This study aimed to explore the relationship between serum magnesium (Mg) levels and incidence of acute kidney injury (AKI) in patients with malignancy. Patients and Methods: Hospitalized patients with malignancy between October 1, 2014 and September 30, 2015 in Zhongshan Hospital were recruited. All relevant data were extracted from the electronic database. Results: All 99,845 patients were enrolled and 16,082 eligible patients were divided into three groups according to admission serum Mg levels in this study. Among them, 2383 (14.8%) cases were diagnosed as AKI. The incidence of AKI showed a V trend with the increase of serum Mg level. The effect of low serum Mg level on the onset of AKI seems to be greater than high serum Mg level. Patients with low serum Mg level spent a longer time in the hospital than those with normal serum Mg level and high serum Mg level. Further, multivariate logistic regression model was used to assess the importance of serum Mg level to influence AKI incidence. There was a higher AKI incidence in patients with magnesium level 0.66mmol/L or less (aOR=2.438, 95% CI=1.696, 3.505). Conclusion: Low serum Mg level might be a independent risk factor for AKI in patients with malignancy. Appropriate clinical intervention for serum Mg disorder may contribute to decreasing the incidence of AKI and the possibility of poor outcomes in cancer patients.

Syndecan-1 (SDC-1), a type of heparan sulfate proteoglycan on the surface of epithelial cells, is involved in maintaining cell morphology. Loss of cell polarity constitutes the early stage of ischemic acute kidney injury (AKI). This study investigated the role of SDC-1 shedding in I/R-induced AKI and the underlying mechanisms. Levels of the shed SDC-1 in the serum were measured with ELISA 12 and 24 h after reperfusion in renal I/R model mice. Na þ /K þ -ATPase-a1 expression was evaluated using western blotting in vivo and immunofluorescence in hypoxia/reoxygenation (H/R) cysts. Renal tubular epithelial cell apoptosis was measured using TUNEL in vivo and flow cytometry in vitro. Furthermore, plasma syndecan-1 (pSDC-1) levels were measured in patients at the time of anesthesia resuscitation after cardiac surgery. We found that shed SDC-1 levels increased and Na þ /K þ -ATPase-a1 expression decreased after H/R in the three-dimensional (3D) tubular model, and this state was exacerbated with extended period of hypoxia. After the inhibition of SDC-1 shedding by GM6001, SDC-1 and Na þ /K þ -ATPase-a1 expression was restored, while H/R-induced apoptosis was decreased. In vivo, SDC-1 shedding was induced by renal I/R and was accompanied with a loss of renal tubular epithelial cell polarity and increased apoptosis. GM6001 pretreatment protected against I/R injury by alleviating the disruption of cell polarity and apoptosis. pSDC-1 levels were significantly higher in AKI patients than in non-AKI patients. ROC curve showed that the accuracy of pSDC-1 for AKI prediction was 0.769. In conclusion, inhibition of I/R-induced SDC-1 shedding could contribute to renal protection by restoring the loss of cell polarity and alleviating apoptosis in tubular epithelial cells.

The aim of this study is to investigate whether Syndecan-1 (SDC-1), an indicator of endothelial glycocalyx injury, would increase the risk of hypercoagulable state and thrombosis in patients with nephrotic syndrome (NS). The prospective study was conducted among patients undergoing renal biopsy in the Department of Nephrology in our hospital from May to September 2018. We enrolled in patients with NS as the experimental group and patients with normal serum creatinine and proteinuria less than 1 g as the control group. Patients’ characteristics including age, sex, laboratory test results and blood samples were collected for each patient. The blood samples were taken before the renal biopsy. The samples were immediately processed and frozen at −80°C for later measurement of Syndecan-1. One hundred and thirty-six patients were enrolled in the study. Patients with NS and hypercoagulability had a higher level of SDC-1 compared with control group. Patients with membranous nephropathy occupied the highest SDC-1 level ( P = 0.012). Logistic regression showed that highly increased level of SDC-1 (>53.18 ng/ml) was an independent predicator for predicting hypercoagulable state. The elevated level of SDC-1 indicated that endothelial injury, combined with its role of accelerating hypercoagulable state, might be considered of vital importance in the pathophysiological progress of thrombosis formation in patients with NS.