Organizing Pneumonia in A Patient Double-Positive for ANCA and Anti-GBM Antibodies: A Case Report.

Both anti-glomerular basement membrane (GBM) disease and the anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are common causes of pulmonary-renal syndrome. Organizing pneumonia (OP), a special pattern of interstitial lung disease, is extremely rare either in AAV or anti-GBM disease. We report an old woman presented with OP on a background of co-presentation with both ANCA and anti-GBM antibodies.

Renal Amyloidosis Secondary to ANCA-Associated Vasculitis: A Case Report.

Renal amyloidosis secondary to anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is extremely rare. Here, we reported a 77-year-old woman with ANCA-associated vasculitis. Renal biopsy with Masson trichrome staining showed pauci-immune crescentic glomerulonephritis, and electron microscopy showed amyloid deposition in the mesangial area. Immunofluorescence revealed kappa light chain and lambda light chain negative. Bone marrow biopsy revealed no clonal plasma cell. Finally, she was diagnosed as ANCA-associated vasculitis with secondary renal amyloid A amyloidosis.

Antiviral treatment and prognosis in patients undergoing maintenance hemodialysis due to hepatitis C virus. / ç»´æŒæ€§è¡€æ¶²é€æžä¸™åž‹è‚ç‚Žç— æ¯’æ„ŸæŸ“æ‚£è€ çš„æŠ—ç— æ¯’æ²»ç–—åŠé¢„åŽ.

OBJECTIVES: Maintenance hemodialysis (MHD) is one of the important renal replacement therapies for patients with end-stage renal disease. Hepatitis C virus (HCV) infection is a serious global public health problem. The proportion of MHD patients complicated with HCV infection and the risk of adverse prognosis are higher than those in the general population. Active antiviral treatment and prevention of reinfection is a combined treatment by nephrology and infection physicians. It is a widely accepted preventive measure to set hemodialysis buffer area for patients in treating HCV infection, but its effectiveness and safety still need to be further explored. Thus, the aim of this study is to explore the antiviral treatment and prognosis of MHD patients with HCV infection during hemodialysis. METHODS: A retrospective analysis for renal disease patients at 10 end-stage with long-term hemodialysis in the HCV area of the Blood Purification Center of Xiangya Hospital, Central South University. After standard antiviral drug treatment, the patient reached the cure standard for HCV infection. The buffer zone was set up in the Blood Purification Center by the Department of Nephrology of Xiangya Hospital since April 2017. Patients cured of HCV infection were transferred from the HCV area to the buffer zone for continuous dialysis, accompanied by monitoring serum HCV-RNA, anti-HCV antibody levels and changes in clinical biochemical indicators following the status of reinfection. RESULTS: Ten patients with HCV infection were finally cured after antiviral treatment, and there were no significant changes in clinical biochemical indicators before and after treatment. In the followed-up period after the transfer, the patient continued to be negative for HCV-RNA and positive for anti-HCV antibody. CONCLUSIONS: Direct antiviral therapy is safe and effective in MHD patients with HCV infection. Active antiviral therapy and transferring to the buffer area for dialysis are new and effective treatment modes for HCV patients during MHD.

Influence of dietary fiber on chronic kidney disease： Base on the gut-kidney axis theory. / åŸºäºŽè‚ -è‚¾è½´ç†è®ºæµ æžè†³é£Ÿçº¤ç»´å¯¹æ ¢æ€§è‚¾ç— çš„å½±å“.

Chronic kidney disease (CKD) can result in alteration of intestinal flora and damage of intestinal barrier function. Intestinal dysbios is contributes to the generation of colon-derived uremic solutes and the translocation of bacteria and endotoxins from gut lumen into the bloodstream, subsequently increasing uremic toxicity and triggering systemic inflammation, which is related to CKD progression and many complications. Studies have revealed that dietary fiber can reduce uremic toxin levels and systemic inflammation in CKD through targeting the "gut-kidney axis". Dietary fiber seems to be a promising measure for CKD treatment.

