Chronic kidney disease promotes chronic inflammation in visceral white adipose tissue.

White adipose tissue plays an important role in the development of metabolic disturbance, which is a common feature in patients with chronic kidney disease (CKD). The effect of CKD on white adipose tissue remains poorly appreciated. Here, we evaluated the inflammatory potential of visceral white adipose tissue in a rat model of CKD.

[Analysis of pregnancy outcomes in 66 patients with systemic lupus erythematosus].

Objective: To analyze the outcomes of pregnancies in women with systemic lupus erythematosus (SLE) and the risk factors affecting the outcomes.

Methods: The data of SLE patients with pregnancy admitted from October, 2006 and September, 2015 were analyzed for assessing the maternal and fetal outcomes and complications. Their risk factors affecting the outcomes of the pregnancies were analyzed.

Enhanced M1 and Impaired M2 Macrophage Polarization and Reduced Mitochondrial Biogenesis via Inhibition of AMP Kinase in Chronic Kidney Disease.

Background: Macrophage polarization plays a pivotal role in the process of inflammation which is common in chronic kidney disease (CKD). Macrophages polarization under the condition of CKD remains poorly understood. Here we tested the hypothesis that CKD promotes macrophage M1 polarization.

The effect of inhibition of endoplasmic reticulum stress on lipolysis in white adipose tissue in a rat model of chronic kidney disease.

Aim: Lipolysis in fat tissue plays an important role in the development of metabolic disturbances, a characteristic feature of chronic kidney disease (CKD). In the present study, we tested the hypothesis that the inhibition of endoplasmic reticulum (ER) stress could alleviate lipolysis in white adipose tissue in a rat model of CKD.

Methods: A rat model of CKD was established by a method of reduced renal mass (RRM).

Current pattern of Chinese dialysis units: a cohort study in a representative sample of units.

Background: Understanding the characteristics of Chinese dialysis patients and the current practice trends is the first step to evaluate the association between practice pattern and outcome in these populations. In the present study, we evaluated the status of medical treatment and characteristic features of chronic dialysis patients in China.

Methods: Through a clustering sampling, we selected 9 centers from the largest dialysis facilities in 6 cities around China.

Vascular insulin resistance related to endoplasmic reticulum stress in aortas from a rat model of chronic kidney disease.

Metabolic insulin resistance has been demonstrated in patients with nondiabetic chronic kidney disease (CKD), yet their vascular insulin signaling remains poorly understood. Here we tested the hypothesis that vascular insulin signaling was impaired and related with endoplasmic reticulum (ER) stress in aortas from the reduced renal mass (RRM) model of CKD. The activity of insulin signaling and markers of ER were determined in aortas from rats with RRM and cultured human umbilical vein endothelial cells.

Changes in pathological pattern and treatment regimens based on repeat renal biopsy in lupus nephritis.

Background: Relapses occur frequently in patients with lupus nephritis. Renal biopsy is the gold standard for assessing renal activity and hence guiding the treatment. Whether repeat renal biopsy is helpful during flares of lupus nephritis remains inconclusive.

VEGF ameliorates tubulointerstitial fibrosis in unilateral ureteral obstruction mice via inhibition of epithelial-mesenchymal transition.

Aim: Vascular endothelial growth factor (VEGF) has been shown to be a survival factor for renal tubular epithelial cells. In the present study, we investigated whether administration of VEGF ameliorates tubulointerstitial fibrosis in a mouse model of unilateral ureteral obstruction (UUO).

Methods: Thirty-six male CD-1 mice were randomly divided into three groups: sham-operation, UUO and UUO+VEGF group.

Advanced oxidation protein products induce inflammatory response and insulin resistance in cultured adipocytes via induction of endoplasmic reticulum stress.

Accumulation of advanced oxidation protein products (AOPPs) is prevalent in metabolic syndrome and type 2 diabetes. Adipocyte dysfunction has been recognized as a link between these conditions. To examine the effect of AOPPs on adipocyte perturbation, 3T3-L1 adipocytes were treated with increased levels of AOPPs as seen in these conditions.

Advanced oxidation protein products inhibit differentiation and activate inflammation in 3T3-L1 preadipocytes.

Accumulation of advanced oxidation protein products (AOPPs) is prevalent in metabolic syndromes, a condition with impaired preadipocytes differentiation. In the present study, we tested the hypothesis that AOPPs disturb preadipocyte differentiation. Exposure of 3T3-L1 preadipocytes to increased levels of AOPPs inhibited accumulation of intracellular triglyceride and decreased the expression of the essential markers of matured adipocytes, such as adipocyte fatty-acid-binding protein (aP2), CAAT/enhancer-binding protein (C/EBP)-alpha, and peroxisome proliferator-activated receptor (PPAR)-gamma, in response to standard adipogenic induction.

Optimal dose of angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker for renoprotection.

Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II type 1 receptor blockers (ARB) have become the cornerstone in the treatment of chronic kidney disease (CKD), as numerous lines of evidence have shown that these agents have a blood pressure lowing independent anti-proteinuric effect. However, despite the benefits of ACEI or ARB therapy, a substantial proportion of patients still experience renal morbidity and mortality. Considering the prognostic impact of proteinuria reduction, it is currently assumed that titration of ACEI or ARB for optimal anti-proteinuric effect would be a logical step towards improvement of renoprotection.

