Review Article

Obesity and Chronic Kidney Disease: The Dual Epidemic in Cardiovascular Health

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Abstract

More than half of adults are overweight/obese and one in 10 has chronic kidney disease (CKD). These patients are at high risk of cardiovascular morbidity and mortality. This review discusses the pathophysiology, epidemiology, therapeutic principles and challenges of obesity management in adults with non-dialysis-dependent CKD. Inflammation, metabolic dysfunction and neurohormonal changes are central processes in the development of obesity-associated kidney disease. Obesity with metabolic syndrome is a risk factor for de novo CKD, progression to end-stage kidney disease and cardiovascular death. Treatment options to address obesity and related sequelae include lifestyle interventions, such as dietary modification and exercise therapy, drug treatment, such as glucagon-like peptide-1 receptor agonists and sodium-glucose cotransporter inhibitors, and metabolic surgery, such as vertical sleeve gastrectomy, Roux-en-Y gastric bypass or gastric banding. Challenges of management include fragmented care, limited evidence and the obesogenic environment. Cardiologists and nephrologists should work collaboratively to proactively screen for and manage cardiorenal risk in obese adults with CKD to mitigate avoidable harm.

Keywords

Obesity, chronic kidney disease, cardiovascular outcomes,

Received:

Accepted:

Published online:

DOI: https://doi.org/10.15420/ecr.2025.33

Disclosure: SB has received consulting fees from AstraZeneca, GSK and Bayer. CHG has no conflicts of interest to declare.

Funding: CHG is funded by a scholarship at the University of Dundee as part of the Multimorbidity PhD Programme for Health Professionals supported by the Wellcome Trust.

Correspondence: Samira Bell, Division of Population Health and Genomics, School of Medicine, University of Dundee, Nethergate, Dundee DD1 4HN, Scotland. E: s.t.bell@dundee.ac.uk

Copyright:

© The Author(s). This work is open access and is licensed under CC-BY 4.0. Users may copy, redistribute and make derivative works, provided the original work is cited correctly.

Nearly half the global adult population is overweight or obese.1 Obesity is associated with excess morbidity and mortality from lifestyle and non-communicable diseases, including but not limited to diabetes, hypertension and ischaemic heart disease.2–4 Its prevalence is rising driven partly by the obesogenic environment common to high- and low-income countries in the context of urbanisation and the social determinants of health.5

Chronic kidney disease (CKD) affects one in 10 adults worldwide and is predicted to be the fifth leading cause of death globally by 2040.6,7 CKD is characterised by a sustained reduction in glomerular filtration and/or structural kidney damage, including albuminuria, for more than 3 months.8 Patients with CKD are at an increased risk of progression to end-stage kidney disease (ESKD), and six times as many patients will die from cardiovascular disease before requiring kidney replacement therapy.9 Consequently, addressing key cardiovascular risk factors, including obesity, is an essential principle of CKD management.

Obesity and CKD are key drivers of the complex cardio-kidney-metabolic syndrome and have shared risk factors, pathophysiology and targets for therapeutic intervention. A comprehensive understanding of the management of obesity in patients with CKD is essential to improve cardiovascular outcomes.

This review will discuss the pathophysiology, epidemiology, therapeutic principles and challenges of obesity management in adults with CKD (Figure 1). We will focus on CKD without kidney failure (characterised by dialysis or transplantation) with an emphasis on improving cardiovascular outcomes, which are directly relevant to both cardiologists and nephrologists.

Figure 1: Obesity and Chronic Kidney Disease: Pathophysiology, Epidemiology, Management, Challenges and Future Directions

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Pathophysiology of Obesity-related Chronic Kidney Disease

Definitions and Concepts

Obesity is defined as an abnormal and/or excessive accumulation of body fat, which creates a material risk to health.10 It is usually, although not exclusively, accompanied by other components of metabolic syndrome (MetS) including hypertension, insulin resistance and dyslipidaemia.11 In clinical practice and research, obesity is typically defined as a BMI of ≥30 kg/m2, while overweight is categorised as ≥25 kg/m2.10 Defining obesity by BMI fails to account for variation in body composition, age, sex, ethnicity, distribution or type of adipose tissue, all of which influence the likelihood of chronic disease development.12 For example, visceral adipose tissue deposition, also known as central obesity, confers far greater cardiometabolic risk than subcutaneous fat.13

The pathophysiological processes underlying the relationship between obesity, CKD and the cardiovascular system that lead to multi-organ dysfunction are often conceptualised as the cardio-kidney-metabolic syndrome. This represents a complex continuum of direct and indirect effects of adipose tissue on inflammatory, metabolic and neurohormonal pathways leading to adverse renal and cardiovascular outcomes.14 The effects of the syndrome are multifaceted, bidirectional, multiplicative and incompletely understood.

