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While β-hemolytic streptococcus (β-HS) infections are known to predispose patients to acute poststreptococcal glomerulonephritis, there is evidence that implicates α-hemolytic streptococcus (α-HS) in IgA nephropathy (IgAN). The alternative pathway of the complement system has also been implicated in IgAN. We aimed to explore the association between α-HS and complement activation in human tonsillar mononuclear cells (TMCs) in IgAN. In our study, α-HS induced higher IgA levels than IgG levels, while β-HS increased higher IgG levels than IgA levels with more activation-induced cytidine deaminase, in TMCs in the IgAN group. Aberrant IgA1 O-glycosylation levels were higher in IgAN patients with α-HS. C3 and C3b expression was decreased in IgAN patients, but in chronic tonsillitis control patients, the expression decreased only after stimulation with β-HS. Complement factor B and H (CFH) mRNA increased, but the CFH concentration in culture supernatants decreased with α-HS. The percentage of CD19 + CD35 + cells/complement receptor 1 (CR1) decreased with α-HS more than with β-HS, while CD19 + CD21 + cells/complement receptor 2 (CR2) increased more with β-HS than with α-HS. The component nephritis-associated plasmin receptor (NAPlr) of α-HS was not detected on tonsillar or kidney tissues in IgAN patients and was positive on cultured TMCs and mesangial cells. We concluded that α-HS induced the secretion of aberrantly O-glycosylated IgA while decreasing the levels of the inhibitory factor CFH in culture supernatants and CR1 + B cells. These findings provide testable mechanisms that relate α-HS infection to abnormal mucosal responses involving the alternative complement pathway in IgAN.

To examine whether platelet-to-lymphocyte ratio (PLR) is associated with 5-year mortality in patients with chronic kidney disease (CKD), we performed this study using data from the National Health and Nutrition Examination Survey (NHANES) through 1999 to 2006. 3285 patients with CKD stage 1–5 were included. Patients’ baseline characteristics were collected. Cox proportional hazards models were used to investigate the association of PLR with 5-year mortality including all-cause and cardiovascular mortality. Subgroup analysis was performed. Within 5 years following the date of the NHANES 1999 to 2006 survey participation, 655 (19.94%) deaths were recorded and 207 patients died from cardiovascular disease. A J-shaped association between PLR and 5-year mortality was observed. In adjusted model 2, the elevated PLR Z-score was not significantly associated with a decreased 5-year all-cause mortality risk (HR: 0.44, 95% CI: 0.16–1.22) when PLR Z-score

Diabetic nephropathy (DN) is a primary cause of renal failure. However, studies providing renal gene expression profiles of diabetic tubulointerstitial injury are scarce and its molecular mechanisms still await clarification. To identify vital genes involved in the diabetic tubulointerstitial injury, three microarray data sets from gene expression omnibus (GEO) were downloaded. A total of 127 differentially expressed genes (DEGs) were identified by limma package. Gene set enrichment analysis (GSEA) plots showed that sister chromatid cohesion was the most significant enriched gene set positively correlated with the DN group while retinoid X receptor binding was the most significant enriched gene set positively correlated with the control group. Enriched Gene Ontology (GO) annotations and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of DEGs mostly included extracellular matrix organization, extracellular space, extracellular matrix structural constituent, and Staphylococcus aureus infection. Twenty hub genes from three significant modules were ascertained by Cytoscape. Correlation analysis and subgroup analysis between hub genes and clinical features of DN showed that ALB, ANXA1, APOH, C3, CCL19, COL1A2, COL3A1, COL4A1, COL6A3, CXCL6, DCN, EGF, HRG, KNG1, LUM, SERPINA3, SPARC, SRGN, and TIMP1 may involve in diabetic tubulointerstitial injury. ConnectivityMap analysis indicated the most significant three compounds are 5182598, thapsigargin and 5224221. In conclusion, this study may provide new insights into the molecular mechanisms underlying diabetic tubulointerstitial injury as well as potential targets for diagnosis and therapeutics of DN.

Background: Aberrant O-glycosylation IgA1 production is a major factor in the pathogenesis of IgA nephropathy, but the underlying mechanism is still unclear. IgA1 glycosylation modification is in Golgi, and downregulation of the Golgi peripheral membrane protein Golgi matrix protein 130 (GM130) could lead to glycosylation deficiency. In this study, we aimed to explore the role of GM130 in glycosylate deficiency IgA1 (Gd-IgA1) production. Methods: We enrolled 27 IgA nephropathy patients, 12 patients with chronic tonsillitis, 15 non-IgAN chronic kidney disease patients, and 15 healthy volunteers as healthy control. We explored GM130 expression in Tonsillar tissue by immunofluorescence staining and Western blotting and expression in peripheral blood mononuclear cells (PBMCs) by flow cytometry. The concentration of IgA1 and level of O-glycosylation were determined by ELISA and Vicia Villosa lectin-binding assay. Real-time PCR and Western blot were used to analyze the levels of β1,3-Gal transferase (C1GALT1) and ST6GalNAC2, respectively. To explore the contribution of GM130 in IgA1 O-glycosylation modification, cells were subjected to experiments for evaluation of GM130 silencing by GM130-siRNA transfection. Results: GM130 expression was significantly decreased in tonsil tissues and PBMC of IgAN patients; the expression of C1GALT1 decreased and Gd-IgA1 level increased significantly in patients with IgAN patients. The expression of GM130 was negatively related to Gd-IgA1 production. By siRNA transfection, our results clearly indicated that the downregulation of GM130 can increase IgA1 O-glycosylation deficiency, which is thought to reduce C1GALT1 expression but not affect the expression of ST6GalNAC2. Conclusion: We identified and demonstrated that GM130 plays an important role in IgA1 O-glycans deficiency in IgAN patients, by negatively regulating C1GALT1 expression. We believe that this finding will provide theoretical foundations for a new mechanism of Gd-IgA1 production in IgAN patients.

Background: Despite the progression of dialysis techniques, the mortality of hemodialysis (HD) patients is still high in China. Here, a retrospective study was performed to investigate the neglected risk factors of all-cause mortality during maintenance HD (MHD). Methods: We investigated 117 MHD patients who died between 2011 and 2016 in the Second Xiangya Hospital of Central South University HD center. In order to analyze the risk factors of 48 months all-cause death, the methods of Kaplan-Meier and Cox regression were used. Results: Multivariate analyses of adjusted age and gender showed that MHD patients with estimated glomerular filtration rate 10 mL/min/1.73 m2 and anemia (hemoglobin Conclusions: This study indicated that the status of HD initiation is a risk factor of long-term survival in MHD patients, which were usually ignored for lacking of nephrology care prior and could potentially be identified and modified to improve the survival prognosis. Video Journal Club “Cappuccino with Claudio Ronco” at https://www.karger.com/Journal/ArticleNews/223997?sponsor=52

