Leptin and Renal Disease

Briley, Libbie P.; Szczech, Lynda A.

doi:10.1111/j.1525-139x.2006.00119.x

Cited by 49 publications

(30 citation statements)

References 78 publications

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“…Leptin is an adipocyte-derived hormone that is structurally similar to IL-2 and is largely considered a cytokine. Increased caloric intake and decreased expenditure result in increased adiposity, which results in increased leptin levels (11,(47)(48)(49). Leptin crosses the blood-brain barrier, and via reducing neuropeptide Y in the hypothalamus suppresses appetite and increases energy expenditure.…”

Section: Role Of Cytokinesmentioning

confidence: 99%

Obesity and Obesity-Initiated Metabolic Syndrome

Wahba

Mak

2007

Clinical Journal of the American Society of Nephrology

453

343

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There is an epidemic of obesity and the metabolic syndrome in the United States and across the world. Both entities are associated with high mortality, mainly as a result of cardiovascular disease. The epidemic of obesity has been paralleled by an increase in the incidence of chronic kidney disease (CKD). Several recent epidemiologic studies have shown that obesity and the metabolic syndrome are independent predictors of CKD. In addition to diabetes and hypertension, several other mechanisms have been postulated to initiate and maintain kidney injury in patients with obesity and the metabolic syndrome. This article reviews the recent epidemiologic data linking obesity and the metabolic syndrome to CKD and summarizes the potential mechanisms of renal injury in this setting, with a focus on the role of inflammation, lipotoxicity, and hemodynamic factors. Potential preventive and therapeutic modalities based on the limited evidence available are discussed.Clin , and the increase occurred for both men and women and for all age groups (2). Since then, the trend for increased prevalence has continued, particularly for adolescents and men (1). Obesity is also on the rise in other industrialized countries (3-5). The metabolic syndrome, previously known as syndrome X and a major consequence of obesity, is also on the rise (6). According to the Third National Health and Nutrition Examination Survey (NHANES III), the prevalence of the metabolic syndrome in the United States is 23% in those who are 20 yr or older and Ͼ40% in those who are 60 yr or older (7). According to the Third Adult Treatment Panel of the National Cholesterol Education Program, the metabolic syndrome is defined as the presence of at least three of the following criteria, with or without diabetes: Central obesity (waist circumference in men Ͼ102 cm and in women Ͼ88 cm), hypertriglyceridemia (Ն150 mg/dl), low HDL cholesterol (men Ͻ40 mg/dl, women Ͻ50 mg/dl), elevated fasting glucose (Ͼ110 mg/dl), and hypertension (Ն130/85 mmHg) (8). A central feature of the metabolic syndrome is insulin resistance, which results in hyperglycemia and hyperinsulinemia, and eventually leads to the development of diabetes (9). Central obesity is the most important predisposing factor for insulin resistance (9). Chronic inflammation is another feature of the metabolic syndrome, which, together with insulin resistance, results in complex metabolic derangements that contribute to the pathogenesis of hypertension, lipoprotein abnormalities, atherosclerosis, coronary artery disease, and other organ dysfunction (10,11). Both obesity and the metabolic syndrome are associated with high mortality, mainly related to cardiovascular disease (12,13). Overweight, obesity, and the metabolic syndrome have recently emerged as strong independent risk factors for chronic kidney disease (CKD) and ESRD. This article reviews the epidemiology of CKD in relationship to obesity and the metabolic syndrome and the possible mechanisms of renal injury that is caused by obesity and obesity-initiated metab...