Synthesis and biocompatibility of an argatroban-modified polysulfone membrane that directly inhibits thrombosis.

Anticoagulation therapy plays a vital role in the prevention of blood clot formation during hemodialysis and hemofiltration, especially for critical care patients. Here, we synthesized a novel argatroban (Arg)-modified polysulfone (PSf) membrane for anticoagulation. Arg was grafted onto the PSF membrane via chemical modification to increase membrane hydrophilicity. Protein adsorption, coagulation, as well as activation of platelets and complement systems were greatly reduced on the Arg-modified PSf membrane. Thus, the recalcification time and the activated partial thrombin time (APTT) were increased after the modification. In comparison with the pristine PSf membrane, the Arg-modified PSf membrane showed better hemocompatibility and anticoagulation properties, indicating its potential for applications in hemodialysis and hemofiltration. Modification of the PSf membrane has been investigated in attempts to further enhance the anticoagulation properties of the hemodialysis membranes, including a heparin-modified PSf membrane. However, heparin can inhibit plasma-free thrombin, and cause the occurrence of heparin-induced thrombocytopenia (HIT), which increases the risk of bleeding during dialysis in critical care patients. To address this problem, we modified PSf membrane with as a novel direct thrombin inhibitors, argatroban (Arg). It can reversibly bind to thrombin, inhibiting not only the plasma-free thrombin in the blood, but also clot-bound thrombin.

High-Flux Hemodialysis Benefits Hemodialysis Patients by Reducing Serum FGF-23 Levels and Reducing Vascular Calcification.

BACKGROUND: High- and low-flux hemodialysis (HFHD and LFHD, respectively) are dialysis procedures designed to eliminate blood toxins that accumulate in end-stage renal disease. HFHD may reduce vascular calcification by removing serum fibroblast growth factor 23 (FGF-23). However, whether HFHD is better than LFHD is still under debate. We therefore compared the efficacy of HFHD and LFHD in controlling FGF-23 and vascular calcification. MATERIAL AND METHODS: Fifty hemodialysis patients were recruited and randomly treated with either HFHD or LFHD. Fasting venous blood was collected at baseline, six months, and twelve months after the treatment. We then measured levels of FGF-23, calcium, phosphorus, parathyroid hormone, and alkaline phosphatase. Further, abdominal lateral radiographs were taken to calculate aorta abdominalis calcification scores (AACs). RESULTS: Compared to the LFHD group, FGF-23 and AACs in the HFHD group significantly decreased after 12 months treatment (p=0.049 and p=0.002, respectively). AACs were positively correlated with FGF-23 in all patients (p=0.004), the HFHD group alone (p=0.040), and the LFHD group alone (p=0.037). We also found that older patients, patients with higher blood phosphorus levels, and higher FGF-23 levels had an increased risk of aorta abdominalis calcification (p=0.048, p=0.003, p=0.001, respectively). HFHD was more able to reduce the risk of aorta abdominalis calcification than LFHD (p=0.003). CONCLUSIONS: FGF-23 is an independent risk factor for the development of vascular calcification. HFHD may benefit hemodialysis patients by reducing serum FGF-23 levels and controlling vascular calcification.

Acute interstitial nephritis caused by ANCA-associated vasculitis: a case based review.

Antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) typically manifests as rapidly progressive glomerulonephritis with crescent formation. In this report, we present a local case of myeloperoxidase (MPO)-AAV-associated acute interstitial nephritis (AIN), showing slight pauci-immune glomerulonephritis and positive MPO-ANCA. This case is characterized by foot process effacement of podocytes in the glomerulus, a favorable prognosis, and an absence of crescentic formation. To further understand this condition, we conducted a comprehensive literature search on Google Scholar and PubMed, employing both free text words and MeSH terms related to "AAV and AIN." This search yielded 24 cases, which we analyzed for their clinical features, laboratory findings, renal pathological characteristics, and therapeutic outcomes. AAV-associated interstitial nephritis predominantly affects elderly patients and is often associated with anemia, proteinuria, hematuria, and nonspecific manifestations, including fever, anorexia, fatigue, edema, and weight loss. Most of the cases in our review were MPO-ANCA-positive and exhibited isolated interstitial inflammation. These patients typically presented with relatively lower levels of serum creatinine, 24-h urine protein levels, and MPO-ANCA titers. All patients in our study received immunosuppressive therapy, including glucocorticoids, immunosuppressants, and rituximab, with the majority achieving clinical remission. Isolated AIN in the context of AAV is a rare occurrence, but it displays distinct clinical, laboratory, and pathological features. Patients with this presentation show a positive response to immunosuppressive treatment. Nevertheless, the establishment of definitive therapy guidelines for AAV-associated AIN remains uncertain and necessitates further investigation to develop comprehensive treatment guidelines. AIN, particularly when lacking typical glomerulus lesions, may represent a novel subgroup within MPO-AAV warranting additional research and clinical attention. Key Points • This study contributes valuable scientific insights by highlighting that MPO-AAV-associated interstitial nephritis, even without crescentic formation, can exhibit podocyte foot process effacement and respond well to treatment. • The presence of AIN, independent of crescentic glomerulonephritis, suggests the potential emergence of a new subclass within MPA-AAV. • Notably, some cases of MPO-AAV-associated AIN may present with normal levels of Scr (Table 5, cases 5, 6, and 17). • This observation highlights the importance of considering renal biopsy, diagnosis, and therapy in a timely manner to prevent the development of chronic kidney disease (CKD).

Rhein inhibits integrin-linked kinase expression and regulates matrix metalloproteinase-9/tissue inhibitor of metalloproteinase-1 ratio in high glucose-induced epithelial-mesenchymal transition of renal tubular cell.

Studies have found overexpressed integrin-linked kinase (ILK) and disturbed matrix metalloproteinase-9/tissue inhibitor of metalloproteinase-1 (MMP-9/TIMP-1) ratio in diabetic nephropathy epithelial-mesenchymal transition (EMT). However, the underlying mechanisms of EMT and the inhibiting effect of rhein need further understanding. The aim of this study was to investigate the possible regulating effects of ILK towards MMP-9/TIMP-1 ratio in EMT and the inhibiting effect of rhein. The characteristic epithelial marker and mesenchymal marker of EMT were examined by cytoimmunostaining, real-time reverse transcription polymerase chain reaction (real-time RT-PCR) and Western blot. To observe the EMT inhibiting effects of rhein, specific ILK-small interfering RNA (ILK-siRNA) was used as a positive control. The results showed that in high glucose conditions, overexpression of ILK and an abnormal changing of MMP-9/TIMP-1 ratio occurred; ILK inhibition by siRNA could adjust MMP-9/TIMP-1 ratio to near normal. Meanwhile, rhein inhibited the overexpressing ILK and inhibits high glucose-induced EMT; the effect was similar to that of ILK-siRNA. The decreased expression of ILK regulated by rhein contributed to the adjustment of the MMP-9/TIMP-1 ratio. Our data indicates that rhein inhibits high glucose-induced-EMT partially through the inhibition of ILK expression and regulates the MMP-9/TIMP-1 ratio in HK-2 cells. This mechanism may be associated with rhein's effect of ILK suppression.

Hemodialysis with a dialyzer loaded with argatroban may be performed in vivo without a systemic anticoagulant.

BACKGROUND/AIMS: Anticoagulation in hemodialysis (HD) patients at high risk of bleeding remains an intractable problem. Simulating endothelial cells by releasing anticoagulant on the membrane may be a promising alternative. METHODS: We modified a polyacrylonitrile (PAN) dialyzer by loading argatroban into its membrane and verified its anticoagulation efficiency and its influence on coagulation markers such as activated partial thromboplastin time (aPTT), D-dimer and thrombin-antithrombin complex (TAT) in an animal HD model. RESULTS: All HD sessions with the argatroban dialyzer were completed successfully with either no or minimal fiber clotting. D-dimer was lower in the argatroban group than in the PAN group; TAT and aPTT values were similar in the two groups, which suggests better anticoagulation and a similar influence on the coagulation system. CONCLUSION: HD with the argatroban dialyzer is feasible, safe and simple, and could be used in patients at high risk of bleeding.