Background Lupus nephritis (LN) is a leading cause of mortality. The activation of NLRP3 inflammasome contributed to LN development and thus became a therapeutic target. Here we assessed the therapeutic potential of piperine, a bioactive compound known to target NLRP3 inflammasome, on LN development both in vivo and in vitro. Methods LN was induced in BALB/c mice via intraperitoneal injection of pristane. Upon treatment with increasing doses of piperine, we assessed renal lesions, measured serum levels of pro-inflammatory cytokines, and examined expressions of key components of NLRP3 inflammasome in kidney. To explore the molecular mechanisms, we treated the proximal tubular epithelial HK-2 cells with lipopolysaccharide (LPS) and ATP, and examined the effects of piperine on pyroptosis and the activation of NLRP3 inflammasome. Furthermore, we assessed the significance of AMPK signaling in piperine functions in HK-2 cells. Results In pristane-injected mice, piperine significantly ameliorated LN development in a dose-dependent manner, which was associated with the inhibition of NLRP3 inflammasome and the reduction of serum IL-1β, but not of IL-18 level. In HK-2 cells, piperine potently inhibited pyroptosis and the activation of NLRP3 inflammasome in response to LPS + ATP. The effects of piperine were mediated by blocking AMPK activation, and the AMPK agonist metformin bypassed the activities of piperine, and resumed pyroptosis as well as the activation on NLRP3 inflammasome. Conclusions By targeting AMPK, piperine significantly suppressed the activation of NLRP3 inflammasome, inhibited the release of pro-inflammatory cytokines, blocked the pyroptosis of tubular epithelial cells, and thus suppressed the development of LN.

IgA nephropathy (IgAN) is the most common primary glomerular disease. The characteristic pathology involves immune complexes formed by the deposition of IgA1 and underglycosylated IgA1 aggregates in the mesangial area, which may be accompanied by the deposition of IgG and/or IgM and complement components. However, the molecular mechanisms of IgAN remain unclear. In the present study, microarray analysis showed that the expression of microRNA-630 (miR-630) was significantly reduced in palatal tonsils from IgAN patients compared with chronic tonsillitis. Additionally, bioinformatic analysis showed that Toll-like receptor 4 (TLR4) was the predicted target gene of miR-630 and was regulated by miR-630. When miR-630 was overexpressed in palatal tonsil mononuclear cells from IgAN patients, the expression of TLR4 was reduced and the content of IgA1 in the cell culture supernatant was decreased, and the level of galactosylation in the IgA1 hinge region was increased. Moreover, immunohistochemical analysis showed that the expression of TLR4 in IgAN patients was significantly increased. After knocking down the expression of TLR4, both the concentration of IgA1 and the binding force of IgA1 with broad bean lectin were significantly reduced in IgAN. Furthermore, the mechanism study demonstrated that TLR4 might regulate the expression of IL-1β and IL-8 through NF-κB signaling pathway to modulate the concentration of IgA1 and the glycosylation level of IgA1. This interesting finding may offer new insight into the molecular mechanism of IgAN.

Introduction Metabolomics has emerged as a valuable tool to discover novel biomarkers and study the pathophysiology of diabetic nephropathy (DN). However, the effect of postoperative acute kidney injury (AKI) on diabetes mellitus (DM) to chronic DN progression has not been evaluated from the perspective of metabolomics. Methods A group of type 2 diabetes mellitus (T2DM) inpatients, who underwent off-pump coronary artery bypass grafting (CABG), were enrolled in our study. According to whether postoperative AKI occurred, patients were grouped in either the AKI group (AKI, n = 44) or the non-AKI group (NAKI, n = 44). Urine samples were collected from these patients before and 24 h after operation. Six patients from the AKI group and six patients from the NAKI group were chosen as the pilot cohort for untargeted metabolomics analysis, with the goal of identifying postoperative AKI-related metabolites. To understand the possible role of these metabolites in the chronic development of renal injury among T2DM patients, trans-4-hydroxy-L-proline and azelaic acid were quantified by targeted metabolomics analysis among 38 NAKI patients, 38 AKI patients, 46 early DN patients (DN-micro group), and 34 overt DN patients (DN-macro group). Results Untargeted metabolomics screened 61 statistically distinguishable metabolites in postoperative urine samples, compared with preoperative urine samples. Via Venn diagram analysis, nine of 61 were postoperative AKI-related metabolites, including trans-4-hydroxy-L-proline, uridine triphosphate, p-aminobenzoate, caffeic acid, adrenochrome, δ-valerolactam, L-norleucine, 5′-deoxy-5′-(methylthio) adenosine, and azelaic acid. By targeted metabolomics analysis, the level of trans-4-hydroxy-L-proline increased gradually from the NAKI group to the AKI, DN-micro, and DN-macro groups. For azelaic acid, the highest level was found in the NAKI and DN-micro groups, followed by the DN-macro group. The AKI group exhibited the lowest level of azelaic acid. Conclusions The detection of urinary trans-4-hydroxy-L-proline after AKI could be treated as an early warning of chronic DN progression and might be linked to renal fibrosis. Urinary azelaic acid can be used to monitor renal function noninvasively in DM and DN patients. Our results identified markers of AKI on DM and the chronic progression of DN. In addition, the progression of DN was associated with AKI-like episodes occurring in DM.

To examine whether albumin-to-globulin ratio (AGR) is correlated with long-term mortality in patients with chronic kidney disease (CKD), we performed this study using data from the National Health and Nutrition Examination Survey through 1999–2006. 3302 CKD patients were included. Patients’ baseline characteristics were collected. Multivariate Cox proportional hazards models were used to investigate the association between AGR and the study outcomes, including long-term all-cause and cardiovascular mortality. Subgroup analysis using the Cox proportional hazards model was performed as a sensitivity test. During a median follow-up duration of 122.00 months, 1627 (49.27%) deaths were recorded and 440 patients died from cardiovascular disease. In adjusted model 1, AGR ≥ 1.26 group was associated with a lower risk of long-term all-cause mortality HR 0.72, 95% CI 0.65–0.81) compared with AGR

Damaged or dysfunctional mitochondria are toxic to the cell by producing reactive oxygen species and releasing cell death factors. Therefore, timely removal of these organelles is critical to cellular homeostasis and viability. Mitophagy is the mechanism of selective degradation of mitochondria via autophagy. The significance of mitophagy in kidney diseases, including ischemic acute kidney injury (AKI), has yet to be established, and the involved pathway of mitophagy remains poorly understood. Here, we show that mitophagy is induced in renal proximal tubular cells in both in vitro and in vivo models of ischemic AKI. Mitophagy under these conditions is abrogated by Pink1 and Park2 deficiency, supporting a critical role of the PINK1-PARK2 pathway in tubular cell mitophagy. Moreover, ischemic AKI is aggravated in pink1 andpark2 single- as well as double-knockout mice. Mechanistically, Pink1 and Park2 deficiency enhances mitochondrial damage, reactive oxygen species production, and inflammatory response. Taken together, these results indicate that PINK1-PARK2-mediated mitophagy plays an important role in mitochondrial quality control, tubular cell survival, and renal function during AKI.

