慢性间质性肾炎肾功能不全伴发甲状旁腺腺瘤一例报告

慢性间质性肾炎肾功能不全伴发甲状旁腺腺瘤一例报告杨军，郑法雷，毕增祺慢性间质性肾炎、肾小管酸中毒、肾功能不全可合并继发性甲旁亢和肾性骨病，但伴发甲状旁腺腺瘤临床非常罕见，现将我院诊治１例报告如下。患者，女性，６３岁，因反复尿频、尿急、排尿不适２０余年...     

Inhibitory effect of vascular endothelial growth factor on transforming growth factor β1-induced epithelial-mesenchymal transition of HK2 cells and its relationship with connective tissue growth factor and PI3K-Akt pathway

Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway.     

多胺与尿毒症

关于尿毒症发病机理的研究,已经有一百六十余年的历史。其中研究得最多的是尿毒症毒素(uremic toxins)或尿毒症毒性物质(toxic substances of uremia)的作用。目前已经知道,尿毒症患者体液内有二百余种物质的浓度比正常升高,其中大多数物质是否具有尿毒症毒性作用尚未进行系统研究;关于尿素、肌酐、尿酸、胍类、酚类等小分子物质的作用,人们已了解较多,对某些中分子(分子量500-5000)及大分子(分子量大于5000)物质的作用也进行了初步的研究,认为上述不同分子量的物质可能具有尿毒症毒性作用。近十余年来,关于多胺(polyamine)与     

大黄提取物对慢性肾功能衰竭进展的作用

在我国,应用中药治疗慢性肾衰已有较长历史,在研究中药延缓慢性肾衰进展方面取得了初步成效.我们在早期研究中曾发现大黄煎剂可使轻、中度尿毒症患者临床症状缓解。为了探索大黄对慢性肾衰进展的作用,我们观察了大黄提取物(RE)对慢性肾衰大鼠肾功能的作用,并在透析前慢性肾衰病人中进行了类似的研究,现将有关资料报告于下。一、RE对慢性肾衰大鼠肾功能的作用方法:应用改良Platts法将雄性Wist-ar大鼠作双肾次全切除(5/6切除),获得慢性肾衰动物模型.第二次肾切除后3周,开始将大鼠分为RE治疗组(n=59)和对照组(n=75)两组,两组动物均给予标准饲料(含蛋白质12.97％,淀粉59.24％,脂肪5.11％)。RE治疗组动物饲以RE100mg/日,每日一次,共给药12天。治疗前后均测定BUN、血肌酐(Scr)、尿蛋白定量     

蔗糖铁注射液治疗血液透析患者肾性贫血的多中心研究

目的比较静脉用铁剂蔗糖铁(维乐福)、口服铁剂琥珀酸亚铁(速力菲)分别与基因重组人红细胞生成素(EPO)联合应用,治疗伴有缺铁的维持性血液透析患者肾性贫血的有效性和安全性。方法采用前瞻性、随机、对照的多中心研究。120例血透患者分为静脉组和口服组,每组各60例。静脉组:200mg蔗糖铁稀释于100ml生理盐水,每次透析时使用,直至完成总预计补铁量。总预计补铁量=体重(kg)×(150-Hb实际值)(g/L)×0.24 500(mg)。口服组:琥珀酸亚铁200mg每日3次,共8周。两组患者均使用EPO治疗,剂量为120～150U·kg-1·周-1,皮下或静脉应用。观察并比较两组患者贫血治疗的效果、铁代谢指标的变化及不良反应发生情况。结果治疗前静脉组与口服组间在男女性别比例、年龄、体重和接受治疗前维持透析时间及血红蛋白(Hb)、铁蛋白和转铁蛋白饱和度等方面均无显著差异。治疗后静脉组Hb犤(90.9±15.8)比(74.6±8.3)g/L,P<0.001犦和口服组Hb犤(84.5±11.9)比(76.6±7.8)g/L,P<0.001犦均较治疗前明显升高。而静脉组Hb上升幅度明显高于口服组犤(17.9±10.1)比(7.9±11.0)g/L,P<0.001犦;其治疗时间明显短于口服组犤(5.2±0.4)比8.0周,P<0.001犦;静脉组Hb上升速度明显快于口服组犤(3.5±2.0)比(1.0±1.4)g·L-1·周-1,P=0.003犦。两组平均EP     

