Expression of Galectin⁃3 in peritoneal dialysate and its clinical significance / 安徽医科大学学报

Objective @#To observe the expression of Galectin⁃3 in peritoneal dialysis ( PD) fluid in patients with different dialysis ages , and to conduct correlation analysis with vascular endothelial growth factor ( VEGF) , fibronectin (FN) and related clinical indicators . @*Methods @#A total of 109 PD patients who were regularly followed up in the department of nephrology were divided into four groups according to different peritoneal dialysis ages . The concentrations of Galectin⁃3 , VEGF and FN were determined by enzyme⁃linked immunosorbent assay . The expression of Galectin⁃3 in peritoneal dialysate of the 4 groups was compared , the correlation with VEGF , FN and clinical related indexes was analyzed , and the correlation was analyzed by Spearman test . @*Results @# The concentration of VEGF in peritoneal dialysis patients in group D significantly increased ( P < 0. 05 ) . Galectin⁃3 expression levels were positively correlated with VEGF ( r = 0. 358 , P = 0. 022) , but not significantly correlated with FN ( r = 0. 121 , P = 0. 452) . Galectin⁃3 was positively correlated with clinical indicators parathyroid hormone (PTH) ( r = 0. 201 , P = 0. 037) , C ⁃reactive protein (CRP) ( r = 0. 357 , P < 0. 001) , left ventricular posterior wall dimensions ( LVPWD) ( r = 0. 213 , P = 0. 026) , and negatively correlated with clinical indicators total cholesterol (TC) ( r = - 0. 316 , P = 0. 001) . @*Conclusion @#The concentration of Galectin⁃3 in the dialysate of long⁃term peritoneal dialysis patients is significantly elevated , indicating that the expression of galectin⁃3 increases with the extension of peritoneal dialysis time , suggesting that the detection of galectin⁃3 levels may be helpful for the evaluation of early peritoneal fibrosis . The positive correlation with VEGF may suggest its role in promoting peritoneal angiogenesis and fibrosis . Moreover , it is positively correlated with clinical indicators PTH , CRP and LVPWD , suggesting that it has certain clinical guiding significance on microinflammatory state and myocardial remodeling .

Different calcium ion concentrations affect epithelial mesenchymal transformation of human peritoneal mesothelial cells via endoplasmic reticulum stress / 中华危重病急救医学

Objective:To study the effects of different calcium ion concentrations on epithelial mesenchymal transformation (EMT) of human peritoneal mesothelial cell (HPMC) via endoplasmic reticulum stress (ERS).Methods:HPMC cell line HMrSV5 was cultured in vitro and treated in groups. The cells in the control group, high calcium group 1, and high calcium group 2 were treated with medium containing calcium ion concentrations of 1.25, 1.75, and 2.25 mmol/L, respectively. The solvent control group was treated with medium containing 1.25 mmol/L physiological calcium ion concentration and 0.1% dimethyl sulfoxide (DMSO), the high calcium+solvent group was treated with medium containing 2.25 mmol/L calcium ion concentration and 0.1% DMSO, the high calcium+4-phenylbutyric acid (4-PBA) group was treated with medium containing 2.25 mmol/L calcium ion concentration and 1 mmol/L ERS inhibitor 4-PBA, and each group was treated for 48 hours. Morphological changes of cells in each group were observed under light microscope. The expressions of epithelial cell phenotype marker zonula occluden-1 (ZO-1) and mesenchymal cell phenotype marker α-smooth muscle actin (α-SMA) in the cells were observed by immunofluorescence staining. The expressions of EMT marker genes E-cadherin, ZO-1, α-SMA and Vimentin were detected by fluorescence quantitative polymerase chain reaction (PCR). The expressions of ERS marker proteins phosphorylated protein kinase R-like endoplasmic reticulum kinase (p-PERK), phosphorylated eukaryotic initiation factor 2α (p-eIF2α), transcription activating factor 4 (ATF4) and C/EBP homologous protein (CHOP) were detected by Western blotting. Results:Compared with the control group, the morphology of HMrSV5 cells became slender and fibrotic, the fluorescence intensity of ZO-1 increased, and the fluorescence intensity of α-SMA decreased in high calcium 1 and high calcium 2 groups, indicating that the cells transformed from epithelial cells to mesenchyme cells. The mRNA expressions of E-cadherin and ZO-1 were significantly decreased, while the mRNA expressions of α-SMA and Vimentin and the protein expressions of p-PERK, p-eIF2α, ATF4 and CHOP were significantly increased, moreover, the expressions of the above marker genes or proteins in the high calcium 2 group was more obvious than those in the high calcium 1 group [E-cadherin mRNA (2 -ΔΔCt): 0.53±0.05 vs. 0.75±0.09, ZO-1 mRNA (2 -ΔΔCt): 0.42±0.06 vs. 0.69±0.06, α-SMA mRNA (2 -ΔΔCt): 1.81±0.16 vs. 1.32±0.14, Vimentin mRNA (2 -ΔΔCt): 2.05±0.22 vs. 1.48±0.16, p-PERK protein (p-PERK/β-actin): 0.81±0.09 vs. 0.59±0.06, p-eIF2α protein (p-eIF2α/β-actin): 0.87±0.10 vs. 0.50±0.06, ATF4 protein (ATF4/β-actin): 0.93±0.10 vs. 0.72±0.06, CHOP protein (CHOP/β-actin): 0.79±0.09 vs. 0.46±0.04, all P < 0.05]. Compared with the solvent control group, the morphological changes of cells, the expressions of EMT marker genes and ERS marker proteins after high calcium ion concentration of 2.25 mmol/L were consistent with those in the high calcium 2 group than control group. Compared with the high calcium+solvent group, the cell morphology recovered the characteristics of polygonal and pebble-like epithelial cells in the high calcium+4-PBA group, the fluorescence intensity of ZO-1 increased, the fluorescence intensity of α-SMA decreased, and the mRNA expressions of E-cadherin and ZO-1 in the cells were significantly increased [E-cadherin mRNA (2 -ΔΔCt): 0.86±0.09 vs. 0.57±0.04, ZO-1 mRNA (2 -ΔΔCt): 0.81±0.06 vs. 0.48±0.05, both P < 0.05], the mRNA expressions of α-SMA and Vimentin and the protein expressions of p-PERK, p-eIF2α, ATF4 and CHOP were significantly decreased [α-SMA mRNA (2 -ΔΔCt): 1.21±0.13 vs. 1.77±0.15, Vimentin mRNA (2 -ΔΔCt): 1.30±0.14 vs. 1.94±0.20, p-PERK protein (p-PERK/β-actin): 0.38±0.04 vs. 0.92±0.11, p-eIF2α protein (p-eIF2α/β-actin): 0.34±0.05 vs. 1.05±0.13, ATF4 protein (ATF4/β-actin): 0.57±0.06 vs. 0.97±0.11, CHOP protein (CHOP/β-actin): 0.51±0.04 vs. 0.90±0.12, all P < 0.05]. Conclusion:High calcium ion concentrations of 1.75 mmol/L and 2.25 mmol/L promote EMT of HPMC via activating ERS.

