Objective To explore the effect of total parathyroidectomy (PTX) with forearm autograft on the anemia and cardiac function in uremic patients with secondary hyperparathyroidism (SHPT). Methods The clinical data of 130 uremic patients who received PTX with forearm autograft in the First Affiliated Hospital of Zhejiang University from October 2010 to December 2015 were retrospectively analyzed. The changes of anemia and echocardiogram before and after operation were compared. According to the presence of left ventricular hypertrophy (LVH) before operation, the patients were divided into LVH group and non-LVH group. Echocardiographic indexes before and one year after operation of the two groups were compared. Results (1) Three months and one year after operation, hemoglobin and hematocrit increased while erythropoietin average usage decreased significantly (P＜0.01). (2) Compared with preoperative period, the dry weight was significantly increased one year after operation, and the cardiac function indexes including left ventricular end diastolic diameter (LVDd), interventricular septum end diastolic thickness (IVSd), left ventricular posterior wall end diastolic thickness (LVPWd), interventricular septum systolic thickness (IVSs), left ventricular systolic diameter (LVDs), left ventricular myocardial mass (LVM), and left ventricular myocardial mass index (LVMI) decreased significantly (P＜0.05). (3) In the non-LVH group, only IVSs decreased one year after operation (P＜0.05). In the LVH group, LVDs, LVDd, LVPWd, LVM, LVMI and IVSs were decreased significantly one year after operation than those in preoperative period (P＜0.05). Conclusions PTX with forearm autograft is an effective treatment for uremic patients with SHPT significantly improving anemia and left ventricular structure and function, especially for patients with ventricular hypertrophy in preoperative.

Objective To investigate the possible risk factors for the progression of abdominal aortic calcification (AAC) in MHD patients. Methods Total of 170 patients on MHD between June 2014 and October 2014 in the dialysis center of the Second Hospital of Tianjin Medical University were included prospectively. Lateral lumbar radiography were applied to evaluate patients' AAC score (AACs) at baseline and after two-years of follow-up respectively. According to the change of AACs, the patients were divided into rapid AAC progression group and non-rapid AAC progression group. Multivariable Logistic regression models were used to determine the risk factors for the progression of AAC in MHD patients. Results At baseline, the presence of AAC (AACs≥1) was 43.5%(74/170). The mean follow-up duration was 27.6(24.7, 28.0) months. AACs were available in 111 patients, and the presence of AAC was 78.4%(87/111). During the follow up, 36 patients developed new AAC; rapid AAC progression was seen in 54 patients, and non-rapid AAC progression was seen in 57 patients. Multivariate Logistic regression analysis demonstrated that hyperphosphatemia (OR=4.373,95%CI 1.562-7.246, P=0.005) and high density lipoprotein (HDL) (OR=0.031, 95%CI 0.003-0.338, P=0.004)were independent risk factors for AAC progression in MHD patients. Conclusions Hyperphosphatemia and low HDL may promote the progression of AAC. Well-controlled serum phosphate and lipid metabolism may slow the progression of vascular calcification, reducing cardiovascular morbidity and mortality.

Objective To explore the association between BMI and the risk of developing cardiac surgery associated acute kidney injury (CS-AKI), mortality of AKI and AKI requiring renal replacement therapy (AKI-RRT) after cardiac surgery. Methods Clinical data of patients undergoing cardiac surgery from January 2011 to December 2015 in Zhongshan Hospital of Fudan University were prospectively collected. Patients were divided into four groups according to BMI classification of Chinese population. Adjustment for selection bias was further assessed using propensity score method (PSM) to evaluate the role of BMI in the development of AKI. Results A total of 8442 patients were enrolled, among which 1092 patients successfully matched through PSM. The AKI incidences were respectively 30.3%, 33.3%, 38.6% and 46.8% in four BMI groups (P＜0.01) before PSM. The AKI incidences were respectively 31.9%, 35.2%, 42.5% and 42.9% in four BMI groups (P=0.016) after PSM. The risk of developing AKI increased by 19.9% as the BMI increased per 5 kg/m2 (95%CI: 1.070-1.344, P=0.002). The hospital mortality of patient (overall, AKI, AKI-RRT) in four groups was not statistically different after PSM (P＞0.05), but overweight group always had the lowest mortality. Conclusions BMI is a risk factor for AKI after cardiac surgery, and the AKI incidence increases with increasing BMI in a certain range.

