ABSTRACT
REVIEW AR
INTRODUCTION Approximately5%ofahospital’spatient population may develop acute renal failure (ARF).1,2This prevalence is even greater amongpatientsinintensivecareunits(ICUs), whereitmayreach16%.3,4ARFisasevere disease associated with significant mortality rates.Intheabsenceofcomorbidityfactors, the mortality rate ranges from 7 to 23%, whereas in large series it is around 50%.2,5 Severalfactorshavebeencorrelatedwiththis extremelyhighmortalityrate,suchassepsis, multipleorganfailureandoliguria.5-8
Thepatient’snutritionalstatushasalso been considered to be a possible mortality factorinARFcases.Althoughmalnutritionis highlyprevalentamonghospitalizedpatients andisassociatedwithincreasedmortality,9-11 the current literature on nutrition in ARF casesisfundamentallybasedonexperimental studies.Mostoftheclinicalstudiesavailable havebeenbasedonsmallnumbersofpatients, retrospectivelyanalyzingsurgicalorintensive careunits(ICU)populations.12-17The sam-plingproblemsmayresultfromdifficulties inassessingthenutritionalstatusofcritically illpatients.
Oneofthemostimportantinitialstudies, aimedatevaluatingtheeffectofnutritional therapyinARFcaseswascarriedoutbyAbel etal.(1973).12Theseauthorsreportedlower mortality among ARF patients receiving a combination of essential amino acids and hypertonic glucose, in comparison with patients receiving hypertonic glucose alone. Subsequently,severalinvestigatorsevaluated the role of nutritional supplementation in morbidityandmortalityamongARFpatients and obtained conflicting results.13-17These studies were the subject of a meta-analysis carriedoutbyNayloretal.(1987-88).18This meta-analysisconcludedthatthesurvivalof ARF patients receiving parenteral nutrition
with essential amino acids and hypertonic glucose solutions was better than for those receivinghypertonicglucosealone.However, mostofthestudiesexaminedhadpoorde-scriptionsoftherandomizationcriteriaand inappropriatestatisticalanalysis,andonlytwo ofthefourrandomizedstudiesincludedmore than10patientsineachstudygroup.Thus, the authors of the meta-analysis concluded thattheefficacyofparenteralnutritionregi-mensinARFcasesremainsunclear.
Energy metabolism
Energy expenditure is defined better in relationtotheunderlyingdiseasethantoacute uremicstatus,thussuggestingthat,whenure-miaiswellcontrolled,thereislittlevariationin energymetabolism.19-21Energyrequirements maybeaccuratelycalculatedusingtheHarris-Benedictequationmultipliedbytheassociated stress factor.22 Even under hypercatabolic conditions,suchassepsisororgandysfunc-tion, the energy requirements rarely exceed 1.3timesthebaselineenergyexpenditure.22 InARFcases,anenergyintakeof25to35 kcal/kg/dayisrecommended,accordingtothe associateddegreeofcatabolism.22
Protein metabolism
Themostmarkedalterationinnutritional status among ARF patients is the presence ofhypercatabolismwithanegativenitrogen balance.23 Severalfactorsmaycontributeto-wardstheincreasedcatabolisminARFcases. Inflammatorymediators,includinginterleu-kinsandtumoralnecrosisfactor,activatethe protein metabolism in the same way as in otherconditionslikesepsisthatareobserved among critically ill patients. Data obtained from animal studies suggest that uremia is associated with increased gluconeogenesis, withincreasedproteincatabolismandreduced proteinsynthesis.24Hormonalandmetabolic
EmmanueldeAlmeidaBurdmann
(Famerp),SãoJosédoRioPreto,SãoPaulo,Brazil
Nutritionalstatushasbeenconsideredtobeone ofthepossibledeterminantsofmortalityratesin casesofacuterenalfailure(ARF).However,most studiesevaluatingpossiblemortalityindicators inARFcaseshavenotfocusedonthenutritional status,possiblybecauseofthedifficultiesinvolved inassessingthenutritionalstatusofcriticallyill patients. Although the traditional methods for assessing nutritional status are used for ARF patients, they are not the best choice in this population. The use of nutritional support for these patients has produced conflicting results regardingmorbidityandmortality.Thisreview coversthemechanismsandindicatorsofmalnu-tritioninARFcasesandthetypesofnutritional supportthatmaybeused.