Targeting STAT3 alleviates peritoneal fibrosis by regulating glycolysis and mesothelial-mesenchymal transition / 安徽医科大学学报

Objective @#To study the effect and mechanism of high glucose on mesothelial-mesenchymal transition (MMT) of peritoneal mesothelial cells (HMrSV5) , and the protective effect of pharmacological blocking of signal transducer and activator of transcription 3 (STAT3) on rat peritoneal fibrosis (PF) model . @*Methods @#The animals were divided into three groups : the sham group , the model group , and the STAT3 inhibitor group . A miniature per- itoneal dialysis catheter was implanted under the dorsal skin of rat and the rat peritoneal fibrosis model was induced by daily injection of high glucose dialysate . After 10 weeks , HE staining was used to evaluate the histology of the peritoneum , and the level of transforming growth factor-β1 (TGF-β1) in the peritoneum was measured by immuno- histochemistry . HMrSV5 was cultured in high glucose and the optimal stimulation concentration of high glucose was determined by Western blot. High glucose was used to stimulate HMrSV5 after successful transfection with si - STAT3 and Western blot was used to measure the protein level of STAT3 , p-STAT3 , and the key enzymes of glycol- ysis 6-phosphofructo-2-kinase/fructose-2 , 6-biphosphatase 3 (PFKFB3) and lactate dehydrogenase A (LDHA) .@*Results @#HE staining showed that administration of STAT3 inhibitor ( BP-1-102) could inhibit the thickening of subperitoneal tissue and the proliferation of vessels in HG dialysis rats . The expression of TGF-β1 in the rats perito- neum of the model group was significantly higher than that in the sham group , and the level of TGF-β1 was marked- ly lower in the STAT3 inhibitor group compared to the model group (P < 0. 05) . Compared to the control group , high glucose induced the up-regulation of α-smooth muscle actin ( α-SMA) , the down-regulation of E-cadherin and STAT3 activation in HMrSV5 (P < 0. 05) . Mesothelial cells treated with high glucose also exhibited high expres- sion of the key enzymes of glycolysis ( PFKFB3 , LDHA) ( P < 0. 05) , and si-STAT3 can effectively inhibit the overexpression of PFKFB3 and LDHA induced by high glucose ( P < 0. 05) . @*Conclusion @#STAT3 is involved in high glucose-induced HMrSV5 hyperglycolysis and MMT , and targeting STAT3 alleviates peritoneal fibrosis and an- giogenesis during peritoneal dialysis treatment in rats .

