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1、RicciandRoncoCriticalCare2013,17:246http://ccforum.com/content/17/6/246REVIEWYearinreview2012:CriticalCare-nephrology1*2,3ZaccariaRicciandClaudioRoncowithout;RIsweresimilarbetweentransientandpersist-AbstractentAKI;RIsdidnotdifferinpatientsreceivingnorepin-Wesumma
2、rizeoriginalresearchinthefieldofcriticalephrineinfusionandwerenotcorrelatedwithcarenephrologyacceptedorpublishedin2012innorepinephrinedose;andonlyinpatientswithoutAKICriticalCareand,whenconsideredrelevantordirectlywereRIsinverselycorrelatedwithmeanarterialpressur
3、elinkedtothisresearch,inotherjournals.Threemainandpartialpressureofarterialoxygen:fractionofin-topicshavebeenidentifiedforarapidoverview:acutespiredoxygenratio,whereastheyhaddirectcorrelationkidneyinjury,detailedinsomepathogeneticandwithage.Theauthorshonestlyconc
4、ludethat,intheepidemiologicalaspects;fluidoverloadasapredictorlightoftheirresults,renalcirculatoryresponsetosepsisofmortalitybothinacutekidneyinjuryandrenalcannotbereliablypredictedbyasingleDopplerultra-replacementtherapy(RRT)patients;andRRT,sonography.Ontheother
5、hand,interestinglythisworkevaluatingsomefeaturesofcitrateanticoagulationconfirmsthat,insepticcriticallyillpatientswithoutanddescribingtheeffectsofRRTmodalitiesortimingAKI,renalperfusionincreaseswithpressureandisprob-onsurvival.ablyassociatedwithreducedrenalvascul
6、arresistance,whereasrenalvasoconstrictionseeninAKIpatientsseemsunresponsivetohemodynamicsupport;however,Acutekidneyinjury2012duetothepoorvalueofsuchcorrelations,theauthorsIntrarenalhemodynamicsinsistthatrenalRIshaveamultifactorialregulationandAcutekidneyinjury(AK
7、I)pathogenesisiscurrentlynodefinitiveconclusioncanbedrawnbythisstudyonwidelydebatedandintensescientificeffortsarebeingtheexactmechanismdeterminingrenalperfusionauto-madetobetterelucidatemechanismsofrenaldamage.regulationinsepticpatients.Inparticular,renalperfusio
8、nisoneofthemostinvesti-InterestinglyacomprehensivereviewonthisfieldbygatedaspectsofsepticAKIpathogenesis:bothhypoper-SchnellandDarmonreachedthesameconclusionsa
