脂联素与肾脏疾病

脂联素是脂肪细胞分泌的一种生物活性分子,是一种蛋白质激素,与代谢综合征、糖尿病、IgA肾病、肾移植、肥胖相关肿瘤等疾病有关,本文对脂联素与肾脏疾病的关系作一综述。     

脂联素在肾脏疾病的研究进展

脂联素是近年来发现的一种由脂肪细胞特异表达和分泌的蛋白质激素,目前对脂联素的研究已涉及到各个学科领域,但在肾脏疾病中的研究较少,多种研究发现,脂联素在慢性肾功能衰竭、肾病综合征、继发性肾病的发生发展中起到了重要的作用。     

脂联素与肾脏疾病

脂联素(Adiponectin—ADPN)是最近发现的一种由脂肪细胞特异性分泌的蛋白质。有关数据显示ADPN与胰岛素抵抗有关，并具有抗炎和抗粥样硬化作用，且ADPN水平随肾功能不全的进展而升高，ADPN在肾脏疾病的发生发展中起着独特作用。     

脂联素与肾脏疾病

脂联素 (Adiponectin -ADPN)是最近发现的一种由脂肪细胞特异性分泌的蛋白质。有关数据显示ADPN与胰岛素抵抗有关 ,并具有抗炎和抗粥样硬化作用 ,且ADPN水平随肾功能不全的进展而升高 ,ADPN在肾脏疾病的发生发展中起着独特作用。     

脂联素在肾脏疾病中的意义

脂联素(adiponectin)是脂肪细胞分泌的一种特异性蛋白质。研究发现脂联素与肥胖、2型糖尿病、胰岛素抵抗、动脉粥样硬化以及糖尿病的血管病变等都有一定的相关性，并证实了脂联素在这些疾病的发生发展中起着重要的作用；脂联素与肾脏病的关系也很密切，肾脏对脂联素的排泄和灭活有着重要作用，血浆脂联素浓度在各种肾脏病病人中均有变化，且与肾功能损害的严重程度密切相关。     

脂联素在肾脏疾病中的意义

脂联素(adiponectin)是脂肪细胞分泌的一种特异性蛋白质。研究发现脂联素与肥胖、2型糖尿病、胰岛素抵抗、动脉粥样硬化以及糖尿病的血管病变等都有一定的相关性,并证实了脂联素在这些疾病的发生发展中起着重要的作用;脂联素与肾脏病的关系也很密切,肾脏对脂联素的排泄和灭活有着重要作用,血浆脂联素浓度在各种肾脏病病人中均有变化,且与肾功能损害的严重程度密切相关。     

脂氧素与肾脏

脂氧素是花生四烯酸的一类脂氧化酶产物，近年来，对脂氧素的合成途径、生物学作用及其机制、对肾赃的作用及在肾小球疾病中的作用、临床应用前景等方面的研究均有许多进展。     

脂氧素与肾脏

脂氧素是花生四烯酸的一类脂氧化酶产物 ,近年来 ,对脂氧素的合成途径、生物学作用及其机制、对肾脏的作用及在肾小球疾病中的作用、临床应用前景等方面的研究均有许多进展     

脂联素与慢性肾脏病

脂联素是脂肪细胞分泌的一种特殊蛋白质,参与多种生理病理过程。随着对脂联素研究的不断深入,发现它与慢性肾脏病的发生、发展、预后等密切相关。我们就脂联素与慢性肾脏病的相关基础及临床研究作一综述。     

脂联素与慢性肾脏病

脂联素是脂肪细胞分泌的一种特殊蛋白质,参与多种生理病理过程.随着对脂联素研究的不断深入,发现它与慢性肾脏病的发生、发展、预后等密切相关.我们就脂联素与慢性肾脏病的相关基础及临床研究作一综述.     

Adiponectin and chronic kidney disease.

Enhanced chronic inflammation and reduced insulin sensitivity are often present in chronic kidney disease (CKD). Cardiovascular disease remains a major cause of morbidity and mortality in end-stage renal patients. Adiponectin (ADP) is a hormone exclusively produced by adipocytes and possesses anti-inflammatory and cardioprotective properties. Despite the high prevalence of insulin resistance and cardiovascular disease, levels of ADP are increased among end-stage renal disease patients on hemo or peritoneal dialysis but also among patients with moderate renal failure or with the nephrotic syndrome. Furthermore, lower ADP levels are associated with poor cardiovascular outcome. In this review, we examine ADP modifications in CKD and discuss the different factors that may have an impact on this adipokine metabolism in renal failure.     

