Background Cardiac valve calcification (CVC) was an important risk factor for cardiovascular complication. But the prevalence, clinical features and risk factors for CVC in ESRD patients were not fully clear at present. In this study, we explored the possible risk factors and clinical characteristics of CVC happened in Chinese ESRD patients. Methods We conducted a retrospective case-control study on 433 cases of ESRD patients who received maintenance dialysis (MHD) for at least 3 months in the First Affiliated Hospital of Chongqing Medical University from October 2014 to December 2015. 93 patients were confirmed to happen cardiac valve calcification (CVC) by echocardiography, and 200 patients without CVC in the same period as control, matched with age and gender. The demographic data, clinical characteristics, and laboratory parameters of the two groups were analyzed. Results Of 433 cases of ESRD patients, the average annual incidence of CVC was 30.3%. The most common calcification was in aortic valve, followed by mitral valve. Dialysis age (P = 0.006, OR = 2.25), serum calcium (P = 0.046, OR = 2.04), diabetes (P = 0.037, OR = 1.81), and pulse pressure ( P < 0.001, OR = 3.22) were the risk factors of CVC, but serum albumin ( P = 0.047, OR = 0.54) was a protective factor for CVC. The ESRD patients with CVC were also more likely to suffer from arrhythmia, heart failure and coronary heart disease (CHD), and the all-cause mortality also increased significantly. Conclusions High prevalence of CVC happened in Chinese ESRD patients, which was a risk signal for severe atherosclerosis, more morbidity and mortality of cardiovascular events in ESRD patients. Dialysis age, serum calcium, diabetes, and pulse pressure were the independent risk factors of CVC in ESRD patients, while serum albumin was a protective factor.

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Background Lipid metabolism disorders lead to lipotoxicity. The kidney is one of the most vulnerable organs in hyperlipidemia. The hyperlipidemia-induced early stage of renal injury mainly manifests as podocyte damage. CD36 mediates fatty acid uptake and the subsequent accumulation of toxic lipid metabolites, resulting in podocyte lipotoxicity. Methods Male Sprague-Dawley (SD) rats (20 rats) were divided into 2 groups: the normal control group (NC) and the high-fat diet group (HFD). Kidney tissue samples were collected for electron microscopy and Western blot analysis. Podocytes were cultured and treated with palmitic acid (PA) and sulfo-N-succinimidyl oleate (SSO). CD36 protein expression was measured by immunofluorescence and Western blot analysis. BODIPY (Boron-dipyrromethene) staining and Oil Red O staining was used to analyze fatty acid accumulation. Foot process damage was assessed by F-actin staining and electron microscopy. Results Podocyte foot process effacement and marked proteinuria occurred in the HFD group but not the NC group. CD36 protein expression was upregulated in the HFD group and in PA-treated podocytes (P < 0.05). PA-treated podocytes showed increased fatty acid accumulation, reactive oxygen species (ROS) production, and actin cytoskeleton rearrangement. However, pretreatment with the CD36 inhibitor SSO decreased lipid accumulation and ROS production and alleviated actin cytoskeleton rearrangement and foot process effacement in podocytes. Furthermore, the antioxidant N-acetylcysteine suppressed PA-induced podocyte foot process effacement and ROS generation. Conclusions CD36 participated in fatty acid–induced foot process effacement in podocytes via oxidative stress, and CD36 inhibitors may be helpful for early treatment of kidney injury.