肾小球高滤过的机制与防治

慢性肾功能衰竭（慢性肾衰）是一种渐进性发展的病症。有哪些因素影响慢性肾衰的病程进展？如何防止或减慢肾衰病程的进展？这是不少学者都在研究的重要课题。目前认为，肾小球高滤过、肾小管高代谢、某些尿毒症毒素、蛋白尿等若干因素，均可能与慢性肾衰病程的进展有关。Ｂｒｅｎｎｅｒ认为，肾小球高滤过是造成慢性肾衰病程进展的重要原因之一，它可导致并加速肾小球硬化，使残余肾单位进一步破坏，肾衰逐渐加重。认识肾小球高滤过在慢性肾衰病程进展中的作用及其可能的机理，并采取相应的防治措施，对延缓慢性肾衰的发展有着重要意义。１…     

Inhibitory effect of vascular endothelial growth factor on transforming growth factor β1-induced epithelial-mesenchymal transition of HK2 cells and its relationship with connective tissue growth factor and PI3K-Akt pathway

Objective To examine the relationship of the inhibitory effect of vascular endothelial growth factor(VEGF) on epithelial-mesenchymal transition (EMT) induced by TGF-β1 in HK2 cells with the expression of connective tissue growth factor (CTGF) and PI3K-Akt pathway. Methods The cultured HK2 cells were divided into the following groups: normal control group, TGF-β1 (5 μg/L) group, VEGF (100 μg/L) group, TGF-β1 plus VEGF group. LY294002 (25 μmol/L), the blocker of PI3K-Akt pathway, was added to each of above-mentioned groups for the second part of the study, α-smooth muscle actin (α-SMA) and E-cadherin expressions of HK2 cells were assessed with double-stain immunocytochemistry method. The mRNA and protein expressions of α-SMA and CTGF of cells were assessed with RT-PCR and Western blot. The expressions of fibronectin (FN) and collagen Ⅰ (Col Ⅰ) in medium were assessed with ELISA. Results The expressions of α-SMA and CTGF significantly increased in HK2 cells treated with TGF-β1 compared with those in normal control (P<0.05), while significantly decreased in cells co-treated with TGF-β1 and VEGF compared with those treated with TGF-β1 alone (P<0.05, respectively). The expression of E-cadherin was exactly opposite to that of α-SMA. When LY294002 was added to TGF-β1 and VEGF co-treated cells, the expressions of α-SMA, CTGF, FN and Col Ⅰ were markedly up-regulated, when compared with those without LY294002 treatment (P<0.05). Conclusion Inhibitory effect of VEGF on TGF-β1-induced EMT of HK2 ceils in vitro may be related to down-regulation of CTGF expression and reduction of FN and Col Ⅰ, which may be partly dependent on PI3K-Akt pathway.     

范可尼综合征的临床特点与生化异常

目的 进一步认识范可尼综合征（FS）的病因、临床特点与生化异常。方法 对我院确诊的42例FS患者进行回顾性分析。结果 42例FS中完全型19例，不完全型23例，主要表现为近端肾小管酸中毒（41例）伴物质转运异常，包括低钾血症（21例）、低磷血症（29例）、低尿酸血症（19例）、肾性糖尿（38例）、氨基酸尿（36/37例）和低分子蛋白尿（21例）。病因：特发性或原因不明21例，继发性21例；其中间质性肾炎8例，干燥综合征5例。临床表现以乏力、多饮、多尿、肾性骨病最常见，伴肾功能不全者18例。14例患者接受肾活检，结果均显示有不同程度的小管-间质病变，其中4例伴有肾小球病变。结论 FS病因多样，继发性FS并不少见，一般均伴有Ⅱ型肾小管酸中毒，并常有肾小管-间质的病理损害。     

马兜铃酸I诱导的LLC—PK1细胞凋亡及其意义

目的探讨在体外条件下马兜铃酸Ｉ（ＡＡＩ）能否诱导肾小管上皮细胞发生凋亡及发生凋亡的条件。方法应用光镜、琼脂糖凝胶电泳、ＡｎｎｅｘｉｎＶＦｌｏｕｓ凋亡检测试剂盒鉴定细胞凋亡，应用流式细胞仪测定凋亡细胞比例。结果００２ｇ／Ｌ，００４ｇ／Ｌ，００８ｇ／Ｌ的ＡＡＩ作用２４小时可明显诱导ＬＬＣＰＫ１细胞凋亡，００１ｇ／Ｌ的ＡＡＩ无此作用。随ＡＡＩ浓度的增高，凋亡细胞比例增加。结论在体外条件下一定浓度的ＡＡＩ能诱导ＬＬＣＰＫ１细胞发生凋亡，其作用与浓度有关。