Construction of novel antiplatelet modified polyethersulfone membrane and study into its blood compatibility.

Blood purification therapy is widely used in patients with renal insufficiency and severe infections, where membrane-associated thrombosis is a side effect. How to improve the hemocompatibility of dialysis membranes and reduce thrombosis is a focus of current research, in which platelets play a key role. However, few dialysis membranes that directly inhibit platelets have been developed to date. In this study, a polyethersulfone (PES) membrane was modified with ticagrelor, a platelet P2Y12 receptor inhibitor, and detailed characterization was performed. The ticagrelor modified PES membrane (TMPES) showed good hydrophilicity and anti-protein adsorption and significantly inhibited platelet adhesion, aggregation, and activation, which demonstrated good antithrombotic properties. In addition, the membrane had excellent red blood cell (RBC) compatibility, anticoagulant, and antiinflammatory effects, which demonstrated superior biosafety in cell and animal experiments. Therefore, the TMPES dialysis membrane could have potential in clinical applications.

Identification of Hub Genes Involved in Tubulointerstitial Injury in Diabetic Nephropathy by Bioinformatics Analysis and Experiment Verification.

Diabetic nephropathy (DN) is the most important cause of end-stage renal disease with a poorer prognosis and high economic burdens of medical treatments. It is of great research value and clinical significance to explore potential gene targets of renal tubulointerstitial lesions in DN. To properly identify key genes associated with tubulointerstitial injury of DN, we initially performed a weighted gene coexpression network analysis of the dataset to screen out two nonconserved gene modules (dark orange and dark red). The regulation of oxidative stress-induced intrinsic apoptotic signaling pathway, PI3K-Akt signaling pathway, p38MAPK cascade, and Th1 and Th2 cell differentiation were primarily included in Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of these two modules. Next, 199 differentially expressed genes (DEGs) were identified via the limma package. Then, the GO annotation and KEGG pathways of the DEGs were primarily enriched in extracellular matrix (ECM) organization, epithelial cell migration, cell adhesion molecules (CAMs), NF-kappa B signaling pathway, and ECM-receptor interaction. Gene set enrichment analysis showed that in the DN group, the interaction of ECM-receptor, CAMs, the interaction of cytokine-cytokine receptor, and complement and coagulation cascade pathways were significantly activated. Eleven key genes, including ALB, ANXA1, ANXA2, C3, CCL2, CLU, EGF, FOS, PLG, TIMP1, and VCAM1, were selected by constructing a protein-protein interaction network, and expression validation, ECM-related pathways, and glomerular filtration rate correlation analysis were performed in the validated dataset. The upregulated expression of hub genes ANXA2 and FOS was verified by real-time quantitative PCR in HK-2 cells treated with high glucose. This study revealed potential regulatory mechanisms of renal tubulointerstitial damage and highlighted the crucial role of extracellular matrix in DN, which may promote the identification of new biomarkers and therapeutic targets.

Immobilizing argatroban and mPEG-NH2 on a polyethersulfone membrane surface to prepare an effective nonthrombogenic biointerface.

