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syndromeatDCMdiagnosisconferredanincreasedriskof5-yearmortality
(hazardratio,2.4;95%confidenceinterval,0.8to7.4),andtheestimated
glomerularfiltrationratewaspositivelycorrelatedwithmeasuresofventricular
function.Thusthesepreliminarystudiessuggestcarefulattentionshouldbepaid
tokidneyfunctioninchildrenwithacutecardiacdysfunction.
ThemanagementofAKIinheartfailurehasalsobeenthesubjectofintense
clinicalstudyoverthepastdecadeinadults,withafocusondiuretic
administrationversusmechanicalfluidremovalviaultrafiltration.64,65Whilethis
focushasgeneratedrandomizedclinicaltrialscomparingdiureticsto
ultrafiltrationwithvaryingresults,apotentiallymorethoughtfulapproachisto
considerdiureticsasafirstlineoftreatmentandthenescalationtoultrafiltration
inpatientswhoareresistanttodiuretics.Patientswithheartfailuremayhave
AKIfromafunctional,prerenalcause,fromstructuralintrinsicrenaldamage,or
both.66PatientswithfunctionalAKImayrespondwelltodiureticsifrenal
perfusionandoncoticpressurearesufficient,whereaspatientswithstructural
AKImaynotrespondwell.
TheadditionalinformationprovidedbystructuralAKIbiomarkersintheacute
heartfailuresettinghasbeenrecentlyaddressed.First,onemeta-analysisof
pediatricandadultstudiesdemonstratedthat41%ofpatientswithelevated
NGALlevelswouldhavehadtheAKIdiagnosismissedbyserumcreatinine
alone,andpatientswithNGAL+/Cr−AKIhassimilarmorbidityandmortalityas
patientswithNGAL−/SCr+AKI.67Second,aprospectiveadultstudyrevealed
thatintegrationofaheartfailuremarker(B-typenatriureticpeptide)anda
kidneydamagemarker(plasmaNGAL)improvedthepredictionof30-day
mortalityandhospitalreadmissionrates.68Finally,inthechronic
cardiomyopathysetting,theurinarybiomarkersinterleukin-18,kidneyinjury
molecule-1,andNGALwereobservedinhigherconcentrationsthaninhealthy
matchedcontrols.69Inaddition,acombinedmodelusingcut-offvaluesof
kidneyinjurymolecule-1of235orgreater,interleukin-18of17.5orgreater,and
B-typenatriureticpeptideof15pg/mLresultedindifferentiationofpatientswith
mildlydepressedLV(55%>LVejectionfraction≥45%)andthosewithaleft