Intervention of modified Shenling Baizhu San on peritoneal fibrosis induced by peritoneal dialysate with different sugar concentration in rats / 中华危重病急救医学

Objective:To investigate the effect of modified Shenling Baizhu San on the pathological changes and extracellular matrix (ECM) in rats with peritoneal fibrosis induced by peritoneal dialysate fluid (PDF) with different sugar concentration and its mechanism.Methods:Seventy male Sprague-Dawley (SD) rats were randomly divided into control group, different sugar content PDF model groups and corresponding traditional Chinese medicine intervention groups, with 10 rats in each group. Peritoneal fibrosis model was reproduced by intraperitoneal injection of 100 mL·kg -1·d -1 PDF containing 1.5%, 2.5% and 4.25% sugar once a day for 8 weeks. The rats in the control group were given the same amount of normal saline. The rats in the traditional Chinese medicine intervention groups were treated with gavage of 10 mL/kg of modified Shenling Baizhu San (containing 2.014 g crude drug per liter) immediately after modeling. The PDF model groups and the control group were given the same amount of normal saline by gavage. After 8 weeks, the peritoneal ultrafiltration volume of rats in each group was measured. The peritoneal tissues were collected and stained with hematoxylin-eosin (HE), and the structural changes and thickness of the parietal peritoneum were observed under a light microscope. After Masson staining, the deposition of collagen fibers was observed under a light microscope. Western blotting was used to detect the protein expressions of E-cadherin,?α-smooth muscle actin (α-SMA) and Vimentin, the main components of ECM in parietal peritoneum. The positive expressions of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), and transforming growth factor-β1 (TGF-β1) were detected by immunohistochemical staining. Results:Compared with the control group, PDF with different sugar contents could induce peritoneal fibrosis in rats, and the degree of fibrosis was gradually aggravated with the increase of sugar content, which was manifested as peritoneal thickening, increased collagen fiber deposition, decreased peritoneal ultrafiltration volume, down-regulated expressions of E-cadherin and MMP-9 in peritoneal tissue, and up-regulated expressions of α-SMA, Vimentin, TIMP-1 and TGF-β1, and the pathological changes and ECM accumulation in peritoneal tissues were more serious in 4.25% PDF model group. After the intervention of modified Shenling Baizhu San, compared with the corresponding PDF model groups, the peritoneal fibrosis of rats was improved to varying degrees, and the effect of the 4.25% PDF+traditional Chinese medicine intervention group was more significant, the parietal peritoneum was significantly thinner (μm: 101.86±16.01 vs. 140.65±10.13, P < 0.05), collagen fiber deposition was significantly reduced, peritoneal ultrafiltration volume was significantly increased (mL: -0.01±3.45 vs. -3.53±1.84, P < 0.05), the expressions of E-cadherin and MMP-9 in peritoneal tissues were significantly up-regulated [E-cadherin protein (E-cadherin/β-actin): 0.84±0.08 vs. 0.28±0.05, MMP-9 ( A value): 0.60±0.15 vs. 0.37±0.01, both P < 0.05], and the expressions of α-SMA, Vimentin, TIMP-1 and TGF-β1 were significantly down-regulated [α-SMA protein (α-SMA/β-actin): 0.36±0.08 vs. 1.05±0.09, Vimentin protein (Vimentin/β-actin): 0.53±0.07 vs. 1.19±0.04, TIMP-1 ( A value): 0.49±0.06 vs. 0.87±0.02, TGF-β1 ( A value): 0.67±0.04 vs. 0.89±0.10, all P < 0.05]. Conclusions:The degree of peritoneal fibrosis gradually increased with the increase of PDF sugar content in rats. Modified Shenling Baizhu San can improve peritoneal fibrosis induced by PDF with different sugar contents in rats, and the mechanism is related to the changes in the expression of fibrosis markers and ECM accumulation.

Research progress on the role of pyroptosis in the occurrence and development of peritoneal fibrosis / 中国医师杂志

Peritoneal dialysis is a recognized renal replacement therapy. Long term peritoneal dialysis will lead to changes in the morphology and function of the peritoneum, that is, peritoneal fibrosis, which is a known cause of the loss of peritoneal ultrafiltration capacity. Pyroptosis is a special type of soluble programmed cell death, characterized by cell swelling, rupture, secretion of cell contents and significant proinflammatory effect. The pyroptosis can be divided into typical and atypical pathways, and the inflammatory body of NOD like receptor heat protein domain related protein 3 (NLRP3) is the most important initiator. Current evidence shows that high glucose peritoneal dialysis fluid can induce peritoneal Mesothelium to scorch, and the inflammation and cell damage caused by it can aggravate the progress of peritoneal fibrosis. Different signal pathways have been proved to regulate the occurrence of pyroptosis. The latest research has proved that some potential targeted methods to inhibit pyroptosis can effectively inhibit the inflammation of peritoneal mesothelium and alleviate peritoneal fibrosis. This article mainly discusses the molecular mechanism of pyroptosis and the relationship between pyroptosis and peritoneal fibrosis.

Primary abdominal cocoon syndrome, situs inversus totalis and bilateral cryptorchidism: a case report / 中华泌尿外科杂志

This paper reviewed the clinical data of a patient with primary abdominal cocoon syndrome, situs inversus totalis and bilateral cryptorchidism admitted to our hospital in March 2021, and discussed the clinical characteristics of the disease based on the literature. This case is relatively rare, and all three diseases involve congenital abnormalities that may lead to developmental disorders in the embryo. The clinical manifestations of abdominal cocoon syndrome lack of specificity, preoperative diagnosis is difficult, often accompanied by partial dysplasia, so it is necessary to improve the awareness of preoperative differential diagnosis.