changes,suchasinsulinresistance,increased glucagon concentrations, secondary hyper-parathyroidismandmetabolicacidosishave alsobeencorrelatedwithmalnutritionamong ARFpatients.25,26
Dialysis procedures cause nutrient loss andstimulateproteincatabolism.Inlow-flux membranedialysis,5to8gofaminoacidsare lostpersession.Whenhigh-fluxmembranes areused,theselossesmayincreaseby30%.27,28 The structural characteristics of the dialysis membranemayalsoinfluencethenutritional status.Thelowerthemembranebiocompat-ibility is, the greater the cytokine release related to increased protein catabolism will be,therebydelayingtherecoveryofARFand producingworseoutcomes.29,30Theamountof dialysismayalsoaffectthenutritionalstatus. Itiswellknownthatinadequatedialysisdoses are associated with worsening of the nutri-tional status of patients with chronic renal failure.31Ithasbeenreportedthatthedelivered dialysisdoseinpatientswithARFisfrequently lowerthantheprescribeddose,32,33andthat uremiainducedbysuboptimaldialysisislikely toaggravatetheproteincatabolism.
InexperimentalARFmodels,inaddition toincreasedproteolysis,reducedproteinsyn-thesisisalsoobserved.Inmuscles,theprotein degradationrateisincreasedatthesametime as protein synthesis is reduced, even in the presenceofinsulin.24Theinabilitytoimprove thenutritionalparametersinmostARFpa-tients,despiteadequatenutritionaltherapy,is probablycausedbyfailuretouptakeanduse theavailablenutrients.Thereisevidencethat uremia causes abnormalities in the growth hormone/insulin-like growth factor-1 axis andinducesresistancetotheactivityofthe growth hormone at a cellular level, thereby hinderingtheoptimaluptakeofnutrients.34 Concomitant diseases and conditions fre-quentlyassociatedwithARF,suchassepsisand organfailure,alsoreduceanabolism.
Nutritional assessment in acute renal failure
Several nutritional assessment methods havebeensuggested,usingclinical,biochemi-cal, anthropometric and body component evaluations. However, no single indicator maybeconsideredtobea“goldstandard”. Manyofthetraditionalnutritionalevaluation methods used in ARF cases are affected by non-nutritionalfactors,andthereforeought nottobeusedinthispatientpopulation.The mostimportantreasonfordiscrepanciesisthat severalprocessesplayaroleinthemalnutrition ofhypercatabolicpatientswithARF.Inthese
patients,malnutritionisametabolicresponse tostressorinflammation,whereasunderother conditions,malnutritionispredominantlya response to chronic inanition. Nutritional marker variations might differ considerably underthesetwoconditions.32,35
Insulin-like growth factor-1 Insulin-likegrowthfactor-1(IGF-1)and insulin-likegrowthfactor-2(IGF-2)arestructur-allyrelatedtoinsulin.HumanIGFs,generically calledsomatomedins,aresimplechainpeptides of7.5kilodaltons(kDa),composedof70(IGF-1)or67aminoacids(IGF-2).36Fourproperties, designated A, B, C and D, are identified in IGFmolecules,andtheAandBpropertiesare homologues for the insulin A and B chains. Somatomedinsaresecretedatthesametime astheyareproduced,andconsequentlythey arenotconcentratedinanyorgan.Therefore, althoughtheliveristhemajorsourceofcirculat-ingsomatomedins,37theirhighestconcentration isobservedintheblood.38IGFsareproduced inseveralorgansandarebiologicallyactivein mostcelltypes.39Thesepeptidesactthrough autocrineandparacrinemechanisms,aswellas throughtheclassicendocrinemechanisms.40The growthhormoneisoneofthemajorhormonal stimuliforIGF-1production.41Lessthan5%of circulatingIGF-1isfree,andover90%istiedto otherbindingproteins.42 IGF-1synthesisisin-fluencedbyhormonalandnutritionalfactors.43 In humans, serum IGF-1 levels are reduced afterprotein-energydeprivation,andreturnto normallevelswithinfewdaysafterfoodintake isresumed.44 IGF-1isareliablemarkerfornu-tritionalstatusandhasbeenshowntobebetter thanotherbiochemicalmarkersforassessingni-trogenbalanceinseverelyillandhypercatabolic patients.45Untermanetal.