Background/Aims: Tonsillectomy may be an important method to achieve a long-term remission of IgAN, but patients’ physical status may limit their access to this surgery. We proposed an encouraging solution through inhibiting GADD34 expression in order to promote tonsillar mononuclear cells (TMCs) apoptosis and reduce nephropathic IgA secretion. Methods: A total of 12 IgAN and 9 non-IgAN patients were involved from March 2015 to May 2016. After TMCs were extracted by density gradient centrifugation and stimulated by inactivated hemolytic streptococcus, the mRNA and protein expression of GADD34, GRP78, CHOP, Bcl-2, Bcl-XL, AID, Iα-Cα, and cleaved caspase-3 were examined by fluorescent RT-PCR and Western blotting. Guanabenz treatment and siRNA interference were applied to downregulate GADD34 in tonsillar mononuclear cells from IgAN patients, and P-eIF2α expression was examined by Western Blotting. Cell apoptosis was evaluated by Annexin V FITC/PI flowcytometry, and IgA secretion in cultural supernatant was inspected by enzyme linked immunosorbent assay. Results: After stimulation, the expression of GADD34 was significantly increased in IgAN patients (P< 0.05). Cell apoptosis was mitigated and IgA secretion level was elevated (P< 0.05). To be noticed, CHOP expression had no significant difference between two groups. After guanabenz treatment and siRNA interference, a prolonged elevation of P-eIF2α expression was observed. Cell apoptosis was reinforced and IgA secretion level was decreased (P< 0.05). Conclusion: GADD34 may be a potential therapeutic target for IgAN treatment due to its effect on cell apoptosis.

Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected. Although AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in patients with CKD, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of transforming growth factor-β, p53, hypoxia-inducible factor, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathologic changes may contribute to the heightened sensitivity of, and nonrecovery from, AKI in patients with CKD.

SUV39H1, the histone methyltransferase (HMTase) of histone H3 lysine 9 trimethylation (H3K9me3), is a known transcriptional repressor of inflammatory genes. The effect of SUV39H1 on inflammatory gene promoters under high-glucose stimulation in vascular smooth muscle cells (VSMCs), macrophages, and cardiomyocytes has been studied, but how SUV39H1 functions in renal tubules under diabetic conditions is unclear. Renal biopsy specimens of ten diabetic nephropathy (DN) subjects and seven non-DN minimal change diseases (MCD) subjects were collected. SUV39H1, IL-6, and MCP-1 expression in renal tissues were measured using immunohistochemical, while SUV39H1, H3K9me3, IL-6, and MCP-1 in human proximal tubular epithelial cells (HK-2) under varying glucose conditions were assayed by Western blot and ELISA. SUV39H1 was overexpressed in HK-2 cells; the regulation of SUV39H1 and H3K9me3 on NF-κB, IL-6, MCP-1, caspase 3, and apoptosis was measured. SUV39H1 was expressed more in diabetic human renal tubules. HK-2 cells with high glucose up-regulated IL-6 and MCP-1 in a dose- and time-dependent manner, and SUV39H1 expression was reduced with greater glucose and prolonged stimulation. Expression of H3K9me3 was synchronized with SUV39H1. Moreover, overexpression of SUV39H1 in high glucose environment was accompanied with increased H3K9me3 and decreased inflammation and apoptosis. SUV39H1 dysregulation may be involved in DN progression. Overexpression of SUV39H1 may reduce renal inflammation and apoptosis via epigenetic modulation, thus plays a protective role in DN.

The predictive effect of combining MEST with clinical data at biopsy on renal survival outcomes has not been investigated in patients with IgA nephropathy (IgAN). MEST of The Oxford classification of IgAN and 24-hour urine proteinuia measured at enrollment. The primary outcome was a composite of either ESRD (eGFR to 2), or a permanent reduction in eGFR to below 50% of the value at biopsy. 742 patients were enrolled and follow-up >3 years, and were divided into two groups according to eGFR levels at biopsy. Multivariable logistical regression revealed that proteinuria at biopsy (OR 5.307 (95% Cl 3.003 to 9.376) p = 0.000), tubular atrophy/interstitial fibrosis scores (T) in MEST (OR 3.915 (95%Cl 2.710 to 5.654) p = 0.000) were the two predictors of eGFR decline for IgAN patients. Kaplan–Meier survival curves show significant difference in renal survival outcome among each T scores groups at biopsy (T0, T1, T2) (P

Many studies have focused on finding predictors for mild IgAN progression. However, the cases of severe IgAN with a high proportion of global glomerulosclerosis have received inadequate attention.A group of 172 primary IgAN patients with 50-75% global glomerulosclerosis was studied retrospectively between April 2007 and October 2017. Patients were divided into three groups according to the serum triglyceride tertiles: 1.42 µmol/L (Group 1), 1.42-2.29 µmol/L (Group 2), and 2.29 µmol/L (Group 3). Groups 1 and 2 comprised non-hypertriglyceridemia subjects, while Group 3 was defined as the hypertriglyceridemia (HTG) group. The patients were followed for 4-96 months (median 39.43 months). The study end point was defined as a 50% decline in estimated glomerular filtration rate (eGFR) or ESRD.A high proportion of global glomerulosclerosis is not absolutely correlated with severe clinical features and poor renal outcome. In our retrospective observation, eGFR decreased by less than 10% of the baseline during follow-up in 43.6% of the patients. However, in our patients with HTG, the cumulative renal survival rate was significantly lower compared to those without HTG. Multivariate Cox regression analysis also showed that triglyceride is an independent predictor of poor renal outcomes. Furthermore, in the HTG group, the cumulative renal survival rates were higher in patients treated with Tripterygium wilfordii Hook F (TwHF) compared to those without TwHF.A high proportion of global glomerulosclerosis combined with HTG at biopsy have better predictive validity for the disease progression of IgAN than global glomerulosclerosis alone. TwHF may partially affect the renal outcome of severe IgAN with HTG, and this may relate to its regulation of lipid metabolism and immunoinflammatory response.

Introduction: Catheter-related blood stream infection (CRBSI), the most common complication of central vein catheter (CVC), was closely associated with high morbidity and mortality in hemodialysis (HD) patients. Conjunction with systemic antibiotic, antibiotic lock (ABL) is an important therapeutic option to salvage the catheter. With extra antimicrobial and biofilm removing properties, urokinase plasminogen activator (uPA)-based ABL could have a potential role in the treatment of CRBSI. Objective: In this study, we aimed to explore effectiveness of uPA-based (ABL) on microorganisms embedded in biofilms in vitro and CVC salvage rate in HD patients with CRBSI. Methods: In vitro, we induced biofilms formation on the surface of HD catheter by mimicking the development of CRBSI. Applying uPA with or without antibiotics on the kinds of microorganism biofilms to explore its antimicrobial and biofilm removing properties. In vivo, 86 HD patients diagnosed as CRBSI were retrospectively enrolled to see effectiveness of uPA-based ABL on catheter salvage rate as compare to heparin-based ABL. Results: uPA was effect to Staphylococcus epidermidis biofilms compared to Staphylococcus aureus, Escherichia coli, and Candida albicans. Less biofilm residues made the regrowth of S. epidermidis also limited. The combination of uPA with antibiotic showed better antimicrobial and antibiofilm activity than uPA alone or heparin-based ABL in vitro and in vivo. Among HD patients, uPA-based ABL did not cause any obvious adverse affects, and it was more effective in treating coagulase-negative Staphylococci related CRBSI than other microorganisms. Conclusions: The combination of uPA and a therapeutic plasma concentration of sensitive antibiotic can work together to effectively remove coagulase-negative S. epidermidis embedded in biofilms in vitro. uPA-based ABL is safe and effective therapeutic intervention for HD patients with CRBSI, especially compared to heparin-based ABL.