Caffeic acid phenethyl ester improves peritoneal dialysis-associated peritoneal fibrosis by alleviating oxidative stress injury through activating nuclear factor erythroid-2-related factor 2/heme oxygenase-1 pathway / 中华肾脏病杂志

Objective:To investigate whether caffeic acid phenethyl ester (CAPE) would improve peritoneal dialysis (PD)-associated peritoneal fibrosis by alleviating oxidative stress through activating nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway.Methods:Thirty-two male Sprague-Dawley rats were randomly divided into four groups by the random number table: control (CON) group (0.9% normal saline 20 ml/d intraperitoneal injection), CAPE group (0.9% normal saline 20 ml/d+CAPE 10 mg·kg -1·d -1 intraperitoneal injection), PD group [4.25% glucose peritoneal dialysis fluid (PDF) 20 ml/d intraperitoneal injection with lipopolysaccharide 0.6 mg/kg intraperitoneal injection at day 1, 3, 5 and 7], and PD+CAPE group (CAPE 10 mg·kg -1·d -1 intraperitoneal injection in addition to PD group), with 8 rats per group. On day 28, rats were euthanized after peritoneal equilibration test, and then the parietal peritoneum and omentum were collected for follow-up tests. To further investigate the mechanism, primary peritoneal mesothelial cells (PMCs) of rats were isolated and cultured. The PMCs were stimulated with 2.5% glucose PDF and added with 5 μmol/L CAPE intervention. The Nrf2 inhibitor (ML385) was used to identify whether CAPE protected PMCs from PDF by activating the Nrf2/HO-1 pathway. Histopathological staining was used to detect structural changes of the peritoneum, and immunohistochemical analysis was performed on cleaved caspase-3, Bax, α-smooth muscle actin (α-SMA), fibronectin (FN), and typeⅠ collagen (Col-Ⅰ) protein. Western blotting was used to detect the protein expression of α-SMA, FN, transforming growth factor-β1 (TGF-β1), HO-1 and nuclear Nrf2 (N-Nrf2). The apoptosis detection kit was used to detect apoptosis and flow cytometry was used to detect reactive oxygen species (ROS) in PMCs. The malondialdehyde (MDA) and superoxide dismutase (SOD) activity detection kit were used to detect MDA content and SOD activity. Cell immunofluorescence was used to analyze the protein expression of Nrf2 in PMCs. Results:Compared with the CON group, the PD group had thicker peritoneum, and the expression levels of cleaved caspase-3, Bax, α-SMA, FN, Col-Ⅰand MDA in peritoneum were significantly higher, while HO-1, N-Nrf2 protein expression and SOD activity were lower (all P<0.05). Compared with the PD group, the parietal peritoneum morphology of CAPE+PD group was improved, accompanied by reduced cleaved caspase-3, Bax, α-SMA, FN, Col-Ⅰ protein expression, and MDA content, while N-Nrf2, HO-1 protein expression, and SOD activity were higher (all P<0.05). Compared with the CON group, the PD group had significantly lower ultrafiltration volume and higher peritoneal permeability (both P<0.05). After CAPE intervention, the peritoneal transport function of the rats was significantly improved ( P<0.05). In cultured PMCs, PDF inhibited nuclear translocation of Nrf2 and protein expression of HO-1, and upregulated intracellular ROS level. In addition, PDF increased cell apoptosis and the protein expression levels of α-SMA, TGF-β1 and FN (all P<0.05). CAPE activated nuclear translocation of Nrf2, increased HO-1 protein expression, downregulated intracellular ROS level, and partially reversed PDF-induced cell apoptosis and epithelial- mesenchymal transition (all P<0.05). The protective effects of CAPE on PMCs were partially abolished by ML385 (all P<0.05). Conclusions:CAPE can reduce PD-induced PMCs apoptosis and epithelial-mesenchymal transition by attenuating oxidative stress, and significantly improve peritoneal fibrosis and ultrafiltration function. The beneficial effects of CAPE on peritoneum are related to activation of Nrf2/HO-1 pathway.

Encapsulating peritoneal sclerosis: from early diagnosis to successful kidney transplantation / Esclerose peritoneal encapsulante: do diagnóstico precoce ao transplante renal bem-sucedido

Abstract Encapsulating peritoneal sclerosis is an uncommon but serious complication of peritoneal dialysis. In most cases, the symptoms appear after peritoneal dialysis withdrawal, which hampers its diagnosis. We present the case of a 44-years-old Caucasian male who had been on peritoneal dialysis for 6 years and 3 months and was switched to hemodialysis due to ultrafiltration failure. During his last months on peritoneal dialysis, he developed anorexia and asthenia, which were initially attributed to dialysis inadequacy. After hemodialysis induction, the patient developed abdominal pain, increased abdominal volume, obstipation alternating with diarrhea, and weight loss. Computed tomography showed de novo ascites. A diagnosis of early encapsulating peritoneal sclerosis was considered, and treatment was promptly initiated with nutritional support, oral prednisolone, and tamoxifen for one year. The patient progressed with resolution of the symptoms. One month after the end of the treatment, he underwent a successful kidney transplant and remain without any major intercurrences. A high level of clinical suspicion is crucial for the early diagnosis of encapsulating peritoneal sclerosis as the disease can be fatal in advanced stages. This case highlights that with early treatment, kidney transplantation can be successfully performed after an episode of encapsulating peritoneal sclerosis.