Systemic anticoagulation is not suitable for hemodialysis (HD) patients with a high risk of bleeding in the clinic. An HD membrane that provides a localized anticoagulation membrane surface may be a promising strategy to solve this intractable problem for HD patients. Herein, we modified a nonthrombogenic polyethersulfone (PES) dialyzer membrane by grafting argatroban (AG) and methoxy polyethylene glycol amine (mPEG-NH2) via a polydopamine (PDA) strategy. The PES substrates were immersed in an alkaline dopamine solution for 24 h, and then, AG and mPEG-NH2 were sequentially grafted covalently onto the resultant membrane. Attenuated total reflection-Fourier transform infrared spectroscopy (ATR-FTIR) and X-ray photoelectron spectroscopy (XPS) were utilized to confirm the successful introduction of PDA and the immobilization of AG and mPEG-NH2. Scanning electron microscopy (SEM) and atomic force microscopy (AFM) were used to observe the surface structure and morphology after the surface modification. The excellent antithrombotic abilities of the modified membrane were demonstrated by the suppression of platelet adhesion and activation, prolongation of clotting times, and inhibition of thrombin generation and complement activation. This work describes an efficient and convenient method to immobilize AG and mPEG-NH2 to create a nonthrombogenic biointerface for blood-contacting devices such as HD membranes.

Acute Peritoneal Dialysis System for Neonates with Acute Kidney Injury Requiring Renal Replacement Therapy: A Case Series.

BACKGROUND: Acute kidney injury (AKI) is common in critically ill neonates, and peritoneal dialysis (PD) can be a lifesaving option. In China, however, much of the equipment for PD in neonates is not available. We describe results with a novel system for PD, which has been developed locally to improve access to therapy and care for critically ill neonates requiring PD in China. METHODS: The system comprises a 14-gauge single-lumen central venous catheter serving as a PD catheter, inserted by Seldinger technique, with an adapted twin bag PD system. Ten neonates with AKI were treated using the novel PD system. RESULTS: The 10 patients ranged in age from 1 day to 22 days, with bodyweights between 700 g and 3,300 g. Average time to renal function recovery was between 14 and 96 hours. Complications related to the novel PD system included leak (n = 1), catheter displacement (n = 1), and catheter obstruction (n = 1). There were no complications related to insertion, no cases of peritonitis or exit-site infection, and no subsequent hernias. A comparison of costs indicated that the novel PD system is less expensive than conventional systems involving open insertion of Tenckhoff catheters. CONCLUSIONS: Peritoneal dialysis using the novel PD system is simple, safe, and effective for suitable neonates with AKI in China.

miR302a-3p May Modulate Renal Epithelial-Mesenchymal Transition in Diabetic Kidney Disease by Targeting ZEB1.

BACKGROUND: Recent study found that microRNA (miRNA) are involved in diabetic kidney disease (DKD). The objective of this study is to determine the role of miR302a-3p in the process of renal epithelial-mesenchymal transition (EMT) in DKD. METHODS: The miRNA expression profiling of the cell line stimulated by high glucose was performed by a microarray analysis. Then real-time polymerase chain reaction (PCR) were used to determine the expression of one of the miRNAs significantly upregulated in cell line stimulated by high glucose, miR302a-3p. miR302a-3p mimics and inhibitor were transfected to HK-2 cells following exposure to high glucose and normal glucose, respectively. The expressions of E-cadherin, vimentin, and Zinc finger E-box-binding protein 1 (ZEB-1) were determined by real-time PCR and Western blot. Finally, the levels of miR302a-3p in the plasma of DKD patients were detected by real-time PCR, and then the relationship of miR302a-3p and urinary albumin excretion (UAE) or estimated glomerular filtration rate (eGFR) was analyzed. RESULTS: The expression of miR-302a-3p, 513a-5p, 1291 and the other 17 miRNA were increased significantly in HK-2 cell line after high glucose stimulation; on the other hand, miRNA490-3p, 638, 3203 and the other 19 miRNA were decreased significantly. In vitro, miR-302a-3p expression in HG group increased at 6 h and ascended to the highest level at 12 and 24 h and then gradually decreased from 48 to 72 h. More interesting, ZEB1 protein expression had an opposite change, which gradually decreased from 6 to 24 h and then gradually increased from 48 to 72 h. Moreover, overexpression of miR-302a-3p suppressed expression of ZEB1 in the post-transcriptional level and reversed high glucose-mediated downregulation of E-cadherin and upregulation of vimentin. Meanwhile, loss of miR-302a-3p expression can lead to EMT of HK-2 cells just as high glucose stimulation. Further study demonstrated that the expression of circulating miR-302a-3p was significantly increased in the diabetes mellitus (DM) with normoalbuminuria (DM group, n = 22) compared with control (healthy persons, n = 30) and then decreased in DM with microalbuminuria (DNE group, n = 20). Furthermore, its expression in DM with macroalbuminuria (DNC group, n = 18) was decreased significantly compared with DM group. Circulating miR-302a-3p had negative relevance with UAE in DNE group (r = -0.649, p = 0.002) and DNC group (r = -0.681, p = 0.006). Circulating miR-302a-3p had positive relevance with eGFR in DNC group (r = 0.486, p = 0.041). CONCLUSIONS: These findings suggest that miR-302a-3p may play a protective role by targeting ZEB1 in renal EMT in DKD. In view of these findings, it is conceivable that miR-302a-3p may serve as a potential novel target in pre-EMT states for the amelioration renal fibrosis seen in DKD.