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Section: Role Of Cytokinesmentioning

confidence: 99%

Obesity and Obesity-Initiated Metabolic Syndrome

Wahba

Mak

2007

Clinical Journal of the American Society of Nephrology

453

343

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“…Patients with CKD have increased circulating levels of both adipokines that may result from an increase in their systemic production and/or decrease in their renal clearance. [24][25][26][27] In KTR, the most common cause of late allograft loss and leading cause of KTR deaths is CVD. 28 There are still unanswered points about how and why KTR keep on suffering from CVD despite the restoration of glomerular dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Adiponectin, leptin, nitric oxide, and C-reactive protein levels in kidney transplant recipients: comparison with the hemodialysis and chronic renal failure

2016

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Background: Cardiovascular disease (CVD) is the leading cause of mortality and morbidity in patients with chronic kidney disease (CKD) including kidney transplant recipients (KTR). Secondary lipid metabolism disorders, endothelial dysfunction, and inflammation enhance the risk of CVD development in these patients. The aim of the present study was to investigate the lipid profile, adiponectin, leptin, nitric oxide (NO), and high sensitivity C-reactive protein (hs-CRP) levels in KTR and to compare these parameters with those of the patients with chronic renal failure (CRF), hemodialysis (HD) patients, and healthy controls. Methods: Serum adiponectin and leptin levels were measured by radioimmunoassay; hs-CRP was determined immunoturbidimetrically. Determination of NO was based on the Griess reaction. Results: Compared with the control group, serum NO and adiponectin levels were significantly higher in the KTR, CRF, and HD groups; hs-CRP levels were significantly higher in the KTR and HD groups; leptin levels were significantly higher in the KTR. In addition, serum NO level was significantly higher in the KTR compared to CRF cases. Adiponectin correlated positively with high density lipoprotein-cholesterol in the control and patient groups. A positive correlation was observed between hs-CRP and NO in the KTR and the patients with CRF. Serum adiponectin levels were inversely correlated with hs-CRP and leptin in the HD group. Conclusion: KTR suffer from inflammation and accompanying changes in levels of adipocytokines and NO which contribute to the increased risk of CVD in these patients.

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“…Elevated serum leptin level in CRF patients could be attributed to the reduced filtering ability of the kidney, causing leptin to accumulate in the serum [17,23]. After renal transplantation the level of serum leptin falls.…”

Section: Discussionmentioning

confidence: 99%

Serum Leptin and Bone Mineral Density in Hemodialysis Patients with or without Liver Diseases

Ghonemy

Salim²,

Atia³

et al. 2011

Arab J. Nephr. Trans

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Introduction: Leptin is a hormone secreted by adipocytes that plays an important role in regulating appetite and energy expenditure. Our aim was to evaluate serum leptin level in hemodialysis (HD) patients with or without chronic liver disease (CLD) and study the relationship between serum leptin level and bone mineral density in these groups of patients.Methods: we recruited 20 healthy volunteers as controls (group I), 20 patients on regular HD with normal liver function (group II), 20 CLD patients with normal kidney function (group III) and 20 patients on regular HD with CLD (group IV). We measured serum calcium, phosphorus, parathyroid hormone (PTH), total alkaline phosphatase (ALP), serum leptin, 24-hours urinary hydroxyproline and bone mineral density (BMD) of the lumber spine and femoral neck by DEXA scan.Results: Serum leptin level was significantly higher (P <0.001) in HD patients and CLD patients compared to controls. Its level was also significantly elevated in HD patients without liver disease (group II) compared to patients with CLD who had no renal failure (group III). Urinary hydroxyproline level was increased in both HD patients and CLD patients. We detected a positive correlation between serum leptin level and urinary hydroxyproline in all patient groups. There was a significant decrease in BMD in HD and CLD patients. BMD was significantly lower in HD patients without CLD compared to HD patients with CLD. There was a significant negative correlation between serum leptin level and BMD in CLD patients without renal disease but not in other groups (r = -0.6, P = 0.01). Conclusion:Serum leptin is elevated in HD patients with or without liver disease and in CLD patients. Serum leptin level is inversely correlated with BMD in CLD patients without renal disease.

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Leptin and Renal Disease

Cited by 49 publications

References 78 publications

Obesity and Obesity-Initiated Metabolic Syndrome

Obesity and Obesity-Initiated Metabolic Syndrome

Adiponectin, leptin, nitric oxide, and C-reactive protein levels in kidney transplant recipients: comparison with the hemodialysis and chronic renal failure

Serum Leptin and Bone Mineral Density in Hemodialysis Patients with or without Liver Diseases

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