Resumo A esclerose peritoneal encapsulante é uma complicação incomum, mas grave, da diálise peritoneal. Na maioria dos casos, os sintomas aparecem após a suspensão da diálise peritoneal, o que dificulta seu diagnóstico. Apresentamos o caso de um homem caucasiano de 44 anos de idade que esteve em diálise peritoneal por 6 anos e 3 meses e foi transferido para hemodiálise devido a falha de ultrafiltração. Durante seus últimos meses em diálise peritoneal, ele desenvolveu anorexia e astenia, que foram inicialmente atribuídas à inadequação da diálise. Após a indução de hemodiálise, o paciente desenvolveu dor abdominal, aumento do volume abdominal, obstipação alternada com diarreia, e perda de peso. A tomografia computadorizada mostrou ascite de novo. Foi considerado um diagnóstico de esclerose peritoneal encapsulante precoce, e o tratamento foi prontamente iniciado com suporte nutricional, prednisolona oral e tamoxifeno por um ano. O paciente progrediu com resolução dos sintomas. Um mês após o término do tratamento, ele foi submetido a um transplante renal bem-sucedido e permanece sem maiores intercorrências. Um alto nível de suspeita clínica é crucial para o diagnóstico precoce da esclerose peritoneal encapsulante, uma vez que a doença pode ser fatal em estágios avançados. Este caso destaca que, com tratamento precoce, o transplante renal pode ser realizado com sucesso após um episódio de esclerose peritoneal encapsulante.

Peritonitis encapsulante esclerosante (síndrome de cocoon): una causa extremadamente rara de obstrucción intestinal. Reporte de un caso y revisión de la literatura / Cocoon syndrome: an extremely rare cause of bowel obstruction. Case report and literature review

La peritonitis esclerosante encapsulante o síndrome de cocoon es una causa rara de obstrucción intestinal, que puede dividirse en pri-maria o secundaria, producida por una membrana fibrocolágena que envuelve el intestino delgado. El diagnóstico es particularmente desafiante, al tratarse de una entidad cuya clínica es inespecífica. El conocimiento de los hallazgos imagenológicos, sumados a una correcta anamnesis, permite una adecuada valoración preoperatoria. Presentamos un caso de interés y de difícil diagnóstico, junto con una revisión de la literatura sobre el tema.

Sclerosing encapsulating peritonitis or cocoon syndrome is a rare cause of intestinal obstruction, that can be divided into primary or secondary. It is produced by a fibro collagenous membrane that surrounds the small bowel. The diagnosis is particularly challenging since it is an entity whose symptoms are nonspecific. Knowledge of the imaging findings, in addition to a well performed anamnesis allows an adequate preoperative assessment. We present a clinical case and a review of the literature.

Encapsulating Peritoneal Sclerosis in a kidney transplant recipient - Case Report / Peritonite esclerosante encapsulante em receptora de transplante renal - relato de caso

Abstract Encapsulating Peritoneal Sclerosis (EPS) is a severe and rare condition frequently associated with peritoneal dialysis, characterized by bowel obstruction, with lethal consequences in 20% of the patients. The disease presents as a mass of fibrous tissue encapsulating visceral organs that may potentially compromise digestive tract function. This report describes the case of a patient under peritoneal dialysis (PD) due to chronic kidney disease secondary to focal segmental glomerulosclerosis diagnosed with EPS. The patient had undergone two living-donor kidney transplant procedures. Surgical techniques and clinical measures employed to unravel bowel obstruction are described, which have been shown to ameliorate EPS secondary complications. Parenteral nutrition has significantly contributed to afford adequate nutrition, improving tissue healing as well as serum protein levels, vitamins and electrolytes. Therapy with tamoxifen and sodium thiosulfate effectively delayed the development of EPS.

Resumo A peritonite esclerosante encapsulante (PEE) é uma condição rara e grave, frequentemente associada à diálise peritoneal, caracterizada por obstrução intestinal, que pode ter uma evolução fatal em 20% dos pacientes. Apresenta-se como uma massa de tecido fibroso, recobrindo os tecidos viscerais, e pode comprometer o funcionamento fisiológico de todo o aparelho digestivo. O presente estudo relata um caso de PEE decorrente de diálise peritoneal (DP) devido à insuficiência renal por glomeruloesclerose focal e segmentar. No caso relatado, a paciente foi submetida a DP e passou por dois transplantes renais intervivos. São descritas as técnicas cirúrgicas e as medidas clínicas adotadas, que se revelaram úteis na resolução da obstrução intestinal, com melhora dos efeitos secundários da PEE. A dieta parenteral mostrou ser um importante fator para a manutenção do aporte nutricional, auxiliando na cicatrização e no nível sérico de proteínas, vitaminas e eletrólitos. A terapia com tamoxifeno e a administração de hipossulfito de sódio foram eficientes para retardar o avanço da PEE.

