氫水治療腎臟移植后腎病
來源： | 發(fā)布時(shí)間：2015/9/24 9:48:54 | 瀏覽次數(shù)：
腎移植通俗的說法又叫換腎，就是將健康者的腎臟移植給有腎臟病變并喪失腎臟功能的患者。人體有左右兩個(gè)腎臟，通常一個(gè)腎臟可以支持正常的代謝需求，當(dāng)雙側(cè)腎臟功能均喪失時(shí)，腎移植是最理想的治療方法，故凡是慢性腎功能不全發(fā)展至終末期，均可用腎移植治療。腎移植因其供腎來源不同分為自體腎移植、同種腎移植和異種腎移植，習(xí)慣把同種腎移植簡稱為腎移植。其他兩種腎移植則冠以“自體”或“異種”腎移植以資區(qū)別。
腎移植可以發(fā)生無腎功能、腎移植術(shù)后發(fā)生早期腎功能不全和腎移植術(shù)后發(fā)生晚期腎功能減退，總之移植后腎功能不全是腎臟移植后的重要并發(fā)癥，是該領(lǐng)域非常關(guān)注的問題。
隨著免疫抑制藥物的發(fā)展，腎移植急性排斥反應(yīng)基本上都可以得到控制，但慢性移植功能不全尚無明確有效的治療藥物和方法，慢性移植腎病是導(dǎo)致移植腎晚期功能喪失的最主要原因。
慢性移植腎病的發(fā)病機(jī)制目前比較公認(rèn)的觀點(diǎn)是：本病是由異種抗原依賴的免疫因素（如急性排斥反應(yīng)、免疫抑制劑不足等）及非異種抗原依賴的因素（如延長的冷缺血時(shí)間、供體年齡、受體脂代謝異常、高血壓、糖尿病或糖耐量異常、移植后6～12月間腎功能受損、巨細(xì)胞病毒感染等）導(dǎo)致的移植腎功能持續(xù)惡化和發(fā)展。本研究作者曾經(jīng)在Fisher344－Lewis大鼠慢性移植腎病模型發(fā)現(xiàn)：成年鼠間腎移植的慢性移植腎病顯著比幼年鼠間腎移植的慢性移植腎病嚴(yán)重。
該研究通過動(dòng)物腎臟移植模型，持續(xù)給動(dòng)物飲用氫水150天，最后比較了不同組的腎臟功能、死亡率、炎癥因子和MAPK細(xì)胞信號(hào)分子系統(tǒng)，結(jié)果證明，長時(shí)間飲用含氫水可以預(yù)防慢性移植腎病的發(fā)生，研究給臨床上治療移植后腎臟功能不全帶來了新希望。這也是氫分子醫(yī)學(xué)研究方面的又一力作。文章來自美國著名氫氣醫(yī)學(xué)研究小組匹茲堡大學(xué)器官移植中心Nakao小組。
不過本人學(xué)術(shù)好友Nakao教授，2012年日本福島海嘯后從美國已經(jīng)返回日本工作，職業(yè)為急救科醫(yī)生，氫氣醫(yī)學(xué)雖然仍然是他的科研內(nèi)容，但已經(jīng)比在美國少多了。
ORALADMINISTRATION OF HYDROGEN WATER PREVENTS CHRONIC ALLOGRAFTNEPHROPATHY IN RAT RENAL TRANSPLANTATION
Tissueinjury, induced by reactive oxygen species (ROS), contributes to thedevelopment of chronic allograft nephropathy (CAN; also known as interstitialfibrosis and tubuar atrophy with unknown etiology [IF/TA]) after renaltransplantation. Molecular hydrogen gas can act as a ROS scavenger. Wehypothesized that administration of hydrogen water (HW) would ameliorate CAN byscavenging ROS. Using a rat model of kidney transplantation, LEW rat allograftswere orthotopically transplanted into BN rat recipients that had undergonebilateral nephrectomy.
Molecularhydrogen was dissolved in water (>0.8 mM) and recipients were given eitherregular water (RW) or HW from day 0 to day 150, or death. RW-treated animalsexperienced a gradual decline in creatinine clearance, associated withproteinuria, which ultimately led to graft failure secondary to CAN. Incontrast, HW administration improved allograft function, slowed the
progressionof CAN, and improved overall survival. HW also reduced oxidant injury andinflammatory mediator production. Additionally, inflammatory signaling pathways(mitogen activated protein kinases) were less activated in renal allograftsfrom HW-treated rats compared to the RW-treated group. These data indicate thatorally administered HW is an effective antioxidant and anti-inflammatory agentthat can prevent CAN and improve survival in a model of rodent renaltransplantation. HW may be of therapeutic value in the setting oftransplantation.