To investigate the correlation of different types of urinary abnormalities or different proteinuria and hematuria with the pathological injury of kidney in IgA nephropathy with isolated hematuria and/or mild proteinuria. Methods: Patients with primary IgA nephropathy, isolated hematuria and/or mild proteinuria were enrolled in the Department of Nephrology, the Second Xiangya Hospital, Central South University from January 2013 to January 2018. According to the difference of red blood cell count in urinary sediment and quantitative of 24-hour urinary protein (24 h-UP) during renal biopsy, the patients were grouped in 3 ways: a simple hematuria group, a hematuria and proteinuria group, and a simple proteinuria group; a proteinuria I group, a proteinuria II group, and a proteinuria III group; a hematuria I group, a hematuria II group, and a hematuria III group. The clinical parameters such as age, mean arterial pressure, blood urea nitrogen, serum creatinine, blood uric acid, 24 h-UP, and renal pathological damage were compared. Results: A total of 157 patients met the inclusion criteria, including 71 males and 86 females. The most common pathological type was focal and/or segmental glomerulosclerosis. The Lee's classification were dominated by grade III and IV, and the renal pathological injury was heavy. Immunoglobulin deposition was dominated by simple IgA deposition. The most common fluorescence intensity of IgA deposition was +++. 97 (61.78%) patients were accompanied by complement deposition and were mainly composed of simple complement C3 deposition. There were 18 patients (11.47%) in the simple hematuria group, 111 patients (70.70%) in the hematuria and proteinuria group, and 28 patients (17.83%) in the simple proteinuria group. Compared with the simple hematuria group, the proportion of patients with mild injury was lower in the simple proteinuria group, and the proportion of patients with moderate-to-severe injuries was increased (χ2=7.053, P=0.008). Compared with the hematuria and proteinuria group, the proportion of patients with mild injury was lower in the simple proteinuria group, and the proportion of patients with moderate-to-severe injury was increased (χ2=4.294, P=0.038). Compared with the proteinuria I group, the proportion of patients with mild injury was lower in the proteinuria III group, and the proportion of patients with moderate-to-severe injury was increased (χ2=5.433, P=0.020). There was no significant difference in the proportion of patients with renal pathological injury among different hematuria groups (P0.05). Conclusion: The clinical manifestations of patients with IgA nephropathy with hematuria and/or mild proteinuria are inconsistent with renal pathological damage. Some patients with mild clinical manifestations have severe renal pathological damage and the renal pathological damage is more serious in simple proteinuria. The more proteinuria, the heavier the renal pathological damage.目的：探讨单纯血尿和/或轻度蛋白尿IgA肾病患者的不同尿检异常类型、不同蛋白尿及血尿程度与肾脏病理的关系。方法：选择在中南大学湘雅二医院肾内科2013年1月至2018年1月经肾活检确诊的、临床表现为单纯血尿和/或轻度蛋白尿的原发性IgA肾病患者。根据肾活检时尿沉渣红细胞计数及24 h尿蛋白定量(quantitative of 24-hour urinary protein，24 h-UP)对所有患者进行3种方式的分组：单纯血尿组、血尿+蛋白尿组、单纯蛋白尿组；蛋白尿I，II，III组；血尿I，II，III组。比较各组患者的年龄、平均动脉压、血尿素氮、血肌酐、血尿酸、24 h-UP等临床指标以及肾脏病理损伤程度。结果：纳入157例患者，其中男71例，女86例。病理类型以局灶和/或节段硬化型最多见，Lee’s分级以III级和IV级为主，肾脏病理损伤较重。免疫球蛋白沉积以单纯IgA沉积为主，IgA沉积荧光强度以+++最多见，97例(61.78%)的患者伴有补体沉积，且以单纯补体C3沉积为主。单纯血尿组18例(11.47%)，血尿+蛋白尿组111例(70.70%)，单纯蛋白尿组28例(17.83%)。单纯蛋白尿组与单纯血尿组相比，轻度肾损伤患者比例降低，中重度肾损伤患者比例增高(χ2=7.053，P=0.008)；单纯蛋白尿组与血尿+蛋白尿组相比，轻度肾损伤患者比例降低，中重度肾损伤患者比例增高(χ2=4.294，P=0.038)；蛋白尿III组与蛋白尿I组相比，轻度肾损伤患者比例降低，中重度肾损伤患者比例增高(χ2=5.433，P=0.020)。不同血尿组肾脏病理损伤差异无统计学意义(P0.05)。结论：单纯血尿和/或轻度蛋白尿IgA肾病患者临床表现与肾脏病理损伤程度不一致。部分临床表现轻微的患者肾脏病理损伤较重，且以出现单纯蛋白尿时更明显；蛋白尿越多，肾脏病理损伤越重。.

Diabetic nephropathy (DN) is a major cause of end-stage renal disease. Although intense efforts have been made to elucidate the pathogenesis, the molecular mechanisms of DN remain to be clarified. To identify the candidate genes in the progression of DN, microarray datasets GSE30122, GSE30528, and GSE47183 were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) were identified, and function enrichment analyses were performed. The protein-protein interaction network was constructed and the module analysis was performed using the Search Tool for the Retrieval of Interacting Genes and Cytoscape. A total of 61 DEGs were identified. The enriched functions and pathways of the DEGs included glomerulus development, extracellular exosome, collagen binding, and the PI3K-Akt signaling pathway. Fifteen hub genes were identified and biological process analysis revealed that these genes were mainly enriched in acute inflammatory response, inflammatory response, and blood vessel development. Correlation analysis between unexplored hub genes and clinical features of DN suggested that COL6A3, MS4A6A,PLCE1, TNNC1, TNNI1, TNN2, and VSIG4 may involve in the progression of DN. In conclusion, DEGs and hub genes identified in this study may deepen our understanding of molecular mechanisms underlying the progression of DN, and provide candidate targets for diagnosis and treatment of DN.

