M型磷脂酶A2受体和1型血小板反应蛋白7 A域的表达与特发性膜性肾病患者病情及临床预后的关系

目的探讨PLA2R和THSD7A表达与特发性膜性肾病患者病情及临床预后的关系。方法随机选取我院60例经肾脏病理确诊为特发性膜性肾病(IMN)的患者作为研究对象,采用酶联免疫吸附法检测患者血清中PLA2R和THSD7A的表达水平,探讨患者血清中PLA2R和THS7A水平与其肾病病情及临床预后的关系。结果 15例肾炎型肾病患者中PLA2R阳性5例(占33.3%)、THSD7A阳性0例,45例单纯型肾病患者中40例PLA2R阳性(占88.9%)、THSD7A阳性4例(占8.89%),两种疾病类型之间PLA2R和THSD7A阳性率比较差异显著(P0.05)。CR患者中PLA2R阳性18例(占94.7%),THSD7A 3例(占15.8%); PR患者中PLA2R阳性15例(占75.0%),THSD7A 1例(占5.0%); PE患者中PLA2R阳性12例(占57.1%),THSD7A阳性0例;不同治疗结果的IMN患者的PLA2R和THSD7A阳性率对比差异有统计学意义(P0.05)。PLA2R阴性(P=0.01)、THSD7A阴性(P=0.02)、病理类型(P=0.01)是患者发生慢性肾功能不全的独立危险因素。结论 M型磷脂酶A2受体和THSD7A阴性患者病情差,是IMN患者预后不良的独立危险因素。     

早期尿激酶应用对慢性肾衰竭静脉置管长期血液透析患者导管纤维蛋白鞘形成防治效果研究

目的探讨早期尿激酶应用对慢性肾衰竭静脉置管长期血液透析患者导管纤维蛋白鞘形成的防治作用。方法选取我院2017年3月-2018年10月收治的慢性肾衰竭静脉置管长期血液透析患者85例,根据防治导管纤维蛋白鞘形成方法的不同分为观察组44例和对照组41例。观察组置管首次透析后即开始采用尿激酶封管法和滴注法防治导管纤维蛋白鞘形成;对照组置管首次透析后先采用常规肝素封管,待出现导管功能不良时再开始采用尿激酶封管法和滴注法防治导管纤维蛋白鞘形成。观察比较两组透析6个月后导管功能不良发生次数和首次导管功能不良出现时间;两组透析1、3及6个月时的血流量及静脉压;两组透析前及透析6个月时凝血酶原时间(PT)、凝血酶时间、纤维蛋白原、部分凝血酶时间;两组治疗期间不良反应发生情况。结果观察组导管功能不良发生次数明显少于对照组,首次导管功能不良出现时间明显晚于对照组,差异均有统计学意义(P<0.05或P<0.01)。透析3、6个月时观察组血流量明显大于对照组,静脉压明显低于对照组,差异均有统计学意义(P<0.05)。透析6个月时两组组内治疗前后比较,仅对照组PT降低(P<0.05);观察组透析6个月时PT明显长于对照组(P<0.05)。两组治疗期间均无严重不良反应发生。结论早期应用尿激酶可有效防治慢性肾衰竭静脉置管长期血液透析患者导管纤维蛋白鞘形成,且安全性良好,是一种防治长期血液透析留置导管功能不良的有效手段。     

Effects of hyperosmolality on expression of urea transporter A2 and aquaporin 2 in mouse medullary collecting duct cells

In this study,the effects of hyperosmolality on the expression of urea transporter A2 (UTA2) and aquaporin 2 (AQP2) were investigated in transfected immortalized mouse medullary collecting duct (mIMCD3) cell line.AQP2-GFP-pCMV6 and UTA2-GFP-pCMV6 plasmids were stably transfected into mIMCD3 cells respectively.Transfected mIMCD3 and control cells were cultured in different hy-pertonic media,which were made by NaCl alone,urea alone,or an equiosmolar mixture of NaCl and urea.The mRNA and protein expression of AQP2 was elevated by the stimulation of NaCl alone,urea alone and NaCl plus urea in AQP2-mIMCD3 cells;whereas NaCl alone and NaCl plus urea rather than urea alone increased the mRNA and protein expression of UTA2 in UTA2-mIMCD3 cells,and all the expression presented an osmolality-dependent manner.Moreover,the mRNA and protein expression of UTA2 rather than AQP2 was found to be synergistically up-regulated by a combination of NaCl and urea in mIMCD3 cells.It is concluded that NaCl and urea synergistically induce the expression of UTA2 rather than AQP2 in mIMCD3 cells,and hyperosmolality probably mediates the expression of AQP2 and UTA2 through different mechanisms.