Effect of KLF-4 on peritoneal fibrosis induced by high glucose peritoneal dialysate via targeting regulation of the expression of E-cadherin / 解放军医学杂志

[Abstract] Objective To explore the relationship between Kruppel-like factor 4 (KLF-4) and E-cadherin in human peritoneal mesothelial cells (HPMCs), and the expression and function of KLF-4 in the animal model of peritoneal fibrosis induced by high glucose peritoneal dialysate. Methods Co-transfection in HPMCs with the plasmid of KLF-4 and the bind site or mutant in the promoter region of E-cadherin, and then the luciferase activity was measured of the each bind site and its matched mutants to estimate whether KLF-4 can combine with the bind site in the promoter region of E-cadherin; Chromatin immunocoprecipitation (CHIP) was exploited to verify if KLF-4 can combine with the bind site in the promoter region of E-cadherin; Real-time PCR and Western blotting were performed to detect the expression of E-cadherin at the bind site and matched mutants of b, d, f and g. Thirty SD rats were randomly divided into saline group, peritoneal dialysate group and experimental group (10 each). Rats in saline group were given intraperitoneal injection with 0.9% NaCl, in peritoneal dialysate group were given with 4.25% high glucose peritoneal dialysate, and in experimental group were given via tail vein with 4.25% high glucose peritoneal dialysate and the mixture of KLF-4 plasmid suspension containing ultrasound microbubble. To observe the peritoneal tissue thickness of the 3 groups of rats by Hematoxylin and Eosin staining. Masson trichrome staining was performed to detect the deposition of collagen fibers in peritoneal tissue of the 3 groups of rats. Immunohistochemistry was used to detect the expression level of KLF-4, E-cadherin, α-SMA and fibronectin (FN) in peritoneal tissue of the 3 groups of rats. Results Promoter luciferase reporter gene and CHIP results showed that KLF-4 can combine with the bind site in the promoter region of E-cadherin in HPMCs. Real-time PCR and Western blotting showed that KLF-4 can positively regulate the expression of E-cadherin. HE staining showed that the peritoneal tissue was obviously thickened in rats of peritoneal dialysate group [(105.91±12.0) μm] than in rats of saline group [(20.89±5.39) μm] and of experimental group [(23.05±6.07) μm] with statistical significance (P0.05). Masson staining showed that the deposition of collagen fiber significantly increased in peritoneal dialysate group (0.89±0.09) than in saline group (0.19±0.03) and experimental group (0.15±0.06) with statistical significance (P0.05). Immunohistochemistry results showed that the expressions of KLF-4 and E-cadherin were obviously lower in peritoneal dialysate group (0.27±0.09, 0.31±0.03) than in saline group (0.79±0.19, 0.83±0.13) and experimental group (0.85±0.11, 0.76±0.11) with statistically significant difference (P0.05). In contrast, the expressions of α-SMA and FN were evidently higher in peritoneal dialysate group (0.83±0.09, 0.63±0.09) than in saline group (0.22±0.08, 0.30±0.07) and experimental group (0.19±0.05, 0.11±0.03) with statistically significant difference (P0.05). Conclusion KLF-4 may positive regulate the expression of E-cadherin by combining with the bind site in the promoter region of E-cadherin, and inhibit the peritoneal fibrosis induced via high glucose peritoneal dialysate.

The diagnosis and treatment of primary abdominal cocoon / 中华普通外科杂志

Objective To investigate the clinical characteristics,diagnosis and treatment of primary abdominal cocoon.Methods The clinical data of 16 cases of primary abdominal cocoon were reviewed and analyzed.Results Only in 2 cases in which correct preoperative diagnosis was estabished by CT scan.The other 14 cases were diagnosed during operation.Parts or all small intestines were covered with a layer of milky white dense fibrous thin membrane,formed mass-likely adhesion,and fibrous film attached to the mesenteric roots.Extensive adhesion existed in between intestines.The operation included lysis of peritoneal adhesion plus fibrous membrane excision in 14 cases,lysis of peritoneal adhesion plus fibrous membrane excision and segmental enterectomy in 2 cases,and in 2 cases appendectomy was done.There was no anastomotic leakage or other major complications except for wound infection in 1 case.All the patients were followed up from 3 months to 7 years with a median follow-up time of 3.6 years,and no recurrent cases were found.Conclusions Surgery is the main method for the treatment of abdominal cocoon with evident clinical symptoms,and the prognosis is largely fair.