[Effect of integrin-linked kinase on renal tubular epithelial cell transdifferentiation in diabetic rats].

OBJECTIVE: To determine the effect of integrin-linked kinase(ILK) in renal tubular epithelial cells and its relation to tubular epithelial-myofibroblast transdifferentiation. METHODS: Wistar rats were randomly divided into 3 groups, Group normal control (n=10), Group diabetic without therapy(n=10) and Group diabetic with Losartan 20mg/(kg . d)(n=10). Five rats were killed in each group at the 8th and 16th week. The left kidneys were kept for HE and Masson staining to observe the pathological variations in the renal interstitium. ILK, alpha-SMA and Vimentin in renal tubular epithelial cells were detected by immunohistochemistry analysis. RESULTS: Compared with the control group, ILK, alpha-SMA and Vimentin in renal tubular epithelial cells in Group diabetes gradually increased in immunohistochemistry (P<0.01); ILK was consistent with the pathological variation of renal interstitium and was positively correlated to alpha-SMA(rs=0.621, P<0.05). In comparison with the Group diabetes, the expression of ILK, alpha-SMA and Vimentin in renal tubular epithelial cells was apparently declined (P<0.01) in Group diabetes with Losartan. CONCLUSION: Tubular epithelial myofibroblast transdifferentiation and the over-expression of ILK, between which there may be significant connections, are important events in the progression of diabetic nephropathy. Losartan, a blocker of angiotension II type I receptor, which may down-regulate the expression of ILK in diabetic renal tubular epithelial cells, can restrain the procession of epithelial-myofibroblast transdifferentiation.

Thrombotic complications and tip position of transjugular chronic dialysis catheter scheduled into superior vena cava: Findings on HR-MRCP and HR-T2WI.

BACKGROUND: Catheter-related thrombotic complications(TCs) can occur during the long term use of a chronic dialysis catheter (CDC), including fibrin sheath (FS), mural thrombosis (MT), venous thrombosis (VT), and intraluminal clots (IC), which has not been reported with MRI. The aim of our study was to evaluate the determination of catheter tip position (TP) and resolution of TCs in patients with transjugular CDC scheduled into the superior vena cava using high resolution magnetic resonance cholangiopancreatography (HR-MRCP) and T2-weighted imaging (HR-T2WI). METHODS: The study protocol was approved by the local Research Ethics Committee. Informed consent was obtained from all patients. In total, 41 consecutively enrolled transjugular CDC patients with suspected catheter dysfunction were scanned with HRMRCP and HR-T2WI. The distance from the top to the tip of the catheter and the presence and nature of catheter TCs were assessed by 2 experienced radiologists. Chest x-ray was taken within 1 to 2 days and CDC was withdrawn within 3 to 10 days from those patients with TCs identified by HR-MRI. RESULTS: A total of 38 subjects successfully underwent HR-MRI, including 13 normal and 25 with TCs (fibrin sheath [FS]: n = 21, mural thrombosis [MT]: n = 7, venous thrombosis [VT]: n = 3, intraluminal clots [IC]: n = 4). There was no significant difference between HR-MRCP and chest x-ray in catheter TP determination (P = .124). Normal catheter appeared as "double eyes" on HR-T2WI and "double tracks" on HR-MRCP. TCs appeared as follows: FS displayed as a "thin ring" (<1mm) around the catheter, MT as patchy hyperintensity and VT as a "thick ring" (>5mm) on HR-T2WI. Unilateral IC appeared as a "single eye" on HR-T2WI and a "single track" on HR-MRCP (n = 3). Bilateral IC appeared as neither "eye" nor "track" (n = 1). Catheter withdrawal confirmed FS (n = 16), MT (n = 6), VT (n = 1), and IC (n = 4). CONCLUSION: HR-MRCP and HR-T2WI are promising methods for visualizing TP and TCs in CDC patients, and are helpful in adjusting the treatment plan and avoiding the risk of pulmonary embolism.