The proteins BAFF, ST6GALNAC2, C1GALT1, and COSMC in peripheral blood mononuclear cells (PBMCs) and plasma levels of IgA1 and galactose-deficient IgA1 (Gd-IgA1) are potential biomarkers for IgAN nephropathy. In this study, we comparatively studied the changes of those biomarkers before and after tonsillectomy.Peripheral blood samples were obtained from 16 IgAN patients with pre- and post-tonsillectomy. IgAN was diagnosed based on results from analysis of percutaneous renal biopsy tissue. Peripheral blood samples from three patients without renal diseases (non-IgAN), before and after tonsillectomy, and 16 healthy controls were also examined. BAFF, ST6GALNAC2, C1GALT1, and COSMC mRNA levels in PBMCs were detected using real-time PCR. Plasma IgA1 content was measured by ELISA. Gd-IgA1 levels were determined using the VV lectin-ELISA method.BAFF, ST6GALNAC2, C1GALT1, and COSMC mRNA levels and the plasma concentrations of IgA1 and Gd-IgA1 in IgAN patients before tonsillectomy were significantly higher than those in healthy controls (P 0.05). Tonsillectomy significantly increased the expression of BAFF and ST6GALNAC2, and plasma IgA1 level, while it downregulated that of C1GALT1 and COSMC (P 0.05). However, in non-IgAN patients, tonsillectomy did not affect the mRNA levels of BAFF, ST6GALNAC2, C1GALT1, and COSMC, plasma IgA1 content and Gd-IgA1 level. Positive correlations were established between BAFF and IgA1 (r = 0.604, P 0.01) and between ST6GALNAC2 and Gd-IgA1 (r = 0.623, P 0.01).Tonsillectomy changes the mRNA levels of BAFF, ST6GALNAC2, C1GALT1, and COSMC in PBMCs, as well as the plasma IgA1 level in IgAN patients. BAFF and ST6GALNAC2 might regulate IgA1 secretion and O-glycosylation.

Background: Immunoglobulin (Ig) A nephropathy (IgAN) is the finding of immune deposits predominantly containing polymeric IgA in the glomerular mesangium on renal biopsy. Increasing evidence suggested that retinoic acid (RA) signaling selectively induces IgA isotype switching and basic leucine zipper transcription factor, ATF-like (BATF) controls the global regulators of class switch recombination (CSR) in lymphocytes. Great effort has been paid to identify whether impaired immune regulation along the ‘mucosa-bone marrow (BM) axis' play an important role in the pathogenesis of IgAN. Methods: The aim of the study was to investigate the expression of all-trans-RA (ATRA) and BATF, and to identify their impact on IgA CSR in IgAN patients and rat animal models. Blood samples and tonsillar tissue specimens were obtained from 22 patients with IgAN and 24 patients with chronic tonsillitis as control. Results: Immunohistochemical, RT-PCR and western blotting examination revealed that RA signaling and BATF productions are activated in IgAN patients compared with controls. Lipopolysaccharide and α-hemolytic streptococcus stimulation upregulated RA receptor (RAR) and BATF expression, promote IgA CSR and ATRA productions in tonsil mononuclear cells. RAR alpha (RARα) or BATF siRNA decreases IgA expression. We also built IgAN rat models and found that RARα, BATF and activation-induced cytidine deaminase were upregulated in the peripheral blood, spleen and BM. With ATRA (500 μg/kg body weight) treatment for 8 weeks, IgA deposition on glomeruli and mesangial cells proliferation increased. It also revealed that ATRA activated BATF and IgA CSR in vivo. Conclusion: These data point toward the role of RA signaling together with BATF in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with neoantigen results in impaired mucosal and systemic IgA responses.

For maintenance hemodialysis (MHD) patients, the blood is in low hypercoagulable state due to the use of heparin or low molecular weight heparin during dialysis. It is not rare to see hematoma in the puncture site. In recent years, several cases have been reported of spontaneous kidney rupture, but no hip hematoma, let alone both occurred in succession. There was one MHD patient with spontaneous kidney bleeding and hip hematoma in our hospital in 2014, and we provided effective treatment and follow-up.

Renal ischemia-reperfusion injury (IRI), a major cause of acute kidney injury as well as a contributor to a rapid kidney dysfunction and high mortality rates, is a complex yet not fully understood process. Investigation on the underlying molecular mechanism including the inflammation initiation and progression can help to have a better understanding of the disease, and thereby lead to a potential therapeutic approach. We established renal IRI mouse model groups differing in their ages. These renal IRI mice were treated either only with si-nuclear receptor subfamily 4, group A, member 1 (NR4A1) or together with si-β-catenin by tail vein injection to analyze the role of NR4A1 and β-catenin in the development of renal IRI. Serum creatinine (SCr) and blood urea nitrogen (BUN) levels were examined for renal function analysis. Levels of the apoptosis markers B-cell lymphoma-2 (Bcl-2), Bcl-2 associated protein X (Bax), and cleaved caspase-3 were determined. NR4A1 gene was up-regulated in the renal tissues of all mice with IRI, which showed a much higher level in the old mice with IRI. si-NR4A1 treatment resulted in reduced SCr and BUN levels and a decrease of cell apoptosis, indicated by lower expression of Bax and cleaved Caspase-3, while in contrast increased levels of Bcl-2 were detected. Interestingly, also the β-catenin level was increased by knockdown of NR4A1. Furthermore, si-β-catenin reversed the effect of knockdown of NR4A1, leading to aggravated renal function damage, severe pathological injury and increased apoptosis. Thus, silencing NR4A1 ameliorates renal IRI via β-catenin signaling pathway activation. Down-regulated NR4A1 confirms renoprotective properties against renal IRI via the activation of β-catenin signaling pathway in old mice.

IgA nephropathy (IgAN) is the finding of immune deposits predominantly containing polymeric IgA in the glomerular mesangium on renal biopsy. Recently studies show that inflammation may involve in the progression of renal glomerulosclerosis and tubulointerstitial scarring in IgAN. This study was designed to evaluate the renoprotective effect of triptolide on IgAN rat model. IgAN was induced in Sprague-Dawley rats by oral and intravenous immunization with BSA for 12 weeks. Rats were treated with triptolide (200 μg/kg/d intragastrically) from 12 to 28 weeks. At Week 28, the rats was sacrificed, kidneys and blood samples were collected for further analysis. Our data shown that IgAN rat model showed marked deterioration of proteinuria together with higher levels of the urine protein:creatinine ratio compared to the normal control. Animals that underwent intermittent exposure to triptolide treatment exhibited significant improvements in the functional parameters without severe side effects. Rats developing IgAN had profound mesangial proliferation and mesangial expansion, intense and diffuse glomerular IgA deposition, while triptolide treatment significantly attenuated it. We also observed that treatment with triptolide significantly decreases serum levels of IL-1β and IL-18, and may exerted anti-inflammatory effects by down-regulating NLRP3 and TLR4 expression. Our study clearly demonstrated that triptolide prevents IgAN progression via an amelioration of inflammasome-mediated proinflammatory cytokine production, thus brought a light of hope for treatment of IgAN.