Inflammation

Obesity is a low-grade pro-inflammatory state and inflammation is itself a well-established risk factor for atherosclerosis and incident cardiovascular disease.15–17 The histological changes seen in the kidneys of obese adults reflect some of those seen in diabetic kidney disease with glomerulomegaly, mesangial expansion and podocytopathy.18,19 These appearances result from an infiltration of pro-inflammatory cytokine-laden macrophages into adipose and renal tissue.18,20 Direct lipotoxicity induced by lipid deposits promotes glomerular injury through upregulation of sterol-regulatory element-binding proteins (SREBP-1 and 2), which lead to cytokine secretion and podocyte damage.18,19

Adipose tissue confers an active endocrine function, stimulating the release of pro- and anti-inflammatory adipokines, such as leptin, adiponectin and tumour necrosis factor α, the balance of which is disrupted in obesity.21 The adiponectin/adenosine monophosphate-activated kinase (AMPK) pathway, for example, is a critical process regulating inflammation and fibrosis in obesity-related kidney disease. AMPK is a stress-activated kinase that is secreted in response to adenosine triphosphate depletion to prevent cell death during periods of low-calorie intake.22,23 Synthesis of AMPK is reduced in obesity with a corresponding increase in renal inflammation, endothelial dysfunction, albuminuria, matrix accumulation and oxidative stress.18,24 Exercise and reduced calorie intake have been shown to increase AMPK and reduce diabetic kidney disease independent of weight loss and lowered glucose levels.25,26 Stimulation of AMPK may therefore be a useful therapeutic target for reducing inflammation and fibrosis in obesity-related nephropathy to improve both renal and cardiovascular outcomes.23

Metabolic, Neurohormonal and Haemodynamic Changes

Progressive metabolic dysfunction in obesity is thought to contribute to kidney damage through ectopic lipid accumulation (i.e. deposition of lipids in non-adipose tissue), insulin resistance, dyslipidaemia and hyperglycaemia.14,27,28 These changes combine synergistically with various neurohormonal and haemodynamic effects to contribute to progressive renal dysfunction. Obesity is a major risk factor for essential (primary) hypertension and is estimated to account for more than two-thirds of cases.3,29 Deposition of visceral, peri-nephric and renal sinus fat leads to renal tubular compression with resultant stimulation of the renin–angiotensin–aldosterone system (RAAS) and sympathetic nervous system. A relative deficiency of atrial and brain natriuretic peptides may also contribute to these combined effects and lead to increased sodium reabsorption by the renal tubules, expansion of extracellular fluid volume and systemic hypertension.29,30 The corresponding reduction in renal distal tubular sodium delivery results in tubuloglomerular feedback-mediated afferent arteriole dilation with glomerular hyperfiltration, which equates to an increase in glomerular filtration per nephron or whole kidney.29,31 Over time, this initially compensatory mechanism becomes maladaptive, with impaired renal autoregulation, increased glomerular capillary pressure, nephron loss, renal injury and a decline in glomerular filtration rate.18,19,29

Understanding these mechanisms creates an opportunity for early and targeted interventions to mitigate the development of renal dysfunction and cardiovascular risk in adults with obesity.