(1985)46reported that,inmalnourishedpatients,IGF-1serum levels were better indicators than laboratory testsandtheclassicanthropometricparameters usedtoevaluatenutritionalstatus.Donahueand Phillips(1989)47showedthatdecreasedIGF-1 serumlevelsinhospitalizedpatientswithprotein orprotein-energymalnutrition(39±7ng/ml) weremoremarkedthaninpatientswithenergy malnutritionalone(109±25ng/ml),thuscon-firmingthemajorroleofproteinintakeinIGF-1 regulation.ThegoodcorrelationofIGF-1with nutrientdeprivationorintake,itsserumstability andshorthalf-liferecommenditsuseasamarker fornutritionalstatusinARFcases.42,45,48 Albumin
Serumalbuminlevelsdecreasemarkedly in response to stress and inflammation,49 and may not accurately reflect nutritional status changes in severely ill patients.The
serumhalf-lifeofalbuminisrelativelylong (20 days) and serum albumin concentra-tionschangeinresponsetocatabolismand nutritionalsupplementationthattakeplace in the late-stage course of acute diseases.50 Hypoalbuminemia has been described as anindependentfactorformortalityamong elderly patients and patients with chronic renal failure undergoing dialysis.51,52 How-ever,thereislittleevidenceforanassociation betweendecreasedserumlevelsofalbumin andmortalityinARFcases.Decreasedserum albuminlevelshavebeendescribedbyCher-towetal.(1998)6aspredictorsofmortality amongpatientswithacutetubularnecrosis. It should be emphasized that, up to that time,therehadnotbeenanyreportsinthe literaturetoassociatehypoalbuminemiawith highermortalityinARFpatients.Inastudy of15,000severelyillpatients,serumalbumin levels<3.4g/dlonadmissionwerestrongly associatedwithhighermortality,prolonged hospitalizationandreadmission.52
Transferrin
Transferrinhasashorterhalf-life(8days) than albumin, but it lacks sensitivity for evaluatingtheshort-termeffectsofrefeeding.53 Transferrinconcentrationissignificantlyinflu-encedbypatients’serumironlevels.54 Prealbumin
Serumprealbuminisanutritionalmarker with a half-life of 1 to 2 days and a good response to nutritional supplementation.53 Similarlytoalbumin,itsserumlevelsdecrease inresponsetostressandinflammation.49Itis excretedmainlybythekidneys.Prealbumin concentrationsmaybefalselyhighinpatients withARF.55
Subjective global assessment Subjective global assessment (SGA) is a techniqueusedforevaluatingnutritionalstatus. Itassessesthenutritionalstatusbasedonclinical experienceandincludesthemedicalandnutri- tionalhistory,physicalexaminationandfunc-tionalassessmentofthepatients.Thismethod wasinitiallydevelopedtoassessthenutritional statusofsurgicalpatients,57,58butithasnowbeen usedinseveralgroupsofpatients.59,60Inpatients withchronicrenalfailure,goodcorrelationhas beenfoundbetweendiagnosesofmalnutrition madeviaSGAandobjectivemethods,includ-ingbiochemistrytestsandbodycomposition measurement.59,61Abdullahetal.(1998)62found lowerlevelsofanabolicfactors,suchasIGF-1, andhighercataboliccytokinelevelsinpatients classifiedasmalnourishedviaSGA.Worsening ofnutritionalstatus,asevaluatedbytheSGA methodinchronicrenalpatientsundergoing peritoneal dialysis, has been correlated with greater mortality risk,63 although the results fromsubsequentstudieshaveconflictedwith this.64,65Fiaccadorietal.(1999)66reportedthat nutritional status changes, as assessed by the SGA method, are frequent findings among ARFpatients.Thesameauthorsreportedthat preexistingmalnutrition,characterizedbySGA classC,wasanindependentpredictorforhos-pitalmortality.