Digestive involvement in retroperitoneal fibrosis

Retro peritoneal fibrosis is a condition rarely seen in gastroenterology. Through these two observations and data from the literature we will address and focus on the digestive tract in the context of this disease and we will detail the different clinical aspects, radiological, pathological and therapeutic of this entity

Encapsulating peritoneal sclerosis: case report / Esclerose peritoneal encapsulada: relato de caso

Abstract Patients with chronic kidney disease (CDK) can develop several diseases caused by the renal replacement therapy. Here we report a rare complication of peritoneal dialysis, the encapsulating peritoneal sclerosis (EPS) in which the peritoneal tissue is gradually replaced by fibrous tissue. The patient in question, after late loss of renal graft and conversion to peritoneal dialysis, evolved with multiple hospitalizations for spontaneous bacterial infections, in recent admission, he was diagnosed with sub-occlusive abdomen secondary to the EPS. Five days after, presented with intestinal obstruction requiring surgical approach by laparotomy, being performed with right colectomy, enterectomy, enteroraphy and ileostomy with drainage. The patient progressed well and follows on prednisone and tamoxifen-associated with intermittent hemodialysis.

Resumo No contexto da insuficiência renal crônica (IRC), os pacientes estão sujeitos a diversas patologias advindas da própria terapêutica de substituição renal. Relatamos aqui uma complicação rara da diálise peritoneal, a peritonite esclerosante encapsulante (PEE), na qual o tecido peritoneal é progressivamente substituído por tecido fibroso. O paciente em questão, após perda tardia de enxerto renal e conversão para terapêutica dialítica peritoneal evoluiu com múltiplas internações por infecções bacterianas espontâneas, em último internamento, foi diagnosticado com abdome sub-oclusivo secundário à PEE. Após 5 dias apresentou quadro de abdome obstrutivo com necessidade de abordagem cirúrgica por laparotomia exploradora, sendo realizado colectomia direita, enterectomia, enterorrafia e ileostomia com drenagem. O paciente evolui bem e segue em tratamento com prednisona e tamoxifeno associado à hemodiálise intermitente.

Diagnóstico y seguimiento de 12 casos de peritonitis esclerosante asociada a diálisis peritoneal crónica en Chile: Experience in 12 patients on peritoneal dialysis / Encapsulating peritoneal sclerosis

Background: Encapsulating peritoneal sclerosis (EPS) is a complication of peritoneal dialysis (PD) with a low prevalence but high mortality. It is characterized by peritoneal inflammation and fibrosis with subsequent development of intestinal encapsulation. It is associated with a long lapse on PD, frequent episodes of peritonitis, high glucose solution use, and high peritoneal transport status. Aim: To report the clinical features of patients on PD, who developed EPS. Material and Methods: Review of medical records of 12 patients aged 43 ± 10 years (eight women) who developed EPS. Results: The mean time spent on PD was 98 months. The main clinical manifestations were abdominal pain in 82% and ultrafiltration failure in 63%. In 92%, there was a history of peritonitis and 75% had high peritoneal transport at the time of diagnosis. The main findings in computed tomography were peritoneal calcification and thickening. There was a biopsy compatible with the diagnosis in 10 cases. Treatment consisted in withdrawal from PD, removal of PD catheter and the use of corticoids and tamoxifen. After withdrawal from PD 50% of patients became asymptomatic. The rest had intermittent abdominal pain and altered bowel movements. Two patients died (17%). Conclusions: EPS is a serious complication of PD, which should be suspected in any patient with compatible clinical symptoms, long time on PD, multiple episodes of peritonitis and high peritoneal transport profile.

Encapsulating peritoneal sclerosis in liver transplant recipients: a report of 2 cases

Encapsulating peritoneal sclerosis (EPS) is a rare cause of intestinal obstruction by a thick fibrous membrane wrapping around the small intestine. It is a possible complication after liver transplantation (LT) that can be fatal. This report describes 2 cases of EPS after LT that were successfully treated with surgery, corticosteroids, tamoxifen, and mammalian target of rapamycin inhibitor. After treatment in both cases, the patients were able to start oral feeding and have been symptom free for more than 1 year. These cases suggests that for the management of EPS, surgical treatment is mandatory when the patients present with symptoms of intestinal obstruction or if there are findings suggestive of decreased mural perfusion. Surgery should be accompanied with medical treatment to prevent the relapse of EPS.

Interleukin-6 induces epithelial mesenchymal transition of human peritoneal mesothelial cells by STAT3 / 中华肾脏病杂志

Objective To investigate the role of STAT3 transcription factor in IL-6 inducing epithelial mesenchymal transition (EMT) of human peritoneal mesothelial cells (HPMCs).Methods HPMCs were cultured in vitro and grouped.(1) According to the stimulation time with 50 μg/L IL-6,HPMCs were divided into 24,48,72 h groups.(2) HPMCs were grouped 50,100 μg/L according to IL-6 concentration.(3) HPMCs were respectively divided into control group,IL-6 group,empty vector group,empty vector+IL-6 group,virus infecting group and virus infecting+IL-6 group,as lenti-virus vector mediating RNA interference targeting STAT3 was applied.The mRNA expressions of E-cadherin,α-smooth muscle actin (α-SMA) and vascular endothelial growth factor (VEGF) were detected by real time PCR;their protein expressions and the phosphorylation of JAK2 and STAT3 were detected by Western blotting;the expressions and distribution of E-cadherin and α-SMA were observed by immunofluorescence.Results Compared with those in control group,the expression of E-cadherin decreased remarkably (P ＜ 0.05),while the expressions of VEGF and α-SMA and the ratio of phosphorylated (p)-JAK2/JAK2 and p-STAT3/STAT3 increased significantly in IL-6 concentration groups and stimulation time groups (all P ＜ 0.05),which had been dose and time dependent.Compared with empty vector+IL-6 group,virus infecting+IL-6 group had decreased expressions of VEGF and α-SMA,while increased expressions of E-cadherin (all P ＜ 0.05).Conclusions IL-6 can promote VEGF and α-SMA gene expression and prevent E-cadherin gene expression by STAT3,which involves in EMT of peritoneum fibrosis.While STAT3 gene is knocked-down,EMT is inhibited in HPMCs.