Objective To evaluate the etiology, epidemiological characteristics, clinical diagnosis, and outcomes of hospitalized patients with AKI in Xinjiang, analyzing the risk factors of their clinical prognosis. Methods A multicenter retrospective survey was conducted, investigating adult patients admitted to four hospitals in Xinjiang in January and July 2013. Patients with AKI were screened out based on KDIGO's inclusion and exclusion criteria. Clinical variables of patients with AKI including demographics, clinical data, laboratory tests, treatment measures and prognosis were collected. Results Among 32,157 adult hospitalized patients, there were 722 AKI patients. Excluding those with incomplete data, 719 patients were enrolled in this study. The detection rate of AKI was 2.25% (722 of 32,157) by KDIGO criteria. The main cause for AKI was pre-renal injury, led mainly by cardiac output, low blood volume, and the use of nephrotoxic drugs. The non-recognition rate of AKI was 72.4%(407/557). Multivariate binary logistic regression analysis showed that AKI stage, peripheral vasodilation and renal parenchyma were protective factors of the omission diagnosis. In the short-term prognostic analysis, the overall mortality rate was 12.8%(92/719). Among the 323 patients with AKI who survived discharge, 43.7%(141) had renal function recovery; 40.2%(130) did not fully recover their renal function but ceased maintenance dialysis; 16.4%(53) were still on dialysis at discharge. Multivariate Cox regression model suggested that DIC, shock and department of obstetrics were independent risk factors for death during hospitalization of AKI. In addition, the risk of death for AKI from department of obstetrics and gynecology patients was higher than that of other departments. Conclusions The most common reason for AKI in hospitalized patients in Xinjiang was pre-renal injury. The main risk factors were low cardiac output and low blood volume. The omission diagnosis of AKI was serious; AKI stage, peripheral vasodilation and renal parenchymal injury however were its protective factors. Poor-DIC, shock, hospitalization in obstetrics were independent risk factors for death in patients with AKI.

Objective To detect the serum microRNA-148b-3p level in patients with diabetes mellitus and diabetic nephropathy, and to analyze its correlation with clinical and pathological indexes. Methods The research crowd was divided into three groups (1) diabetic nephropathy group: biopsy with diabetic nephropathy (n=25, 14 males, 11 females); (2) type 2 diabetes mellitus group: type 2 diabetes mellitus patients with normal urinary microalbumin /urinary creatinine value (n=10, 4 males, 6 females); (3) normal control group: healthy subjects (n=9, 3 males and 6 females). Clinical indicators included gender, age, 24-hour urine protein, systolic blood pressure (SBP), diastolic blood pressure (DBP), serum creatinine (Scr), urea (Urea), cystatin-C (Cys-C), blood albumin (ALB), urine microalbumin (UMA), triacylglycerol (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), serum uric acid (UA), fasting blood glucose (FBG), glycated hemoglobin (HbA1c), urine microalbuminuria / urinary creatinine (UACR), and estimated glomerular filtration rate (eGFR) calculated by CKD-EPI formula. Real-time quantitative PCR was applied to verify the expression of microRNA-148b-3p in serum samples of the research crowds. The relationships between microRNA-148b-3p level and clinical features was also analyzed. Results The levels of serum microRNA-148b-3p in diabetic nephropathy group and in type 2 diabetes mellitus group were 1.82 times and 1.73 times of that in normal control group (P＜0.05, respectively). The level of serum microRNA-148b-3p was significantly correlated with HDL-C (r=-0.374, P=0.013), UMA (r=0.426, P=0.004), FBG (r=0.330, P=0.046) and TG (r=0.423, P=0.005). Multiple linear regression analysis showed that UMA level was independently associated with serum microRNA-148b-3p level (β=0.338, P=0.044). The area under the receiver operating characteristic curve (ROC) of serum microRNA-148b-3p in diagnosing type 2 diabetes mellitus and diabetic nephropathy was 0.835 and 0.665, respectively. Conclusions The level of serum microRNA-148b-3p of patients with type 2 diabetes mellitus or diabetic nephropathy significantly increases. The level of UMA is independently associated with serum microRNA-148b-3p level. Serum microRNA-148b-3p is expected to be a potential biomarker for the diagnosis of diabetic nephropathy.

