ratio following gastric bypass compared with adults [41].

Table 1.

Clinical characteristics and outcomes of patients with CKD that underwent bariatric surgery reported in the literature

Clinical characteristics and outcomes of patients with CKD that underwent bariatric surgery reported in the literature
Clinical characteristics and outcomes of patients with CKD that underwent bariatric surgery reported in the literature

Bariatric surgery is a rather safe surgical procedure, but the rate of peri-surgical complications is usually higher in patients with the double condition of morbid obesity and renal disease. Patients with serum creatinine higher than 2 mg/dL before surgery have a higher risk of re-intervention, readmission, and severe kidney injury. Also, malabsorptive bariatric procedures must be kept in mind as they are also associated with risk of oxalate nephropathy, which may have serious consequences for kidney function. Nevertheless, the absolute risk is still low and mortality risk does not increase [42]. In a prospective cohort study, bariatric surgery resulted in lower CKD risk after a 7-year follow-up period. Reduction in risk was most pronounced in persons with high baseline risk; nevertheless, improvements were also observed in patients with moderate risk at enrollment. This finding has been supported by several studies, with Fischer et al. [43] recently reporting that bariatric surgery slowed declines in eGFR up to 3 years after surgery, although changes in eGFR tracked poorly with changes in BMI. Some authors emphasize the consideration of CKD risk in evaluation for bariatric surgery and propose bariatric surgery as a treatment for high-risk obese patients with CKD [37].

The benefits in terms of weight loss and slowing progression of CKD can be present as early as 1 year after surgery (Fig. 1). A meta-analysis from Huang et al. [44] including 49 articles involving 8,515 patients showed that bariatric surgery significantly reduced serum creatinine levels, uACR, and albuminuria. There was significant increase of GFR in the CKD subgroup, yet a noticeable decrease in the hyperfiltration subgroup. The most significant improvement in GFR was seen 6–12 months after surgery, while uACR dropped most dramatically at 12–24 months [44]. In another systematic review and meta-analysis of patients with at least stage 3 CKD and obesity undergoing bariatric surgery, improved eGFR (mean difference +11.64 mL/min/1.73m2) and reduced serum creatinine (mean difference −0.24 mg/dL) were observed after surgery. There was no significant difference in the relative risk of having CKD stage 3 after bariatric surgery, but there was reduced likelihood of having uACR >30 mg/g or above, with a relative risk of 3.03. This review included studies where bariatric surgery was performed in patients on maintenance hemodialysis [45].

Fig. 1.

Beneficial effects of bariatric surgery on CKD. Created with BioRender.com.

Fig. 1.

Beneficial effects of bariatric surgery on CKD. Created with BioRender.com.

Close modal

As for long-term kidney outcomes after bariatric surgery, the evidence is not entirely clear. In the SOS study, independently of procedure type, after a median 10-year follow-up both patients in the control group and in the bariatric surgery group had developed albuminuria. Nevertheless, the analysis of cumulative incidence rates of CKD stages 4 and 5 (that is, eGFR ≤30 mL/min/1.73 m2) in the SOS study showed a hazard ratio of 0.53 (0.32–0.89) for surgery recipients. This protective effect was markedly accentuated in those patients with a baseline uACR >34 mg/mmol (HR 0.14; 95% CI: 0.04–0.44). A single-center retrospective study in patients treated with bariatric surgery who had baseline CKD-related albuminuria graded as moderate or severe, found that this group had the most marked treatment benefit at 12-month follow-up and that their relative risk of progression to kidney failure was reduced by 70% at 2 years and 60% at 5 years [5].

Effects on Inflammatory, Adipokine Markers, and Lipidomics

On this matter, a recent study by Morales et al. [40] demonstrated the beneficial effects of bariatric surgery to prevent kidney damage in obese subjects with CKD by improving hyperfiltration. This was the first study showing benefits in GFR measured by plasma clearance of iohexol. The important decrease in proteinuria, improvement of kidney function and the excellent control of metabolic parameters was associated with a reduction in both adipose tissue-derived molecules and inflammatory parameters [40]. This study highlighted the emerging role of adipose tissue-derived molecules, such as adiponectin, a fat tissue secreted protein that improves insulin sensitivity in cells, which is reduced in obese patients and may become a target for future therapies. The combination of increased fetuin A and decreased adiponectin stimulates pro-inflammatory and profibrotic mechanisms in hepatocytes and podocytes, promoting kidney and liver injury, thus the importance of adiponectin reduction after bariatric surgery. Comprehensive lipidome analysis may be an important tool to identify potential markers of risk of CKD during obesity. Lanzon et al. [46] recently showed that patients with severe obesity and CKD displayed significant differences in lipid signature, changes in specific amino acids and downregulation of levels of triglycerides and diglycerides when compared to obese subjects without CKD. These changes in lipid signature also play a role in the development of nonalcoholic fatty liver, a highly prevalent condition in diabetic and obese patients which has recently been proven as a key factor in the progression of diabetic kidney disease [47].

The use of albuminuria and/or decreased GFR is late biomarkers in the combination of obesity and kidney damage. One of the challenges of the coming decades is to have new early biomarkers that allow early diagnosis and intervention so that patients do not develop kidney disease and reach the point of no return. On the other hand, efforts should be directed toward therapeutic strategies aimed at slowing the progression of kidney disease. The use of multitarget therapies with appropriate dietary education and the combination of SGLT2i or GLP-1 agonists with RAAS inhibitors and bariatric surgery could allow a comprehensive improvement of inflammatory parameters, adipocyte cytokines and finally achieve the desired nephroprotection.

An ethics statement is not applicable because this study is based exclusively on published literature.

The authors have no conflicts of interest to declare.

E.M. holds a research grant (2015/0117) “Efectos de la pérdida de peso sobre la función renal en pacientes obesos con enfermedad renal” from Fundación SENEFRO.

Lucia Cordero Garcia-Galán, Lucia Aubert Girbal, and Manuel Praga have contributed substantially to the conception and design of the manuscript. Enrique Morales, Justo Sandino, and Julio Pascual have contributed to the drafting of the paper, the critical review of the paper for its important intellectual content and their final approval of the version to be published.

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