Interleukin-6 induces epithelial mesenchymal transition of human peritoneal mesothelial cells by STAT3 / 中华肾脏病杂志

Objective To investigate the role of STAT3 transcription factor in IL-6 inducing epithelial mesenchymal transition (EMT) of human peritoneal mesothelial cells (HPMCs).Methods HPMCs were cultured in vitro and grouped.(1) According to the stimulation time with 50 μg/L IL-6,HPMCs were divided into 24,48,72 h groups.(2) HPMCs were grouped 50,100 μg/L according to IL-6 concentration.(3) HPMCs were respectively divided into control group,IL-6 group,empty vector group,empty vector+IL-6 group,virus infecting group and virus infecting+IL-6 group,as lenti-virus vector mediating RNA interference targeting STAT3 was applied.The mRNA expressions of E-cadherin,α-smooth muscle actin (α-SMA) and vascular endothelial growth factor (VEGF) were detected by real time PCR;their protein expressions and the phosphorylation of JAK2 and STAT3 were detected by Western blotting;the expressions and distribution of E-cadherin and α-SMA were observed by immunofluorescence.Results Compared with those in control group,the expression of E-cadherin decreased remarkably (P ＜ 0.05),while the expressions of VEGF and α-SMA and the ratio of phosphorylated (p)-JAK2/JAK2 and p-STAT3/STAT3 increased significantly in IL-6 concentration groups and stimulation time groups (all P ＜ 0.05),which had been dose and time dependent.Compared with empty vector+IL-6 group,virus infecting+IL-6 group had decreased expressions of VEGF and α-SMA,while increased expressions of E-cadherin (all P ＜ 0.05).Conclusions IL-6 can promote VEGF and α-SMA gene expression and prevent E-cadherin gene expression by STAT3,which involves in EMT of peritoneum fibrosis.While STAT3 gene is knocked-down,EMT is inhibited in HPMCs.

Effect of Bailing Capsules on the Expressing of TGF-β1 in the Peritoneal Dialysis Solution for Peritoneal Di-alysis Patients / 中国药师

Objective:To investigate the effects of Bailing capsules on the expression of TGF-β1 in the peritoneal dialysis solution for peritoneal dialysis patients. Methods: Totally 40 patients treated with peritoneal dialysis ( PD) were randomly divided into two groups (20 cases in the control group and 20 cases in the experimental group). All the patients were treated with PD by 1. 5% perito-neal dialysis effluent (6 000 ml everyday), and the patients in the experimental group were additionally treated with Bailing capsules (5 capsules each time, three times a day after meals) for 6 months. The adequacy of PD (including Kt/V and Ccr) of the two groups was examined after the one-month treatment. The renal function and the level of TGF-β1 in the effluent in 1, 3 and 6 month were com-pared between the two groups. Results:The adequacy of PD ( Kt/V and Ccr ) had no significant difference between the two groups (P0. 05). In the control group, the expression of TGF-β1 in the effluent in 1, 3 and 6 month was increased gradually with significant difference (P0. 05), which was lower than that in the control group (P<0. 05). Conclusion:Bailing capsules can decrease the expression of TGF -β1 in the effluent for the patients treated with PD and inhibit the peritoneal fibrosis.

Experimental systems to study the origin of the myofibroblast in peritoneal fibrosis

Peritoneal fibrosis is one of the major complications occurring in long-term peritoneal dialysis patients as a result of injury. Peritoneal fibrosis is characterized by submesothelial thickening and fibrosis which is associated with a decline in peritoneal membrane function. The myofibroblast has been identified as the key player involved in the development and progression of peritoneal fibrosis. Activation of the myofibroblast is correlated with expansion of the extracellular matrix and changes in peritoneal membrane integrity. Over the years, epithelial to mesenchymal transition (EMT) has been accepted as the predominant source of the myofibroblast. Peritoneal mesothelial cells have been described to undergo EMT in response to injury. Several animal and in vitro studies support the role of EMT in peritoneal fibrosis; however, emerging evidence from genetic fate-mapping studies has demonstrated that myofibroblasts may be arising from resident fibroblasts and pericytes/perivascular fibroblasts. In this review, we will discuss hypotheses currently surrounding the origin of the myofibroblast and highlight the experimental systems predominantly being used to investigate this.