The diabetic milieu is believed to change the activity, or result in damage of podocytes-a key component of the glomerular filtration barrier and known to secrete matrix for glomerular basement membrane. This in turn contributes to diabetic nephropathy. However, how podocyte dysfunction is triggered in diabetic nephropathy remains ambiguous. Galectin-1 belongs to Galectin family that bind to β-galactoside residues of glycosylated proteins. We explored whether Galectin-1 is dysregulated in diabetic nephropathy using three different techniques, namely real-time polymerase chain reaction, western blotting, and immunofluorescent staining, to follow the expression of Galectin-1 under high glucose levels in podocytes. High glucose consistently induced Galectin-1 expression. Immunohistochemistry using a Galectin-1-specific antibody also showed elevated Galectin-1 in renal tissues of diabetic patients with manifestation of nephropathy, indicating a correlation of Galectin-1 overexpression with diabetic nephropathy. Upregulation of Galectin-1 is associated with loss of podocin, which is important for the physiological function of podocytes and decreases in the renal tissues of diabetic nephropathy. Increased Galectin-1 is a causal event for the high glucose-induced loss of podocin, since silencing Galectin-1 in podocytes increased podocin expression in the presence of 25 mM glucose. Thus expression of Galectin-1 in diabetic nephropathy may serve as a marker and contribute to disease progression by interfering with podocin expression.

The relationship between tonsillar autoimmune response and the pathogenesis of IgA nephropathy (IgAN) has been previously demonstrated. However, the role of CD4 (+)CD25 (+)Treg cells, which play critical roles in maintaining peripheral tolerance and preventing autoimmunity, has not yet been defined in IgAN.Thirty-five patients with IgAN and 35 patients without renal disease were studied. The CD4 (+)CD25 (+)Treg cells were examined by flow cytometry. Clinical and laboratory data, such as serum creatinine and urinary samples, were obtained from each patient. Glomerular injury was assessed by histopathology. Serum IgA, C3, IL-2, IL-4 and IL-6 were analyzed by ELISA.CD4 (+)CD25 (+)Treg cells significantly decreased in IgAN patients compared with the controls before tonsillectomy (p0.05). CD4 (+)CD25 (+)Treg cells were negatively correlated with blood urea nitrogen, supernatant IL-4 and proteinuria in IgAN patients, and positively with estimated glomerular filtration rate. CD4 (+)CD25 (+)Treg cells gradually decreased as the severity of renal histology increased. In addition, serum IgA, IL-2, IL-6 and supernatant IL-4 elevated while CD4 (+)CD25 (+)Treg cells decreased in IgAN patients. CD4 (+)CD25 (+)Treg cells were significantly increased when serum IgA, IL-2, IL-6 and supernatant IL-4, urine protein and urine erythrocytes were decreased after tonsillectomy in patients with IgAN, but were still lower than those of the controls (p0.05).CD4 (+)CD25 (+)Treg cells were associated with IgAN, and tonsillectomy may increase CD4 (+)CD25 (+)Treg cells in IgAN patients, leading to clinical improvement.

Background IgA nephropathy (IgAN) is the most common type of primary glomerulonephritis in the world. Hot pepper is the most favorite vegetable for Chinese in Hunan and Sichuan provinces. It can be assumed that capsaicin, the active ingredient of hot pepper, is a possible risk factor in diet in the pathogenesis of IgAN. Methods 22 subjects, including 11 IgAN patients and 11 non-IgAN patients were enrolled in this study. Tonsillar mononuclear cells were isolated and cultured for 3 days with or without capsaicin. Results In the absence and presence of capsaicin, the BAFF expression and IgA1 secretion were higher in IgAN patients than that in non-IgAN patients, meanwhile, the gene expression of C1GALT1 and Cosmc and IgA1 O-glycosylation level were significantly lower. In IgAN group, coincubated with capsaicin, IgA1 and BAFF secretion and BAFF expression by TMCs were significantly higher than that without capsaicin, furthermore, the level of mRNA encoding C1GALT1 and Cosmc and the level of IgA1 O-glycosylation were evidently lower. Conclusion Capsaicin may induce IgA1 secretion by activating BAFF expression, and bring to aberrantly IgA1 O-glycosylation by suppressing C1GALT1 and Cosmc expression. Therefore, to limit the consumption of hot pepper would be beneficial to patients with IgA nephropathy.

Proteinuria and decline of renal function are associated with progression of kidney disease. The Renin Angiotensin Aldosterone System (RAAS) plays an important role in blood pressure regulation, fluid volume, and sodium balance. Overactivity of RAAS contributes to the pathogenesis of a variety of clinical conditions including progress of chronic kidney disease (CKD). This review summarizes the use of RAAS inhibitors as dual therapy or monotherapy in different stages of kidney disease. Experimental and clinical studies have demonstrated RAAS inhibitors prevent proteinuria, kidney fibrosis and slow decline of renal function and thus play a protective role in both early and end stages of kidney disease. While combination use of RAAS inhibitors showed higher efficiency compared with monotherapy, it is also associated with higher incidence of adverse events. Besides ACEI/ARBs, more mechanism research of mineralocorticoid receptor antagonists in kidney disease should be performed.

Background/Aim: Focal segmental glomerulosclerosis (FSGS) typically presents with nephrotic range proteinuria, which could eventually develop into end-stage renal disease. Resveratrol (RSV) is a natural polyphenol compound, which has been reported to suppress inflammatory response and renal interstitial fibrosis. This study is aimed at evaluating the renoprotective effect of RSV treatment on adriamycin-induced FSGS. Methods: In Balb/c mice, adriamycin nephropathy was induced by adriamycin (10 mg/kg body weight, diluted in normal saline) via a tail vein on day 0. Then the mice were treated with RSV (40 mg/kg body weight) once daily by oral gavage, again starting on the day of adriamycin injection and continued for 6 weeks. At 6 weeks, the mice were sacrificed; kidneys and blood samples were collected for further analysis. Results: When treated with adriamycin, the expressions of C3aR, C5aR, sphingosine kinase 1 (Sphk1), and soluble urokinase-type plasminogen activator receptor (suPAR) were upregulated, while RSV treatment could inhibit the expressions of C3aR, C5aR, Sphk1, and suPAR, eventually leading to anti-inflammatory and anti-fibrosis conditions. Conclusion: RSV attenuates adriamycin-induced FSGS through C3aR/C5aR-Sphk1 pathway.

Many studies found that hemoglobin (Hb) fluctuation was closely related to the prognosis of the maintenance hemodialysis patients. We investigated the association of factors relating dialysis dose and dialyzer membrane with Hb levels. We undertook a randomized clinical trial in 140 patients undergoing thrice-weekly dialysis and assigned patients randomly to a standard or high dose of dialysis; Hb level was measured every month for 12 months. In the standard-dose group, the mean (±SD) urea reduction ratio was 65.1% ± 7.3%, the single-pool Kt/V was 1.26 ± 0.11, and the equilibrated Kt/V was 1.05 ± 0.09; in the high-dose group, the values were 73.5% ± 8.7%, 1.68 ± 0.15, and 1.47 ± 0.11, respectively. The standard deviation (SD) and residual SD (liner regression of Hb) values of Hb were significantly higher in the standard-dose group and low-flux group. The percentage achievement of target Hb in the high-dose dialysis group and high-flux dialyzer group was significantly higher than the standard-dose group and low-flux group, respectively. Patients undergoing hemodialysis thrice weekly appear to have benefit from a higher dialysis dose than that recommended by current KDQQI (Kidney Disease Qutcome Quality Initiative) guidelines or from the use of a high-flux membrane, which is in favor of maintaining stable Hb levels.