Epidemiology and Clinical Associations

Obesity and Incident Chronic Kidney Disease

Obesity, by various measures, is an independent risk factor for the development of de novo CKD in general population cohorts.32–39 A systematic review and meta-analysis of individual participant data (n=5,459,014 in 39 studies) reported a graded increase in the association between BMI and adverse kidney events – 40% estimated GFR (eGFR) decline, eGFR <10 ml/min/1.73 m2 or initiation of kidney replacement therapy, such as dialysis or transplant, for ESKD – following adjustment for age, sex, ethnicity, smoking and comorbidities (BMI 30: HR 1.03; 95% CI [0.95–1.11]; BMI 35: HR 1.28; 95% CI [1.14–1.44]; BMI 40: HR 1.46; 95% CI [1.28–1.67] versus reference BMI 25). Other measures of obesity, such as waist-to-height ratio and waist circumference, showed similar associations, suggesting that BMI is a useful measure for prognostication in clinical practice despite its limitations.32 The findings were supported by another systematic review of general population cohorts (n=630,677 in 39 studies) which reported that obesity increased the relative risk of de novo CKD stage III–V and albuminuria. However, being overweight (BMI 25–30) did not confer additional risk compared to individuals with a healthy BMI.33 The findings of both systematic reviews suggest that BMI is only implicated at higher ranges in the absence of additional metabolic risk factors.32,33

The effect of raised BMI on the development of CKD appears to be independent of genetic predisposition and persists when assessing for the onset of advanced CKD (eGFR<30 ml/min) among people with normal baseline eGFR.34,35 In the largest study to assess BMI and adverse renal outcomes in primary care (n=1,405,016), Herrington et al. demonstrated a graded relationship between BMI and incident CKD stage IV or V (BMI 25–30: HR 1.34; 95% CI [1.30–1.38]; BMI 30–35: HR 1.94; 95% CI [1.87–2.01]; BMI ≥35: HR 3.10; 95% CI [2.95–3.25]).36 Other studies have reached similar conclusions even after controlling for the presence of diabetes and hypertension.37–39 However, such epidemiological studies frequently assess for the presence or absence of such pertinent comorbidities only at baseline, therefore introducing the risk for exposure misclassification over time and missing the potential mediating effect of these conditions within the causal pathway from obesity to CKD.37,38

Obesity-related Glomerulopathy

Obesity-related glomerulopathy (ORG) is a distinct entity within the spectrum of obesity-related kidney diseases. The incidence of ORG is unknown, due to substantial variation in the availability and application of kidney biopsy around the world.40 Obesity itself makes obtaining an adequate kidney biopsy sample more technically challenging, which may influence clinician decision-making.41 Pathologically, the disease is usually characterised by glomerular hypertrophy and perihilar focal segmental glomerulosclerosis (FSGS) with modest foot process effacement, which is generally less pronounced than in primary FSGS.42 Clinically, ORG typically presents with proteinuria in the sub-nephrotic range with or without renal dysfunction. Nephrotic syndrome is rare, however, and up to one-third of patients with ORG may progress to ESKD.40,43 There is no role for immunosuppression in the management of obesity-related FSGS and there is a pressing need for long-term studies of effective interventions.40,44

Obesity and CKD Progression

Obesity has also been shown to increase the likelihood of disease progression including to ESKD among individuals with established CKD.32 A meta-analysis of 18 CKD cohorts (n=91,607) found that obesity (BMI >35) was associated with a composite of eGFR decline ≥40%, receipt of kidney replacement therapy or eGFR <10 ml/min/1.73 m2 (HR 1.17; 95% CI [1.04– 1.31], reference BMI 25). The risk was more pronounced (HR 1.75; 95% CI [1.30–2.37]) when the first 3 years of follow-up data were excluded, suggesting that raised BMI confers greater prognostic importance in determining long-term rather than short-term kidney function. Interestingly, in the subgroup of cohorts at high baseline CV risk (n=84,417 in 6 studies), BMI was not significantly associated with eGFR decline.32 This provides further evidence that raised BMI in isolation may not confer additional harm to patients who are already at high risk of incident vascular disease. Indeed, obesity without other components of MetS has been reported to be associated with a lower likelihood of ESKD compared to patients with a healthy BMI.45 This highlights the essential role of other components of cardio-kidney-metabolic syndrome on the causal pathway between obesity and adverse renal outcomes in patients with CKD and the difficulty in isolating the individual prognostic contribution of obesity.