Since SGA is a subjective technique, it doesnotmeasurevisceralproteinsanddoes notprovidefollow-upfornutritionaltherapy. Moreover, because it requires information from patients, this methodology may not alwaysbeapplicabletoARFpatientsinthe ICU, due to their decreased consciousness levels caused by their underlying disease or bytheuseofsedatives,orbecauseoftheuse ofmechanicalventilation.
Total cholesterol
Serum cholesterol is an independent predictor for mortality among hemodialysis patients.Individualsundergoinghemodialysis withnormalorlow(from150to180mg/dl) serumcholesterollevelshavehighermortality than those with higher cholesterol levels.67,68 However,theassociationbetweenhypocholester-olemiaandmortalityduetonon-cardiovascular causes is unclear.69 Hypocholesterolemia and decreasedlowdensitylipoprotein(LDL)have beendescribedinseverelyillsurgicalpatientsin theICUwithevidenceofsepsis.70Itisnotclear under what circumstances serum cholesterol mightbeareliableindicatorofprotein-energy malnutrition.Additionaldataontheassociations betweenserumcholesterol,nutritionalstatusand morbidityandmortalityarerequired.
Table1.Estimatingtheextentofproteincatabolism
Ureanitrogenappearance(UNA)(g/day)
=urinaryureanitrogenexcretion+changeinureanitrogenpool =(UUNxV)+(BUN2–BUN1)0.006xBW+(BW2–BW1)xBUN2/100
Iftherearesubstantialgastrointestinallosses,addureanitrogeninsecretions: =volumeofsecretionsxBUN2
Netproteinbreakdown(g/day)=UNAx6.25 Muscleloss(g/day)=UNAx6.25x5
UUN=urinaryureanitrogenconcentrationingramsnitrogen/day;V=urinaryvolumeinliters;BUN1andBUN2=bloodurea nitrogeninmgnitrogen/dlondays1and2;BW1andBW2=bodyweightsinkgondays1and2.
Patient classification and nutritional therapy
Theuseofadequatenutritionaltherapy amongpatientssufferingfromdifferentdis-easesisrequiredinordertomaintainprotein storageandregulateleanbodymassdeficits. Theobjectivesofnutritionaltherapyamong ARFpatientsarenodifferentfromthoseun-derotherhypercatabolicconditions.However, they are different from the objectives to be achievedamongpatientswithchronicrenal failure (CRF), since therapies meeting the minimum requirements for CRF are insuf-ficientforARFpatients.22
Since not all ARF patients necessarily require nutritional support, it is important to identify those who will benefit from it, as well as to establish the optimal time to start therapy.The decision to start therapy isinfluencedbytheindividual’scapacityto adequately intake the nutritional require-ments,bynutritionalstatusandbythetype ofunderlyingdisease.Whenthereisevidence ofmalnutritionorhypercatabolism,therapy shouldbestartedearlyon.