Aim: Treg cells are of critical importance for maintenance of tolerance. The purpose of the this study was to observe the number of Treg cells in the patients with thrombotic thrombocytopenic purpura (TTP) associated with systemic lupus erythematosus (SLE), and to study pathogenesis of TTP with SLE. Methods: Seven patients with TTP associated with SLE and seven healthy volunteers were studied. The Treg cells were examined by flow cytometry. Clinical and laboratory data, such as urinary protein, serum creatinine, endothelial markers and immunologic serologics, were obtained from each patient and healthy volunteer. Glomerular injury was assessed by histopathology. Serum IL-2, IL-4, IL-6 and anti-endothelial cell antibody were analyzed by ELISA and anti-ADAMTS13 antibody were detected by Western blotting. Results: Treg cells significantly decreased in TTP with SLE patients compared with controls (p

Background Clinical deterioration of IgA nephropathy (IgAN) is frequently preceded by episodes of upper respiratory tract infection such as tonsillitis. The aim of this study was attempt to investigate the expression and correlation of IL-4, IFN-γ and FcαRI in tonsillar mononuclear cells under stimulations of α-hemolytic streptococcus (HS) or lipopolysaccharide (LPS) in patients with IgA nephropathy. Methods Tonsillar mononuclear cells isolated from 26 patients with IgAN and 25 patients with chronic tonsillitis (CT) as controls were cultured for 72 h with or without α-hemolytic streptococcus (HS) and lipopolysaccharide (LPS) stimulation. Concentration of IL-4 and IFN-γ level were determined by ELISA. Expression levels of IL-4, IFN-γ and FcαRI mRNA were measured by real-time PCR, respectively. FcαRI expressing cells were tracked by flow cytometry. Results The supernatant concentration of IL-4, IFN-γ and the expression of IL-4, IFN-γ and FcαRI mRNA in the IgA nephropathy group was markedly increased compared with the non-IgAN group. With the stimulation of HS, the production of IL-4 and the FcαRI expressing cells in the IgA nephropathy group was significantly increased than the non-IgAN group, while the secretion of IFN-γ was remarkably decreased in the IgA nephropathy group than the non-IgAN group. Upon the LPS stimulation, the concentration of IL-4, IFN-γ in the supernatant of the IgA nephropathy group was markedly increased compared with the non-IgAN group. However, there wasn’t significant difference in the FcαRI expressing cells between the LPS stimulated IgAN group and the non-IgAN group. The expression of FcαRI is in a negative correlation with IL-4 while positive with IFN-γ. Conclusion The tonsillar mononuclear cells of IgAN may in a state of overactive immune response, which probably can promote the secretion of Th cytokines, involving in the pathogenesis of IgAN.

Background: Urgent-start dialysis is a major problem for incident dialysis population. Urgent start on hemodialysis is associated with an increased risk of infectious or mechanical complications, and its mortality is equal to or higher than that of urgent start on peritoneal dialysis (PD). However, compared to patients starting PD in a planned setting, those on urgent-started PD have an increased risk of mechanical complications and lower technique survival. Methods: In this study, 101 adult incident dialysis patients (≥18 years old) who underwent Tenckhoff catheter implantation were enrolled. All of the patients were grouped according to the urgent PD mode: the intermittent PD (IPD) or automatic PD (APD) group, and patients were followed for 1 year. The paired or independent t test was used to analyze the change of laboratory variables. Pearson chi-square test was applied to compare the short outcome between the 2 groups. Results: When PD was treated for 7 days and 1 month, the APD group has the lower serum potassium and phosphorus levels than the IPD group. The incidence of catheter dysfunction was significantly lower in the APD group. The morbidity of infection associated with PD in the first year was lower in the APD group despite no significant difference existing. The technique survival and patient survival rate have no evident difference between the 2 groups. Conclusion: Compared to IPD, urgent start on APD could reduce the risk of mechanical complication, which could be considered a gentle, safe, and feasible alternative to urgent start on IPD.

To examine levels of M-type phospholipase A2 receptor (PLA2R) and its antibody in the patients with hepatitis B virus-associated membranous nephropathy (HBV-MN), and to explore the correlation of PLA2R with laboratory parameters and pathological characteristics. Methods: A total of 49 adult patients with biopsy-proved HBV-MN were enrolled in this study. Levels of anti-PLA2R antibody in serum and PLA2R in renal tissue were detected. Patients were assigned into two groups: a positive PLA2R group and a negative PLA2R group. Differences in laboratory parameters and pathological characteristics were compared between the two groups. Results: Of 49 patients with HBV-MN, 17 had positive PLA2R expression in renal tissues. In the positive PLA2R group, 10 patients were positive for serum anti-PLA2R antibody. Patients with positive PLA2R expression in renal tissues showed higher levels of 24 hour urinary protein [(4.6±3.9) g/d], serum HbsAg (70.5%) and renal HbsAg expression (71%), while lower level of serum albumin [(24.1±7.5) g/L] than those of the negative group. Conclusion: PLA2R is expressed in the renal tissues and serum anti-PLA2R antibody can be detected in some HBV-MN patients. Positive PLA2R expression in renal tissue might be related to HbsAg deposition in serum and renal tissues. Patients with positive PLA2R expression in renal tissue have more severe glomerular sclerosis.目的：研究M型磷脂酶A2受体(phospholipase A2 receptor，PLA2R)在乙肝病毒相关性膜性肾病(hepatitis B virus-associated membranous nephropathy，HBV-MN)患者血液及肾组织中的表达情况，并探讨肾组织PLA2R阳性表达在乙型肝炎相关性肾小球肾炎(hepatitis B virus associated glomerulone nephritis，HBV-GN)患者中的临床和病理特点。 方法： 选取经肾活检确诊的49例HBV-MN患者。检测血清抗PLA2R抗体以及肾组织PLA2R的表达，将患者分为肾组织PLA2R表达阳性组和阴性组，比较两组间临床指标、病理改变、血抗PLA2R抗体表达水平的差异。结果：17例患者存在肾组织PLA2R阳性表达，其中10例患者血清抗PLA2R抗体阳性。肾组织阳性组较阴性组24 h尿蛋白水平升高，血白蛋白水平下降，血清HbsAg阳性比例更高(70.5%)，肾组织HbsAg表达比例更高(71%)。结论：肾组织PLA2R以及血清抗PLA2R抗体在HBV-MN患者中有一定表达，其表达可能与HBV-MN患者血清以及肾组织中HbsAg沉积有关。肾组织PLA2R阳性患者肾小球慢性损伤可能相对更重。.

