[Analysis of clinical state for arteriosclerosis obliterans in lower extremity of diabetic patients on peritoneal dialysis].

OBJECTIVE: To investigate the prevalence of arteriosclerosis obliterans in lower extremity and its influence factors in diabetic patients on peritoneal dialysis. METHOD: In this single center cross-sectional study, 74 with diabetic patients on peritoneal dialysis were recruited. The general information, dialysis program, laboratory examination and dialysis adequacy test results were recorded.Their symptoms and signs of arteriosclerosis obliterans in lower extremities were investigated and ankle brachial index (ABI) was determined. RESULT: In this study,70.3% of the patients had different degrees of symptoms and signs of arteriosclerosis obliterans in lower extremity. With Fortaine classification, 13.5% of the patients were in early lesions phase, 28.8% in local ischemic phase, 51.9% in nutritional disturbance phase, and 5.8% in gangrene phase. The patients were divided into three groups base on Fontaine classification: control group (no symptoms), mild group(early lesions phase and local ischemic phase) and severe group(nutritional disturbance phase and gangrene phase). There was a significant difference between the insulin dose, left foot ABI levels, plasma albumin levels and total Kt/V levels among the three groups (P<0.05). The plasma albumin levels and insulin doses were independent factors associated with arteriosclerosis obliterans in lower extremity (P<0.05). CONCLUSION: In diabetic patients on peritoneal dialysis, there is a high prevalence of arteriosclerosis obliterans in lower extremity, which is related to high insulin dosage and low serum albumin levels.

Association between serum cartilage oligomeric matrix protein and coronary artery calcification in maintenance hemodialysis patients.

BACKGROUND: Coronary artery calcification (CAC) is common in end-stage renal disease (ESRD) patients, and the extent of CAC is closely related to cardiovascular outcomes in ESRD patients. Cartilage oligomeric matrix protein (COMP), as a component of the vascular matrix, has been found to be an inhibitor of arterial calcification in basic studies. However, there is no clinical research on the correlation between COMP and CAC in maintenance hemodialysis (MHD) patients. The aim of this study was to explore the relationship between serum COMP levels and CAC and cardiovascular events in MHD patients. METHODS: Serum COMP levels were compared between 54 MHD patients and 66 healthy people. MHD patients were then divided into three groups according to the tertiles of the concentration of COMP level and were followed up for major adverse cardiac events (MACEs), which were defined as a combined end point of new onset angina pectoris, nonfatal myocardial infarction, heart failure, coronary artery revascularization, hospitalization due to angina pectoris and all-cause deaths. The CAC score was calculated based on computed tomography scans. RESULTS: The serum COMP level in MHD patients was significantly higher than that in the general population [984.23 (248.43-1902.61) ng/mL vs. 219.01 (97.26-821.92) ng/mL, P < 0.01]. Serum COMP levels were positively correlated with CAC (r = 0.313, P = 0.021) and serum parathyroid hormone in MHD patients (r = 0.359, P < 0.01). Linear regression suggested that after adjusting for age, fasting blood glucose (Glu) and glycosylated hemoglobin (HbAlc), CAC score was an independent predictor in the final model for COMP level (ß = 0.424, t = 3.130, P < 0.01). The receiver operating characteristic (ROC) curve showed that COMP ≥ 994 mg/mL had 68.0% sensitivity and 72.4% specificity for the prediction of severe CAC [area under the curve (AUC): 0.674, P = 0.030, 95% CI: 0.526-0.882]. After a median follow-up of 16 months (8-24 months), there was no difference in the incidence rate of MACEs between the upper, middle and lower serum COMP groups. CONCLUSIONS: Our study found that MHD patients have higher levels of circulating COMP than controls. The serum COMP level is positively correlated with CAC score and could be used as a biomarker of severe CAC in MHD patients. However, there is no obvious correlation between serum COMP levels and the incidence of cardiovascular events.

Retraction statement: 'Urotensin II inhibits autophagy in renal tubular epithelial cells and induces extracellular matrix production in early diabetic mice' by Guan­Jong Chen, Fei Wu, Xin­Xin Pang, Ai­Hua Zhang, Jun­Bao Shi, Min Lu and Chao­Shu Tang

AIMS/INTRODUCTION: Urotensin II (UII) and autophagy have been considered as important components in the pathogenesis of diabetic nephropathy. The present study explores whether UII can regulate autophagy in the kidney, and its effect in diabetes. MATERIALS AND METHODS: Immunohistochemistry and western blot were carried out on the kidney tissues of diabetic UII receptor (UT) gene knockout mice, wild-type diabetic mice and normal control mice. For the in vitro experiment, HK-2 cells were treated with UII (10-7 mol/L) in the presence or absence of UT antagonist, SB-657510, (10-6 mol/L) or autophagy inducer, rapamycin (10-3 mol/L), for 12 h. Markers for autophagy (LC3-II, p62/SQSTM1) and extracellular matrix (fibronectin, collagen IV) were analyzed. RESULTS: In diabetic UT knockout mice, expression of LC3-II is increased and p62 was reduced in comparison with that of the normal diabetic mice. Fibronectin and collagen IV were downregulated in diabetic UT knockout mice when compared with that of the normal diabetic mice. For the in vitro cell experiment, UII was shown to inhibit expression LC3-II and increase expression of p62 in comparison with that of the normal control. Treatment with SB-657510 can block UII-induced downregulation of LC3-II and upregulation of p62 while inhibiting UII-induced upregulation of fibronectin and collagen IV. Adding autophagy inducer, rapamycin, also inhibited UII-induced upregulation of fibronectin and collagen IV. CONCLUSIONS: The present study is the first to show that UII can downregulate autophagy in the kidney while accompanying the increased production of extracellular matrix in early diabetes. Our in vitro study also showed that upregulation of autophagy can decrease UII-induced production of extracellular matrix in HK-2 cells.