Nutritional requirements are often ne-glected in clinical practice. Urea nitrogen appearancerate(UNA)measurements,which reflect protein catabolism,22 and the assess-mentofenergyrequirementsarenotroutine practice.Theformulaeusuallyusedtocalcu-lateenergyrequirementsmayunderestimate theserequirementsamongARFpatients,since they are based on healthy individuals with normalbodyfluiddistribution.
The undesirable effects of nutritional therapyareanotherlimitationonitsuse.Ex-cessive supplementation of proteins increases theendproductsofproteinmetabolism.The provisionoflargeamountsofnutrientsrequires theinfusionofconsiderablequantitiesoffluids, carbohydratesandlipids,andthismaycause volume overload and undesirable electrolytic andmetabolicchanges,suchashyperglycemia, hyperlipidemia,hypernatremiaorhyponatremia.
Althoughmostofthesechangesmaybecon-trolledbydialysis,thepossibilityofsuchchanges induces physicians to use more conservative approachestowardsnutritionaltherapy,thereby inadvertentlycontributingtoaworseningofthe nutritionalstatusofARFpatients.
Nutritionalprogramsmustbeindividu-allydesignedforeachARFpatient.Inclinical practice,patientsmaybedividedintothree groups,22 accordingtothedegreeofcatabo-lism,whichmaybeevaluatedbycalculating theUNArate(Table1).
GROUPI:LowUNArate.Thesepatients aremildlycatabolic,i.e.thosewhoseARFwas causedbynephrotoxinsalone(aminoglycosides, contrastmediaandothers).Dialysisisseldom required and the use of nutritional therapy containing25kcal/kg/dayand0.6g/kg/dayof proteinsrichinessentialaminoacidsisusually sufficient.Suchpatientsareusuallyfedorally and the prognosis for the recovery of renal functionandsurvivalisexcellent.22
GROUPII:ModerateUNArate.These areARFpatientswithmoderatecatabolism, frequentlysufferingfrominfectiousorsurgical complications.Theuseofenteralorparenteral nutritionanddialysisisoftenrequired.These patientsshouldreceiveessentialandnon-es-sential amino acids at a dose of 0.8 to 1.2 g/kg/dayandcalorieintakeof25to30kcal/ kg/day.Themortalityrateinthispopulation isapproximately60%.22
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Sourcesoffunding:Notdeclared
Conflictofinterest:Notdeclared
Dateoffirstsubmission:March24,2004
Lastreceived:April7,2005
Accepted:April7,2005
AUTHOR INFORMATION Sérgio Mussi Guimarães, MD. Assistant professor, IntensiveCareUnit,DepartmentofMedicine,Hospitalde Base,FaculdadedeMedicinadeSãoJosédoRioPreto (Famerp),SãoJosédoRioPreto,SãoPaulo,Brazil. JoséPauloCipullo,MD,PhD.
Adjunctprofessor,Ne-phrologyDivision,DepartmentofMedicine,Hospitalde Base,FaculdadedeMedicinadeSãoJosédoRioPreto (Famerp),SãoJosédoRioPreto,SãoPaulo,Brazil. Suzana Margareth Ajeje Lobo, MD, PhD. Adjunct
professor,IntensiveCareUnit,DepartmentofMedicine, HospitaldeBase,FaculdadedeMedicinadeSãoJosédo RioPreto,SãoJosédoRioPreto,SãoPaulo,Brazil. Emmanuel de Almeida Burdmann, MD, PhD.
As-sociate professor, Nephrology Division, Department of Medicine,FaculdadedeMedicinadeSãoJosédoRioPreto (Famerp),SãoJosédoRioPreto,SãoPaulo,Brazil.
Addressforcorrespondence: SérgioMussiGuimarães
RuaDr.CarlosdeArnaldoSilva,110 —JardimPalmeiras
SãoJosédoRioPreto(SP)—Brasil—CEP15093-000 Tel.(+5517)227-8239
E-mail:sergiomussi@terra.com.br
Copyright©2005,AssociaçãoPaulistadeMedicina
RESUMO
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