Obesity and Cardiovascular Morbidity and Mortality

Obesity in the general population is an established risk factor for death and cardiovascular morbidity and mortality.46 However, whether this relationship extends to patients with CKD and obesity but without MetS remains contested. In their meta-analysis, Chang et al. concluded that higher BMI (35 versus 25) was associated with an increased risk of death (HR 1.17; 95% CI [1.01–1.37]).32 However, there was no association following adjustment for potential mediators.32 On the contrary, other systematic reviews have suggested that obesity may confer an apparent survival advantage in patients with advanced CKD.47,48

In their meta-analysis of two studies (n=2,101 patients) published in 2017, Ladhani et al. found that a 1 kg/m2 increase in BMI had no impact on cardiovascular mortality in patients with CKD III–V. However, there was an apparent reduction in all-cause mortality with increasing BMI (n=10,443 patients in five studies; HR 0.99; 95% CI [0.97–1.00] per 1 kg/m2 increase in BMI).48 These findings were supported by a recent study by Kang et al., which found that among CKD patients without MetS (defined as three or more metabolic risk factors), obesity was not associated with an increased risk of cardiovascular events or mortality. Among CKD patients without MetS, obesity conferred a survival advantage (mortality for obese versus non-obese HR 0.82; 95% CI [0.75–0.90]).49

Many studies have demonstrated this apparent ‘obesity paradox’ where higher BMI and/or weight gain appears to confer a survival advantage compared to low/normal BMI and/or weight loss in advanced CKD.47,50,51 This paradox has been described in other chronic disease states, such as heart failure.52 It has been suggested that any apparent survival advantage associated with weight gain determined by BMI may relate to the protective effect of muscle tissue rather than adipose tissue or due to the short-term protective effects among people at risk of malnutrition, as in advanced CKD.32,53 Chang et al. cautiously suggested their results supported the use of waist circumference over BMI in estimating mortality risk in CKD.32 However, differentiating fat versus lean body weight gain due to muscle is not well established in routine clinical practice for nephrologists or cardiologists, in part due to practical difficulties.50 The concept of healthy versus unhealthy weight loss has been explored in a recent analysis of the participants of the CRIC study, where the authors reported that rapid and/or substantial weight loss (>10% BMI decline) was associated with the highest mortality risk, while modest weight loss (<10% BMI decline) carried the lowest risk of death among patients with CKD and obesity.54

Overall, these findings support that obesity in patients with CKD should be considered as part of an overall assessment of cardiovascular risk rather than a binary standalone measure determined by unidimensional measures, such as BMI categorisation at a single point in time.

Management of Obesity in Patients with Chronic Kidney Disease

There are important implications for nephrologists, cardiologists, and general and primary care physicians when treating people with obesity and CKD. Management approaches to address obesity and related sequelae can include lifestyle interventions, pharmacotherapy and bariatric surgery, with the dual aim of weight reduction and cardiorenal protection.

Lifestyle Interventions

There is limited evidence to support the impact of dietary and/or exercise interventions on renal or cardiovascular outcomes for obese patients with CKD.55–57 A Cochrane systematic review evaluating the efficacy of weight loss interventions in obese adults with CKD published in 2021 (n=988 in 19 studies) found that no trials measured cardiovascular events or death as outcomes of interest. Consequently, it is unclear whether such interventions can lower the risk of incident cardiovascular disease or mortality for obese patients with CKD due to an absence of evidence. Furthermore, the authors reported that neither dietary nor exercise interventions specifically demonstrated a consistent benefit in preservation of GFR or reduction of albuminuria when compared to any weight loss intervention. The level of evidence was judged to be very low to low quality and the studies were deemed insufficiently robust to inform clinical practice.55 Other studies have highlighted the potential benefits of a low protein diet in improving uraemic symptoms in advanced CKD, while more recent studies have shown the beneficial effects of exercise therapy on blood pressure (BP) control and BMI in obese adults with non-dialysis CKD. 58–60 A previous systematic review included observational evidence and synthesised 11 studies (n=604) of various dietary interventions, with most reporting no change in eGFR but a modest reduction in proteinuria. Most of the studies (n=10) followed patients for 1 year or less, suggesting the need to assess long-term outcomes.56 Lifestyle interventions have been shown to improve BP, albuminuria, body weight and quality of life in patients with CKD without obesity; however, dietary interventions have an uncertain impact on progression to ESKD, cardiovascular events and mortality. 61,62

Pharmacological Therapy

Glucagon-like peptide-1 receptor agonists (GLP-1-RAs) have transformed the pharmacological treatment of obesity in adults with and without diabetes.63–65 GLP-1 is a neuroendocrine hormone endogenously secreted following food ingestion which alters insulin and glucagon release, delays gastric emptying and leads to centrally mediated appetite suppression.66,67 GLP-1-RAs have been shown to improve glycaemic control, weight and major adverse cardiovascular and kidney events in trials of patients with type 2 diabetes with and without obesity.68,69 Similar benefits in cardiovascular risk reduction have been demonstrated among adults with obesity but without type 2 diabetes. However, despite the presence of many patients with concurrent type 2 diabetes, CKD and obesity among these studies, there are no trials assessing the cardiorenal benefits of GLP-1-RAs exclusively in patients with obesity and stage III–V CKD.70

