為重-急性腎損傷

急性腎損中國醫(yī)學附屬第一醫(yī)重癥醫(yī)學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RocclZ,etal.KidneyIntAKI覆蓋的腎損傷GRF正常伴腎臟損傷標志物改GRF開始下GRF明顯異PathogenesisofReducedBloodReducedBloodReducedRenalCompensatory ReducedGFRReducedGFRAcid-BasedistrubancesNormalAschemaofthePathogenesisofPrerenal最常腎臟低灌注后的反腎實質(zhì)保持完灌注恢復(fù)后腎功能可迅速恢復(fù)正持續(xù)嚴重低灌注可轉(zhuǎn)變?yōu)檠軆?nèi)容量下心排量下外周血管擴腎臟血管收腎動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 腎小管上皮細胞腫脹剝形成管細胞粘附分子使壞死的腎小管上皮細胞在一起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Responsiblefor5%ofmedicalhospitaladmissionand30%ofIntensiveCareunit臨床評詳細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AKI的預(yù)