Objective To explore the effects of C/EBPα knockout in podocyte on diabetic nephropathy and its mechanisms. Methods C/EBPαloxp/loxp mice were crossed with podocin-cre mice to obtain F1 hybrids and then propagated until homozygous mice (C/EBPαf/f) were obtained. Diabetic nephropathy (DN) models were established by low-dose streptozotocin (STZ, 100 mg/kg) administration after 25 weeks of normal diet or 45% high-fat diet treatment, and biochemical indicators of blood and urea were measured. The morphological characteristics and the proteins regulating oxidative stress and mitochondrial function were detected. Results The type 2 DN models were successfully constructed based on transgenic mice. The kidneys of 8-month-old C/EBPαf/f mice did not show obvious morphological changes, but after constructing DN models, they showed obvious renal impairment, inflammation and oxidative stress. Compared with wild-type DN mice, the protein levels of nephrin and E-cadherin in DN C/EBPαf/f mice with DN were significantly decreased (P＜0.01); fibronectin and Nrf2 protein levels were all increased (all P＜0.05). Keap1, phospho-AMPK and mitochondrial function-related genes Pgc-1α protein levels were all decreased (all P＜0.05). Conclusion Podocyte C/EBPα knockout exacerbates diabetic nephropathy by promoting fibrosis and inhibiting Pgc-1α-mediated mitochondrial antioxidant function.

Objective To investigate whether the JAK2/STAT3 signaling pathway is involved in the epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells in uremic peritoneal dialysis (PD) rats. Methods A total of 48 male Sprague-Dawley (SD) rats were randomly separated into six groups: normal control group (NC group, n=8), sham group (n=8), uremic group (n=8), PD group (n=8), S3I-201 control group (n=8) and S3I-201 group (n=8). Uremic model generated by 5/6 nephrectomy surgery in rats was established. The rats of PD group, S3I-201 control group and S3I-201 group received daily infusion of 4.25% glucose-based peritoneal dialysate fluid (3 ml/100 g) from PD catheters for 28 days. Rats of S3I-201 group were injected with STAT3 inhibitor S3I-201 (2.5 mg/kg) solution from the catheters every other day; the same dose of the solvent of S3I-201 was simultaneously given to S3I-201 control group rats. After PD for 28 days, peritoneal function, pathologic changes, and microvessel density (MVD) were evaluated. Creatinine, urea nitrogen and interleukin-6 (IL-6) concentration in blood and dialysate, and protein and mRNA levels of phospho-JAK2 (p-JAK2), phospho-STAT3 (p-STAT3), E-cadherin, alpha-smooth muscle actin (α-SMA) and vascular endothelial growth factor (VEGF) in peritoneum were determined. Results Uremia and peritoneal dialysate could aggravate the peritoneal function and elevate peritoneal thickness and MVD. They could also increased the concentration of IL-6 in blood and dialysate and the expression levels of α-SMA, VEGF, p-JAK2 and p-STAT3 in peritoneum, while lowering E-cadherin expression in peritoneum. These manifestations were even more remarkable in PD group compared to those in uremic group. There was no statistical difference between the S3I-201 control group and the PD group as regards all the index (all P＞0.05). Compared with the S3I-201 control group, the rats treated with S3I-201 showed better peritoneal function. S3I-201 could reduce peritoneal thickness (P＜0.05), MVD (P＜0.05), the concentration of IL-6 in blood and dialysate, the mRNA and protein expression of α-SMA, VEGF, p-JAK2 and p-STAT3 (all P＜0.05), while enhance the mRNA and protein expression of E-cadherin (all P＜0.05). Conclusions After STAT3 is inhibited, the peritoneal thickness, MVD and IL-6 concentration in PD rats are decreased, and EMT is also inhibited, while peritoneal function is improved. The JAK2/STAT3 signaling pathway may thus be involved in the process of EMT of peritoneum in uremic peritoneal dialysis rats by regulating the expression of IL-6.