The FLOW trial demonstrated renal, cardiovascular and survival benefits from weekly 1 mg subcutaneous semaglutide among adults with proteinuric CKD (eGFR 25–75 ml/min/m2) and type 2 diabetes. The effect size for the primary composite outcome (kidney failure, 50% GFR decline or death from kidney-related or cardiovascular cause) was larger in the subgroup of patients with BMI>30 (HR 0.73; 95% CI [0.61–0.89]; n=2,060) than in those with BMI<30 (HR 0.82; 95% CI [0.65–1.03]). It is unclear from this trial if these benefits would be observed in addition to sodium-glucose cotransporter 2 inhibitors (SGLT2i) as less than one in six patients were established on one at trial enrolment.65 The SELECT trial and a subsequent analysis demonstrated cardiovascular and renal benefits of semaglutide 2.4 mg/week subcutaneously among overweight/obese adults (defined as BMI ≥27) with pre-existing vascular disease but without diabetes.64,71 One-fifth of patients in the SELECT trial had baseline CKD (eGFR <60ml/min/1.732), among whom there was greater cardiovascular risk reduction (HR 0.69; CI 95% [0.52–0.90]) than among non-CKD participants (HR 0.82; CI 95% [0.72–0.92]).64 However, the observed 22% reduction in the main composite kidney endpoint (death from kidney disease, initiation of chronic kidney replacement therapy, onset of persistent eGFR<15 ml/min/1.73 m2, persistent ≥50% reduction in eGFR or onset of persistent macroalbuminuria) was not demonstrated in the CKD subgroup (n=148).71 The results suggest that patients with CKD and obesity with or without diabetes benefit from GLP-1-RAs in terms of cardiovascular risk reduction and therefore it is likely that these drugs will become a mainstay of CKD therapy in the future. Currently, access to treatment remains limited by cost and location, potentially exacerbating health inequalities through inequitable access to treatment.63

SGLT2i have become a central tenet of CKD management, particularly in patients with concurrent diabetes, in addition to RAAS inhibitors and non-steroidal mineralocorticoid receptor antagonists.72–74 SGLT2i have been shown to lead to mild-to-moderate weight reduction (1–3 kg body weight); however, they are not primarily indicated for weight loss in obese patients.75 These treatments should be considered in addition to standard components of cardiovascular risk assessment and reduction in CKD patients including RAAS inhibition, blood pressure control, lipid-lowering therapy and smoking cessation.8

Bariatric Surgery

Options for bariatric (metabolic) surgery include vertical sleeve gastrectomy, Roux-en-Y gastric bypass or adjustable gastric banding.76 Such procedures lead to substantial weight loss (about 25% total body weight) and improved long-term survival for patients with morbid obesity in the general population.77 Surgical intervention can also address related cardiovascular risk factors including hypertension and dyslipidaemia and induce remission of type 2 diabetes. 78,79

Bariatric surgery for obese patients with renal dysfunction improves hyperfiltration, albuminuria and proteinuria compared to standard care.80–83 A meta-analysis of six studies involving patients with CKD III (eGFR<60 ml/min/1.73 m2) at baseline reported a post-operative mean increase in eGFR of 11.64 ml/min/1.73 m2 (95% CI [5.84–17.45]; I2=66%) and a threefold improvement in albuminuria in three studies.83 Similar results were found in another meta-analysis with a post-operative reduction in hyperfiltration and improvement in eGFR among patients with early-stage CKD. No randomised controlled trials were included in these syntheses and most studies were limited to short-term (<1 year) follow-up.80,83 Other work suggests that long-term renal outcomes are favourable. A Swedish study of incident ESKD (median follow-up 18 years; n=4,047 patients) among obese patients treated with banding, gastroplasty or gastric bypass showed a significant reduction in ESKD compared to controls (HR 0.27; 95% CI [0.12–0.61]). However, the event rate was small (n=13 in surgery group versus n=26 in controls) and patients had normal secretory renal function at baseline.82 Chang et al. assessed the risk of doubling serum creatinine or ESKD among 985 severely obese patients undergoing bariatric surgery compared to matched controls. Surgery was associated with a 51% reduction in risk following adjustment for incident hypertension and diabetes (HR 0.49; 95% CI [0.30–0.82]) over 9 years of follow-up.84 Given the prevalence of obesity in the CKD population, bariatric surgery could serve as a useful addition to achieve normotension and minimise proteinuria in patients already established on a maximum tolerated dose of RAAS and SGLT2i.76