Level of asymmetric dimethylarginine and carotid atherosclerosis in patients with chronic kidney disease.

OBJECTIVE: To determine the association between asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase, with atherosclerosis in patients with chronic kidney disease (CKD). METHODS: One hundred thirty-eight CKD patients were enrolled in this study. Serum levels of L-arginine, ADMA, and SDMA were measured by high-performance liquid chromatography (HPLC). Common carotid arteries intimae-medial thickness (CCA-IMT), cross-sectional calculated intimae-medial thickness (cIM area) and atherosclerotic plaque were detected by noninvasive high-resolution B-mode ultrasonography. RESULTS: Serum levels of ADMA and SDMA were significantly increased in CKD patients (n=138) compared with age matched healthy subjects (n=42, P<0.01). ADMA and SDMA levels increased with the progression of renal dysfunction and were negatively related to creatinine clearance (Ccr) in pre-dialysis patients (r=-0.315, P<0.05; r=-0.426, P<0.01). Serum levels of ADMA and SDMA in dialysis patients (n=74) were significantly higher than those in pre-dialysis patients (P<0.05). Patients with carotid artery plaques showed significantly higher levels of ADMA compared with those without plaques. Serum levels of ADMA closely correlated with the mean IMT (r=0.471, P<0.01) and cIM area value (r=0.430, P<0.01). These correlations remained significant even after adjusting GFR, age, gender ,and other risk factors for atherosclerosis in the multiple regression analysis. CONCLUSION: Serum levels of ADMA increased with the progression of CKD and may play a role in the pathogenesis of accelerated atherosclerosis in CKD patients.

Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer.

Prostate cancer is a common malignant tumor in urinary system. Curcumin has curative effect on many kinds of cancers and can inhibit prostate cancer (PC)-3 cells proliferation. This study aimed to explore the curcumin induced prostate cancer cell apoptosis and apoptosis related proteins Bcl-2 and Bax expression. PC-3 cells were injected subcutaneously to the nude mice to establish the tumor model. The nude mice were randomly divided into group C (normal saline), group B (6% polyethylene glycol and 6% anhydrous ethanol), group H, M, L (100 mg/kg, 50 mg/kg, and 25 mg/kg curcumin). The tumor volume was measured every 6 days to draw the tumor growth curve. The mice were killed at the 30(th) day after injection to weight the tumor. TUNEL assay was applied to determine cell apoptosis. Immunohistochemistry was used to detect Bcl-2 and Bax expression. The tumor volume and weight in group H, M, L were significantly lower than the control group (C, B) (P<0.05), and the inhibitory rate increased following the curcumin dose increase. Compared with the control group, Bcl-2 expression in group H, M, L gradually decreased, while Bax protein expression increased (P<0.05). The cell apoptosis rate showed no statistical difference between group B and C, while it increased in curcumin group H, M, and L (P<0.05). Curcumin could inhibit PC-3 growth, decrease tumor volume, reduce tumor weight, and induce cell apoptosis under the skin of nude mice by up-regulating Bax and down-regulating Bcl-2.