Adiponectin and mortality in patients with chronic kidney disease

Adiponectin is presumed to possess antiatherogenic and cardioprotective properties. Limited data exist on the relationship between adiponectin and mortality in the earlier stages of chronic kidney disease. The Modification of Diet in Renal Disease study was a randomized, controlled trial that was conducted between 1989 and 1993. Adiponectin was measured in frozen samples that were obtained at baseline (N = 820). Survival status and cause of death, up to December 31, 2000, were obtained from the National Death Index. Multivariable Cox models were used to examine the relationship of adiponectin with all-cause and cardiovascular mortality. Mean +/- SD age was 52 +/- 12 yr, and mean +/- SD glomerular filtration rate (GFR) rate was 33 +/- 12 ml/min per 1.73 m2. Eighty-five percent of participants were white, and 60% were male. Mean +/- SD adiponectin was 12.8 +/- 8.0 mug/ml. Triglycerides, insulin resistance, glucose, body mass index, GFR, C-reactive protein, and albumin were inversely related and proteinuria and HDL cholesterol were directly related to adiponectin. During the 10-year follow-up period, 201 (25%) participants died of any cause, and 122 (15%) from cardiovascular disease. In multivariable adjusted Cox models, a 1-mug/ml increase in adiponectin was associated with a 3% (hazard ratio 1.03; 95% confidence interval 1.01 to 1.05; P = 0.02) increased risk for all-cause and 6% (hazard ratio 1.06; 95% confidence interval 1.03 to 1.09; P < 0.001) increased risk for cardiovascular mortality. High, rather than low, adiponectin is associated with increased mortality in this cohort of patients with chronic kidney disease stages 3 to 4. Further studies are necessary to confirm this association and to elucidate the underlying mechanisms.     

Adiponectin and risk of new-onset diabetes mellitus after kidney transplantation

BACKGROUND: New-onset diabetes mellitus after transplantation (NODAT) is a severe complication of kidney transplantation (KTx) with negative effects upon patient and graft survival. Several risk factors for NODAT have been described; however, the search for an early predictive marker is ongoing. It has recently been demonstrated that high concentrations of adiponectin (APN), which is an adipocyte-derived peptide with antiinflammatory and insulin-sensitizing properties, protect against future development of type 2 diabetes in healthy individuals. The purpose of this report was to study pretransplant insulin resistance and analyze pretransplant serum leptin and APN levels as independent risk factors for the development of NODAT. METHODS: A total of 68 KTx patients were studied [mean age, 48 +/- 11 years; 70% males; body mass index (BMI), 25 +/- 3 kg/m]; 31 KTx patients with NODAT and 37 KTx patients without NODAT (non-NODAT) with similar age, sex, BMI, immunosuppression, and posttransplant time were studied. All patients received prednisone and calcineurin inhibitors (75% tacrolimus and 25% cyclosporine A), and 76% of patients received mycophenolate mofetil. Family history of diabetes mellitus was recorded. Pretransplant homeostasis model assessment for insulin resistance (HOMA-IR) index was calculated from fasting plasma glucose and insulin. Pretransplant serum leptin and APN levels were determined by radioimmunoassay. RESULTS: NODAT patients showed higher pretransplant plasma insulin concentrations [NODAT, 13.4 (11-22.7) microIU/mL; non-NODAT, 10.05 (7.45-18.4) microIU/mL; P=0.049], HOMA-IR index [NODAT, 4.18 (2.49-5.75); non-NODAT, 2.63 (1.52-4.68); P=0.043], and lower pretransplant serum APN concentration [NODAT, 8.78 (7.2-11.38) microg/mL; non-NODAT, 11.4 (8.56-15.27) microg/mL, P=0.012]. Inverse correlations between APN and BMI (r=-0.33; P=0.014) and APN and HOMA-IR index (r=-0.39; P=0.002) and between APN and NODAT (r=-0.31; P=0.011) were observed. Multiple logistic regression analysis showed the patients with lower pretransplant APN concentrations to be those at greater risk of developing NODAT [Odds Ratio=0.832 (0.71-0.96); P=0.01]. CONCLUSION: Pretransplant serum APN concentration is an independent predictive factor for NODAT development in kidney-transplanted patients.     

Ferroptosis and kidney diseases

International Urology and Nephrology - Ferroptosis is a form of iron-dependent, non-apoptotic regulated cell death, which is characterized by the accumulation of lipid hydroperoxides to lethal...     

Review Article: Adiponectin: Its role in kidney disease

The multifactorial glycoprotein, adiponectin has demonstrable insulin-sensitizing, anti-atherogenic and anti-inflammatory properties. However, despite the prevalence of both insulin-resistance and vascular disease in patients with end-stage kidney disease, levels of adiponectin are high. Adiponectin circulates in different sizes (the high-molecular-weight (HMW) isoform is thought to be the most insulin-sensitizing type) and binds to two receptors, adiponectin receptors (AdipoR) 1 and 2. The adiponectin/receptor system appears to be upregulated in end-stage kidney disease possibly as an appropriate counter-regulatory response to the uraemic milieu. In contrast, adiponectin and its HMW isoform, AdipoR mRNA expression on peripheral blood mononuclear cells decrease after kidney transplantation, likely secondary to immunosuppression and/or an improvement in glomerular filtration rate and the uraemic environment. Adiponectin has also been detected in the urine of patients with proteinuric kidney disease. The presence of AdipoR on an immortal cell line of proximal tubular epithelial cells (HK-2) and an increased amount of intact HMW isoform in the urine of patients with various forms of proteinuria lead us to speculate about the potential role of urinary adiponectin. This review will also discuss the structure and function of adiponectin and its potential relevance to patients with kidney disease and the different factors that may influence the metabolism of this protein in kidney failure.