Bariatric surgery has been reported to markedly reduce mortality over 5 years in obese patients with CKD stage III–V compared to matched controls (HR 0.21; 95% CI [0.14–0.32]).85 Similar reductions in long-term (5-year) mortality largely from cardiovascular causes have been observed in patients with obesity and treated kidney failure but at the expense of an increase in short-term (1-year) mortality.86 Therefore, perioperative risks are not insignificant in the CKD population, hence, surgery should be limited to patients who have failed to achieve the desired weight loss via lifestyle or pharmacological means.63 It remains unclear whether the long-term cardiovascular and survival benefits of surgical intervention outweigh the perioperative risks of bariatric surgery in the non-dialysis CKD population.83 Furthermore, a 2021 Cochrane systematic review found that no studies of surgical versus non-surgical intervention for weight loss evaluated death or cardiovascular events as outcomes of interest in the CKD population.55 These outcomes warrant attention through empirical study.

Challenges and Future Directions

There are substantial challenges in addressing obesity among patients with CKD at both an individual and societal level. Half of patients with CKD are undiagnosed and most who receive a diagnosis are managed entirely in primary care.87,88 Guideline-supported referral criteria, such as those that incorporate the kidney failure risk equation, do not include obesity as a prognostic factor to inform referral to secondary care.89 As such, nephrologists and cardiologists only directly manage a small proportion of these patients who are typically at the greatest risk of harm. Other risk prediction tools, such as PREVENT-CVD, incorporate BMI and kidney function to model long-term cardiovascular risk but do not focus on renal risk.90 Multimorbidity is common in CKD and obesity with patients typically navigating a healthcare system that is complex, fragmented and siloed. This increases the likelihood of a lack of ownership of care, which can lead to treatment inertia.91,92

There is a pressing need for joint models of care, integrating primary and secondary care practitioners and the wider multidisciplinary team, to tailor management to individuals at the greatest risk of adverse cardiorenal outcomes. Cardiologists and nephrologists should work synergistically to engage healthcare colleagues in primary care and address lifestyle, pharmacological and, if necessary, surgical management priorities outlined to tackle obesity in patients with CKD much earlier in the life course to prevent an accrual of metabolic morbidity.93 There is also a need for measures of obesity beyond BMI, which accurately estimate the distribution of adipose tissue and are easy to implement in routine clinical practice. Further research is required to substantiate the superiority of, for example, waist circumference or waist-to-hip ratio over BMI in patients with CKD. Other evidence gaps remain, including understanding the existence of and mechanisms underlying the apparent obesity paradox in CKD. Dedicated trials of obesity treatment, including metabolic surgery for patients with CKD, are required with a focus on long-term cardiorenal and patient-reported outcomes, particularly given the under-representation of CKD patients in cardiovascular trials.94 Comparative outcome trials are required to determine the efficacy and relative safety of GLP-1-RAs compared to bariatric surgery. Improving access to treatment is important, specifically for GLP-1-RAs, given that, currently, demand vastly outstrips supply and cost is prohibitively expensive for most patients. Governments must do more to tackle the upstream factors that are leading to an epidemic of obesity, particularly among children. This would include improving access to affordable, healthy food and implementing policies to address the social determinants of health.

Conclusion

Obesity in the context of associated metabolic dysfunction is a key risk factor for the development and progression of CKD and related cardiovascular morbidity. The cardio-kidney-metabolic syndrome complex highlights the many shared pathophysiological and clinical manifestations that exist among patients with CKD, obesity and cardiovascular disease and offer an opportunity for early and targeted treatment. Cardiologists and nephrologists should work in tandem to proactively screen for and manage cardiorenal risk in obese adults with CKD to mitigate avoidable morbidity and mortality. The cost of obesity to individuals and societies necessitates action from patients, clinicians, governments and key stakeholders.

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