Imbalance of Th1/Th2 pro-inflammatory cytokines plays an important role in the development and progression of IgA nephropathy (IgAN). Clinical development and exacerbation of IgAN are frequently preceded by episodes of upper respiratory tract infection, and palatine tonsils represent the predominant immunocompetent tissue of the upper respiratory tract. This study examined tonsillar lymphocytes of IgAN who suffered from tonsillitis (n = 22), and using tonsils derived from patients with chronic tonsillitis (n = 24) but without renal disease as a control. We identified a polarization toward Th2 response in tonsils of IgAN patients. TH0 cells are differentially mobilized during contact sensitization and by adjuvants such as lipopolysaccharide (LPS) that induce T-helper type 1 (Th1) responses, or α-hemolytic streptococcus (HS) that induces T-helper type 2 (Th2) responses. Th1:Th2 ratio is correlated with proteinuria and renal pathologic changes in IgAN group. Our study suggests that IgAN is associated with the change in Th1/Th2 balance in favor of Th2 lymphocytes.

To determine functional and structural alterations of peritoneum and fibrotic cytokines expression in peritoneal dialysis (PD) rats.28 Sprague-Dawley (S-D) rats were randomly divided into four groups and dialyzed with various solutions daily for four weeks: (1) no solution (CON group), (2) 0.9% Saline solution (NS group), (3) 1.5% Dianeal (LG group), (4) 4.25% Dianeal (HG group). Peritoneal equilibration tests, ultrafiltration function and effluent protein quantification were measured. Peritoneum morphology was studied and immunohistochemistry were performed for detection of transforming growth factor β1 (TGF-β1), connective tissue growth factor (CTGF), and fibronectin (FN) proteins. Reverse transcriptional-polymerase chain reaction was used to analyze the expression of TGF-β1, CTGF mRNA.Administration of 4.25% Dianeal caused functional and structural changes of peritoneum, including protein loss through the transport process, decrease of peritoneal solute transport rate and ultrafiltration capacity. The collagen of peritoneum in the HG group was thicker than the other groups. The levels of CTGF, TGF-β1, and FN proteins were significantly the highest in the HG group, followed by the LG group. The liner correlation analysis showed positive correlations between the levels of CTGF, TGF-β1, and FN proteins and the collagen thickness. The expression of TGF-β1 and CTGF mRNA in the HG group were significantly higher than those in the other groups and were indicated positive correlation.Using high glucose peritoneal dialysis solutions in rats may not only lead to processing of peritoneal fibrosis, which is promoted by ectopic expression of TGF-β1, but also increase the expression of CTGF. CTGF is an important fibrotic media of peritoneal fibrosis in PD rats.

Background Mechanical catheter dysfunction caused by omentum entrapment remains a major complication of peritoneal dialysis (PD) therapy. The purpose of this study was to determine the outcomes of omentum folding at the time of primary open catheter insertion. Methods From March 2008 to December 2012, a total of 67 PD subjects were enrolled in the study and randomly assigned to receive either regular open insertion (ROI group, n = 33) or open insertion with omentum folding (OIOF group, n = 34). The primary outcome was defined as PD catheter tip migration with dysfunction. A systematic review was performed to analyze the outcomes of omentum management in PD catheter implantation, based on published data from 1990 to 2013. Results There was no statistical difference in baseline patient characteristics between the ROI and OIOF groups. Nine (27.3%) patients in the ROI group presented with catheter malposition in the late stage (>60 days) of the study, significantly more than in the OIOF group (two; 5.9%) (P = 0.049). Significant differences in catheter survival rate between the two groups were observed in the late stage (P = 0.030) and over the entire study period (P = 0.028). A higher incidence of irreversible catheter dysfunction was shown in the ROI group (15.2%), whereas none occurred in the OIOF group (P = 0.031). No statistical difference was determined in other catheter-related complications or patient survival rate. There were no statistical differences in peritoneal transport characteristics or dialysis adequacy between the two groups upon evaluation at 3, 6 and 12 months. Systemic review of current publications suggested that PD catheter placement with omentum management could lead to less irreversible catheter dysfunction and improved outcome of catheter survival. Conclusions Our data suggest that omentum folding at the initial time of open catheter placement can significantly reduce the risk of catheter tip migration with dysfunction and improve the outcome of the PD technique.

The purpose of the present study was to detect bacterial strains and antibiotic susceptibility in chronic tonsillitis patients with IgA nephropathy (IgAN) and without nephritis, in order to provide evidence for clinical therapy and pathogenesis of IgAN.A total of 53 patients with IgAN (group A) and 53 chronic tonsillitis patients without nephritis (group B) underwent tonsillectomy. The tonsil tissues of patients were collected under sterile condition. The bacteria in the tonsil crypt of patients in both groups were isolated and identified for antibiotic susceptibility test by the manual routine of the laboratory and also with the autoScan/Microscan system.There were bacteria in each specimen in both groups. The bacteria detection rate was 100%, but there was no significant difference between two groups (p 0.05). The 522 strains of bacteria in group A and 494 strains of bacteria in group B were isolated. Streptococcus. Neisseria, Hemophilus parainfluenzae. Staphylococcus. Bacillus proteus and Streptococcus pneumoniae were detected in both groups, but there was no significant difference in the types of bacteria between the two groups (all p 0.05). Alpha streptococcus was the most common in both groups. The antibiotic susceptibility test showed that there was no significant difference in the susceptibility to penicillin, chloramphenicol, macrolides, cephalosporin, gentamicin, amikacin sulphate, norfloxacin, ciprofloxacin, rifampicin and vancomycin between two groups (all p 0.05).Alpha streptococcus in both two groups can be detected and is the most common. There was no significant difference in bacterial strains and antibiotic susceptibility between two groups.

Patients with nephrotic syndrome carry a high risk of pulmonary embolism due to the abnormalities in coagulation and fibrinolysis. Thrombolytic therapy for critical pulmonary embolism in nephrotic syndrome patients was rarely reported and remains controversial in the regimen selection so far. We reported a case of fatal pulmonary embolism, complicating in hepatitis B virus-associated nephrotic syndrome. The patient presented with chest pain, hemoptysis and shortness of breath on admission and his initial vital signs showed a high risk of developing hypotension. Urgent radiological examinations confirmed massive embolisms in bilateral pulmonary arteries. Prompt thrombolytic therapy was performed right after the diagnosis of pulmonary embolism with an intravenous infusion of urokinase (20 000 U/kg) in 2 h. Complete resolution of pulmonary embolism was achieved after urokinase administration and the patient was discharged in good conditions. This report highlighted the efficacy and safety of prompt thrombolytic therapy with urokinase for nephrotic syndrome patients presented with massive pulmonary embolism. In this study, we also briefly discuss the recent findings on the current state of urokinase in the clinical practice of thrombolysis.