The Kidney-Heart Connection in Obesity

García-Carrasco, Almudena; Izquierdo‐Lahuerta, Adriana; Medina‐Gómez, Gema

doi:10.1159/000515419

Cited by 9 publications

(5 citation statements)

References 13 publications

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“…Chronic renal insufficiency in obese persons with or without diabetes mellitus is associated with disruptions of heart function (cardiometabolic syndrome) [44]. In populations with end-stage renal disease, additional renal toxins not associated with lipids may further impact cardiac function.…”

Section: Intra-nephric Fatmentioning

confidence: 99%

Lipid Toxicity in the Cardiovascular-Kidney-Metabolic Syndrome (CKMS)

D’Elia,

Weinrauch

2024

Biomedicines

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Recent studies of Cardiovascular–Kidney–Metabolic Syndrome (CKMS) indicate that elevated concentrations of derivatives of phospholipids (ceramide, sphingosine), oxidized LDL, and lipoproteins (a, b) are toxic to kidney and heart function. Energy production for renal proximal tubule resorption of critical fuels and electrolytes is required for homeostasis. Cardiac energy for ventricular contraction/relaxation is preferentially supplied by long chain fatty acids. Metabolism of long chain fatty acids is accomplished within the cardiomyocyte cytoplasm and mitochondria by means of the glycolytic, tricarboxylic acid, and electron transport cycles. Toxic lipids and excessive lipid concentrations may inhibit cardiac function. Cardiac contraction requires calcium movement from the sarcoplasmic reticulum from a high to a low concentration at relatively low energy cost. Cardiac relaxation involves calcium return to the sarcoplasmic reticulum from a lower to a higher concentration and requires more energy consumption. Diastolic cardiac dysfunction occurs when cardiomyocyte energy conversion is inadequate. Diastolic dysfunction from diminished ATP availability occurs in the presence of inadequate blood pressure, glycemia, or lipid control and may lead to heart failure. Similar disruption of renal proximal tubular resorption of fuels/electrolytes has been found to be associated with phospholipid (sphingolipid) accumulation. Elevated concentrations of tissue oxidized low-density lipoprotein cholesterols are associated with loss of filtration efficiency at the level of the renal glomerular podocyte. Macroscopically excessive deposits of epicardial and intra-nephric adipose are associated with vascular pathology, fibrosis, and inhibition of essential functions in both heart and kidney. Chronic triglyceride accumulation is associated with fibrosis of the liver, cardiac and renal structures. Successful liver, kidney, or cardiac allograft of these vital organs does not eliminate the risk of lipid toxicity. Lipid lowering therapy may assist in protecting vital organ function before and after allograft transplantation.

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Section: Intra-nephric Fatmentioning

confidence: 99%

Lipid Toxicity in the Cardiovascular-Kidney-Metabolic Syndrome (CKMS)

D’Elia,

Weinrauch

2024

Biomedicines

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“…Zucker-diabetic fatty rats (159) both organs (178). CKD is strongly associated with CVD, it has been reported that patients with advanced kidney disease are at high risk of CVD mortality and morbidity (179).…”

Section: Main Findingmentioning

confidence: 99%

Perirenal Adipose Tissue Inflammation: Novel Insights Linking Metabolic Dysfunction to Renal Diseases

et al. 2021

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A healthy adipose tissue (AT) is indispensable to human wellbeing. Among other roles, it contributes to energy homeostasis and provides insulation for internal organs. Adipocytes were previously thought to be a passive store of excess calories, however this view evolved to include an endocrine role. Adipose tissue was shown to synthesize and secrete adipokines that are pertinent to glucose and lipid homeostasis, as well as inflammation. Importantly, the obesity-induced adipose tissue expansion stimulates a plethora of signals capable of triggering an inflammatory response. These inflammatory manifestations of obese AT have been linked to insulin resistance, metabolic syndrome, and type 2 diabetes, and proposed to evoke obesity-induced comorbidities including cardiovascular diseases (CVDs). A growing body of evidence suggests that metabolic disorders, characterized by AT inflammation and accumulation around organs may eventually induce organ dysfunction through a direct local mechanism. Interestingly, perirenal adipose tissue (PRAT), surrounding the kidney, influences renal function and metabolism. In this regard, PRAT emerged as an independent risk factor for chronic kidney disease (CKD) and is even correlated with CVD. Here, we review the available evidence on the impact of PRAT alteration in different metabolic states on the renal and cardiovascular function. We present a broad overview of novel insights linking cardiovascular derangements and CKD with a focus on metabolic disorders affecting PRAT. We also argue that the confluence among these pathways may open several perspectives for future pharmacological therapies against CKD and CVD possibly by modulating PRAT immunometabolism.

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“…However, BMI fails to encompass various metabolic markers, such as adipokine and inflammatory markers, which often play pivotal roles in the onset and progression of CVD and CKD [ 15 , 16 ]. Furthermore, BMI, monocytes, and HDL interact complexly, and individuals with high BMI may also exacerbate cardiorenal syndrome due to complications from adipose tissue dysfunction [ 16 – 19 ].…”

Section: Introductionmentioning

confidence: 99%

Independent and joint associations of monocyte to high-density lipoprotein-cholesterol ratio and body mass index with cardiorenal syndrome: insights from NHANES 2003–2020

Lin,

Li,

et al. 2024

Lipids Health Dis

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Background With the development of pathophysiology, cardiorenal syndrome (CRS), a complex and severe disease, has received increasing attention. Monocyte to high-density lipoprotein-cholesterol ratio (MHR) and body mass index (BMI) are independent risk factors for cardiovascular diseases, but their association with CRS remains unexplored. This study aims to explore the independent and joint effects of MHR and BMI on CRS. Methods We included 42,178 NHANES participants. The determination of CRS referred to the simultaneous presence of cardiovascular disease (identified through self-report) and chronic kidney disease (eGFR < 60 mL/min per 1.73 m²). We employed multivariate weighted logistic regression to evaluate the odds ratio (OR) and 95% confidence interval (CI) for the independent and joint associations of MHR and BMI with CRS. We also conducted restricted cubic spines to explore nonlinear associations. Results The prevalence of CRS was 3.45% among all participants. An increase in both MHR and BMI is associated with a higher risk of CRS (MHR: OR = 1.799, 95% CI = 1.520–2.129, P < 0.001, P-trend < 0.001; BMI: OR = 1.037, 95% CI = 1.023–1.051, P < 0.001). Individuals who simultaneously fall into the highest quartile of MHR and have a BMI of 30 or more face the highest risk of CRS compared to those in the lowest MHR quartile with a BMI of less than 25 (OR = 3.45, 95% CI = 2.40–4.98, P < 0.001). However, there is no interactive association between MHR and BMI with CRS. Conclusions Higher MHR and BMI are associated with higher odds of CRS. MHR and BMI can serve as tools for early prevention and intervention of CRS, respectively.

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The Kidney-Heart Connection in Obesity

Cited by 9 publications

References 13 publications

Lipid Toxicity in the Cardiovascular-Kidney-Metabolic Syndrome (CKMS)

Lipid Toxicity in the Cardiovascular-Kidney-Metabolic Syndrome (CKMS)

Perirenal Adipose Tissue Inflammation: Novel Insights Linking Metabolic Dysfunction to Renal Diseases

Independent and joint associations of monocyte to high-density lipoprotein-cholesterol ratio and body mass index with cardiorenal syndrome: insights from NHANES 2003–2020

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