為重-急性腎損傷

急性腎損中國(guó)醫(yī)學(xué)附屬第一醫(yī)重癥醫(yī)學(xué)A“syndrome”involvingarapidreductioninrenalexcretorycapacitywithaccumulationofnitrogenwasteproductssuchascreatinineandurea.KidneyInt2008;73:538-AKI的病因和各臨床表現(xiàn)可從輕度肌酐升高直至急性AKI影響危重癥的預(yù)后，增加AKI存在發(fā)展至慢性腎臟病的風(fēng)RocclZ,etal.KidneyIntAKI覆蓋的腎損傷GRF正常伴腎臟損傷標(biāo)志物改GRF開(kāi)始下GRF明顯異PathogenesisofReducedBloodReducedBloodReducedRenalCompensatory ReducedGFRReducedGFRAcid-BasedistrubancesNormalAschemaofthePathogenesisofPrerenal最常腎臟低灌注后的反腎實(shí)質(zhì)保持完灌注恢復(fù)后腎功能可迅速恢復(fù)正持續(xù)嚴(yán)重低灌注可轉(zhuǎn)變?yōu)檠軆?nèi)容量下心排量下外周血管擴(kuò)腎臟血管收腎動(dòng)脈梗藥物所致的自我調(diào)節(jié)受損或GRF下腎血管病腎小球病腎小管壞死腎小管-間質(zhì)病 腎小管上皮細(xì)胞腫脹剝形成管細(xì)胞粘附分子使壞死的腎小管上皮細(xì)胞在一起ATN特 理改變：顆粒管腎小管壞死缺血：持續(xù)低灌外毒素：抗生素、化療藥、造影劑、毒3lastshoursto InitialperiodofrenalhypoperfusionduringwhichischeamicinjuryisevolvingGFRdeclines(i.eUltrafilterationpressureisreducedduetofallinrenalbloodflowObstructiontoflowoffiltratebycastsderivedfromischaemictubularepithelimBackleakoffilterateviainjuredtubularLasts1-2RenalcellinjuryisGFRisatitslowest(5-10mL/min)i.eurineoutputisatitslowestUraemiccomplicationsThereisrenalparenchymalandtubularcellrepairandregenerationGradualreturnofGFRtonormalorpremorbidlevelsMaybecomplicatedbymarkeddiuresisdueExcretionofretainedsaltandContinueduseofDelayedrecoveryofepithelialcellfunction(solute&waterreabsorption)relativetoglomerularIncreasedpolyuria,腎盂梗輸尿管梗頸梗梗AKI流行病學(xué)現(xiàn)患病率：1%（社區(qū)）----7.1%（醫(yī)院人病率：486-AKI需要RRT：22-醫(yī)院獲得AKI率：10-合并多臟器功能衰竭率需要RRT治療者率：高達(dá)Responsiblefor5%ofmedicalhospitaladmissionand30%ofIntensiveCareunit臨床評(píng)詳細(xì)的病史和體格檢查有助于AKI病因析和泌尿系超聲（懷疑有梗阻者）（1A）評(píng)AKI的預(yù)