Advanced oxidation protein products decrease expression of nephrin and podocin in podocytes via ROS-dependent activation of p38 MAPK.

Accumulation of plasma advanced oxidation protein products (AOPPs) promotes progression of proteinuria and glomerulosclerosis. To investigate the molecular basis of AOPPs-induced proteinuria, normal Sprague-Dawley rats were treated with AOPPs-modified rat serum albumin. The expression of glomerular podocyte slit diaphragm (PSD)-associated proteins, nephrin and podocin, was significantly decreased coincident with the onset of albuminuria in rats treated with AOPPs.

[Estrogen reduces the expressions of ryanodine receptor type 1 and Cav1.3 L-type calcium channel in the vaginal smooth muscle cells of rats].

Objective: To determine the expressions of ryanodine receptor type 1 (RyR1) and Cav1.3 L-type calcium channel (Cav1.3) in the vaginal smooth muscle cells of castrated rats and investigate the correlation of RyR1 and Cav1.

Asymmetrical dimethylarginine triggers lipolysis and inflammatory response via induction of endoplasmic reticulum stress in cultured adipocytes.

Protein energy wasting, a state of decreased stores of body protein and fat, is a risk factor for mortality in advanced chronic kidney disease (CKD). Little is known about the mechanism underlying loss of fat in CKD. Accumulation of asymmetric dimethylarginine (ADMA) is prevalent in advanced CKD.

Inhibition of tubulointerstitial fibrosis by pentoxifylline is associated with improvement of vascular endothelial growth factor expression.

Aim: Recent information indicates that pentoxifylline (PTX) has the ability to suppress inflammation and profibrotic cell proliferation. In this study, we investigated the effect of PTX on tubulointerstitial fibrosis and the expression of vascular endothelial growth factor (VEGF) in a rat model of obstructive nephropathy.

Methods: Wistar rats with left ureteral ligation were divided into control and PTX-treated groups.

Advanced oxidation protein products induce mesangial cell perturbation through PKC-dependent activation of NADPH oxidase.

Mesangial deposition of extracellular matrix (ECM) is a hallmark of several glomerular diseases including diabetic nephropathy. Accumulation of advanced oxidation protein products (AOPPs) has been found in diabetes and chronic kidney disease and linked to mesangial ECM deposition and progressive glomerulosclerosis in these disorders. Although emerging evidence implicates AOPPs as the renal pathogenic factors, the underlying mechanisms have not been investigated.

1,25-Dihydroxyvitamin D improved the free fatty-acid-induced insulin resistance in cultured C2C12 cells.

Background: Epidemiological evidence has indicated that vitamin D deficiency increased the risk of insulin resistance in metabolic syndrome. The present study was conducted to test the hypothesis that 1,25-dihydroxyvitamin D may improve the free fatty-acid (FFA)-induced insulin resistance in muscle cells.

Method: The insulin resistance of muscle cell model was established by treatment of FFA in differentiated C2C12 cells.

[Effect of bone morphogenetic protein-7 on monocyte chemoattractant protein-1 induced epithelial-myofibroblast transition and TGF-beta1-Smad 3 signaling pathway of HKC cells].

Objective: To examine the effect of Bone Morphogenetic protein-7 (BMP-7) on Monocyte chemoattractant protein-1 (MCP-1) induced epithelial-myofibroblast transition (EMT) in cultured renal proximal tubular cells (HK-2) and the relationship between TGF-beta1-smad 3 expressions and MCP-1 induced EMT.

Methods: The cultured HK-2 cells were divided into six groups: a, negative control, b, treated with TGF-beta1 (5 ng/ml) as positive control, c, treated with MCP-1 (0.1, 1, 10, 50 ng/ml), d, treated with BMP-7 (0.

[Altered expression of vascular endothelial growth factor and its receptors in transdifferentiated human proximal tubular epithelial cells induced by transforming growth factor beta1].

Objective: To examine the expression of vascular endothelial growth factor (VEGF) and its receptors (VEGFR1, VEGFR2) in transdifferentiated human proximal tubular epithelial (HK-2) cell induced by transforming growth factor beta1 (TGFbeta1).

Methods: The transdifferentiation of HK-2 cells was detected by evaluation of expression of alpha-SMA by cytoimmunochemistry and RT-PCR. The VEGF mRNA was evaluated with RT-PCR.

[Effect of BMP-7 on the transdifferentiation of cultured human tubular epithelial cell induced by TGF-beta1].

Objective: To observe the effect of bone morphogenetic protein-7 (BMP-7) on the transdifferentiation of cultured human tubular epithelial cell (HKC) induced by TGF-beta1 and to elucidate its possible mechanism.

Methods: The cultured HKC cells were divided into 5 groups: serum-free group (negative control); single TGF-beta1 treated group (positive control); single BMP-7 treated group; combined TGF-beta1 and BMP-7 treated group; and BMP-7 pre-treated group. Expression of keratin of HKC cells was assessed by indirect enzyme immunohistochemistry (IEI), expression of alpha-smooth muscle actin (alpha-SMA) and E-cadherin by immunohistological method, percentage of alpha-SMA positive HKC cells by flow cytometry, and mRNA expression of alpha-SMA, TGF-beta1, and TGF-beta type II receptor by reverse transcription PCR.