Understanding urine output in critically ill patients 英文参考文献.docVIP

LegrandandPayenAnnalsofIntensiveCare2011,1:13 /content/1/1/13 REVIEW OpenAccess Understandingurineoutputincriticallyillpatients MatthieuLegrand*andDidierPayen Abstract Urineoutputoftenisusedasamarkerofacutekidneyinjurybutalsotoguidefluidresuscitationincriticallyill patients.Althoughdecreaseofurineoutputmaybeassociatedtoadecreaseofglomerularfiltrationratedueto decreaseofrenalbloodfloworrenalperfusionpressure,neurohormonalfactorsandfunctionalchangesmay influencediuresisandnatriuresisincriticallyillpatients.Thepurposeofthisreviewistodiscussthemechanismsof diuresisregulation,whichmayhelptointerprettheurineoutputincriticallyillpatientsandtheappropriate treatmenttobeinitiatedincaseofchangesinurineoutput. Introduction WhyshouldwewonderaboutoliguriaandAKI? Acute renal failure or acute kidney injury (AKI) is Thereisaccumulatingevidencethatcriticallyillpatients definedbyanacutedeclineofglomerularfiltrationrate developing AKIhaveanincrease relative riskofdeath. (GFR).OccurrenceofAKIisassociatedwithsubstantial OccurrenceofAKIisamarkerofseverityoftheunderly- in-hospital mortality, exceeding 50% when AKI is part ingacuteillnessbutalsoappearsasanindependentfactor of a multiple organ failure syndrome [1,2]. Therefore, associatedwithmortalityinunselectedcriticallyillpatients early recognition of AKI, better understanding of its [7],insepsis[8],pneumonia[9],orcardiacsurgery[10]. pathogenesis, and development ofpreventing strategies Themechanisticpathwaysofsuchanassociationremain appeartobepotentialareasofimprovementofpatient’s elusive,withintricationofinflammation,metabolism,and prognosis.Thedecreaseofglomerularfiltrationrateand apoptoticphenomena.Remoteorgansdamagehasbeen urine output in response to a decrease of renal blood suggested in several experimental studies [11,12]. flowisclassically referred aspre-renal azotemia, which Ischemic-inducedAKIhasbeenfoundtoinducemyocar- canevolveintostructuraldamageifrenalhypoperfusion dial apoptosis [13],