Objective To investigate the effect and mechanism of emodin (EM) in renal interstitial fibrosis of unilateral ureteral obstruction (UUO) mice. Methods Male C57BL/6J mice were randomly divided into 4 groups, including sham operation group (n=8), UUO operation group (n=8), UUO operation+losartan (LST) group (n=8) and UUO operation+EM group (n=8). The mice in each group were ingested the suspensions by gavage for 14 days after surgery. Mice in UUO+LST and UUO+EM groups were given 10 mg?kg-1?d-1 LST and 20 mg?kg-1?d-1 EM, respectively. LST and EM were mixed with 0.5% sodium carboxymethyl cellulose. Mice in sham group and UUO group were given 0.5% sodium carboxymethyl cellulose. The mice were sacrificed at the 14th day. Interstitial fibrosis was observed by HE, Masson and PAS stain. Real-time PCR was used to detect LC3, Beclin-1 and mTOR mRNA. Protein expressions of TGF-β1, α-SMA, E-cadherin, LC3, Beclin-1, PI3K, p-Akt and mTOR were detected by Western blotting. The autophagy was observed with transmission electron microscopy in the renal tissue. Results Compared with sham mice, UUO mice at the 14th day displayed obvious renal fibrosis. Meanwhile, UUO mice had increased expressions of TGF-β1 and α-SMA (all P＜0.01), and decreased expressions of E-cadherin (P＜0.01). Their renal expressions of PI3K, p-Akt and mTOR were also raised (all P＜0.01). Compared with those in UUO group, in UUO+LST group and UUO+EM group, expressions of autophagy protein LC3 and Beclin-1 were increased (all P＜0.01), and the number of autophagic was increased. Additionally, expressions of TGF-β1 and α-SMA were reduced in UUO+LST group and UUO+EM group (all P＜0.01), while the expression of E-cadherin was increased by emodin treatment (P＜0.05). And expressions of PI3K, p-Akt and mTOR were decreased in UUO+LST group and UUO+EM group (all P＜0.05), meanwhile renal tissue fibrosis significantly reduced. Conclusions Emodin can promote autophagy, ameliorate renal interstitial fibrosis and protect renal function through PI3K/Akt/mTOR signaling pathway.

Objective To investigate the effect of lycium barbarum polysaccharides (LBP) on oxidative stress in renal tissue of rats with renal interstitial fibrosis (RIF). Methods The RIF rat model was established by unilateral ureteral obstruction (UUO). A total of 108 specified pathogen free (SPF) class healthy adult male Sprague-Dawley (SD) rats were randomly divided into sham operation group, UUO model group and treatment group. The treatment group was further divided into low, medium and high dose of LBP groups and benazapril group. From the next day of the operation, the rats were given continuous intragastric administration for 3 weeks. The LBP low, medium and high dose groups were given 400, 600, 800 mg?kg-1?d-1 LBP, respectively. The benazapril group was administered with 1.05 mg?kg-1?d-1 benazepril hydrochloride. The sham operation group and UUO model group were daily fed normal saline solution by gavage. Six rats were sacrificed randomly at 7, 14 and 21 days after operation. Their blood samples were collected to detect the serum creatinine (Scr) and the kidney organ index was calculated. The pathological changes on the surgical side were observed by both HE staining and Masson staining. Meanwhile, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the renal tissue were detected by colorimetry detection. The expression of transforming growth factor-β1 (TGF-β1) protein was detected by immunohistochemical staining and the expression of TGF-β1 mRNA was detected by real time PCR. Results (1) Compared with the sham group, the Scr and kidney organ index of the UUO model group and treatment groups increased at each time point (all P＜0.05). Compared with the UUO model group, the kidney organ index of LBP low dose group in the 7th days, the LBP medium and high dose group in the 21st days as well as benazapril group in the 7th and 21st days were significantly lower (all P＜0.05). (2) Renal pathological change: compared with the sham operation group, both the renal tubular interstitial injury index and collagen positive area of the else groups were higher at each time point (all P＜0.05). Compared with the UUO group, the tubulointerstitial injury index and collagen staining positive area of LBP dose groups and benazapril group significantly decreased at different time points (all P＜0.05). (3) Compared with the sham group, in renal tissue of the other groups the level of MDA increased, SOD level decreased, while the expressions of TGF-1 mRNA and protein increased (all P＜0.05). Compared with the UUO model group, LBP low, medium and high dose group as well as benazapril group had lower MDA level, higher SOD level as well as lower expressions of TGF-1 mRNA and protein at each time point (all P＜0.05). Conclusions The pathological injury in UUO rats can be improved by the LBP. The LBP can alleviate the oxidative stress status of the kidney tissue by decreasing MDA and increasing SOD. The further study on the LBP delaying the progression of RIF is to be conducted.