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Causesofmetabolicalkalosis

OfficialreprintfromUpToDate
www.uptodate.com2015UpToDate

Causesofmetabolicalkalosis
Author
MichaelEmmett,MD

SectionEditor
RichardHSterns,MD

DeputyEditor
JohnPForman,MD,MSc

Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.
Literaturereviewcurrentthrough:May2015.|Thistopiclastupdated:Jul01,2014.
INTRODUCTIONMetabolicalkalosis,whichproducesanelevationoftheserumbicarbonate,isarelatively
frequentclinicalproblemthatismostcommonlyduetothelossofhydrogenionsfromthegastrointestinaltractor
intheurine.Theselosthydrogenionsarederivedfromthedissociationofwaterintohydrogenandhydroxylions.
Whenthehydrogenionisremoved,theremaininghydroxylioncombineswithcarbondioxidetoformbicarbonate.
Gastrointestinalandrenalhydrogenlossisusuallyaccompaniedbythelossofchlorideandpotassiumaswellas
thedevelopmentofhypochloremiaandhypokalemia.
Theplasmabicarbonateconcentrationmayalsobeincreasedbyhydrogenmovementintothecells,alkali
administration,orvolumecontractionaroundarelativelyconstantamountofextracellularbicarbonate(calleda
contractionalkalosis)(table1)[14].
Patientswithpreservedrenalfunctionwillmostoftenrapidlyexcreteexcessbicarbonateintheurine.Thus,for
metabolicalkalosistopersist,theremustbeareductionintheabilitytoexcretetheexcessbicarbonateinthe
urine.Thisisusuallyduetohypovolemia,reducedeffectivearterialbloodvolume(includingheartfailureand
cirrhosis),chloridedepletion,hypokalemia,renalimpairment,hyperaldosteronism,orcombinationsofthesefactors
[3,5,6].
Thecausesofmetabolicalkalosiswillbereviewedhere.Thepathogenesis,evaluation,andtreatmentofthis
disorderarediscussedseparately.(See"Pathogenesisofmetabolicalkalosis"and"Clinicalmanifestationsand
evaluationofmetabolicalkalosis"and"Treatmentofmetabolicalkalosis".)
GASTROINTESTINALHYDROGENLOSSGastrointestinalhydrogenlosscanresultfromtheremovalof
gastricsecretions(vomitingornasogastricsuction)orlossofintestinalsecretions(someunusualcausesof
diarrhea).
RemovalofgastricsecretionsGastriccontentshaveahighconcentrationofHClandlesseramountsofKCl
andNaCl.Innormalsubjects,gastrichydrogenionsecretiondoesnotleadtometabolicalkalosissinceitisnot
removedfromthebody,butinsteadisneutralizedbybicarbonatesecretedbythepancreasinresponsetotheacid
thatenterstheduodenum.Withintheintestinallumen,thehydrogenandbicarbonateionscombinetoform
carbonicacidandwater,andthesecretedNaandClionsarereabsorbedintothesystemiccirculation.When
vomitingornasogastrictubesuctionremovesHClfromthebodyandpreventsitfromreachingtheduodenum,
bicarbonateisaddedtotheextracellularfluid[79].Insomecases,ahistoryofvomitingmaynotbeapparent.The
patientmaydenyvomitingorbeunabletoprovideahistory[10].Inthesesituations,measurementoftheurine
chlorideconcentrationmayprovideahelpfuldiagnosticclue.(See"Clinicalmanifestationsandevaluationof
metabolicalkalosis".)
Theadministrationofpoorlyabsorbedantacidsdoesnotusuallygeneratemetabolicalkalosis.Althoughthe
hydroxideorcarbonatecomponentoftheantacidbuffersgastrichydrogenions,thecationcomponentofthe
antacid(magnesium,aluminum,orcalcium)combineswithbicarbonateinthemoredistalgastrointestinallumen
andisexcretedinthestool[11].Theneteffectisthattheingestionofpoorlyabsorbedalkaliismatchedbya
virtuallyidenticalexcretionofalkaliinthestool.Anexceptionoccursifpatientswithrenalfailurearetreated
simultaneouslywithbothapoorlyabsorbedantacidandacationexchangeresinsuchassodiumpolystyrene
sulfonate.Usually,thiscationexchangeresinreleasessodiumandbindspotassium.However,ifgivenwithan
antacid,thecationexchangeresinmaybindthemagnesium,aluminum,orcalciumfromtheantacidinsteadof
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potassium.Thesodiumreleasedfromthecationexchangeresinandthecarbonatereleasedfromtheantacidare
absorbedtogetherwhilethecationexchangeresinisexcretedinthestoolcombinedwiththemagnesium,
aluminum,orcalcium[12].Therenalfailureplaysanimportantroleinthispathophysiologybecauseitperpetuates
thealkalosisbypreventingexcretionoftheexcessbicarbonate.
LossofintestinalsecretionsIntestinalsecretionstypicallyhavearelativelyhighbicarbonateconcentration.
Asaresult,lossofthesesecretions(asindiarrhea)typicallyleadstometabolicacidosis.However,inrare
instances,diarrheacanproducemetabolicalkalosis[8].Thismayoccurinsomepatientswithavillousadenoma
andinsomewhoabuselaxatives.Themechanismresponsibleforthemetabolicalkalosisinsuchpatientsisnot
wellunderstood,buthypokalemiaisinvariablyprominentandprobablyplaysamajorpathophysiologicrole[13].
Theconcurrentsurreptitioususeofdiureticsmayalsocontribute.(See"Factitiousdiarrhea"and'Hypokalemia'
below.)
Inaddition,patientswithcongenitallydefectiveintestinalchlorideabsorption(congenitalchloridediarrheaor
chloridorrhea)developdiarrheaandmetabolicalkalosis.Thisrarecongenitalsecretorydiarrheaiscausedby
mutationsinthedownregulatedinadenoma(DRA)gene,whichdirectssynthesisoftheintestinalanionexchanger
responsibleforchloridereabsorptionandbicarbonatesecretion.(See"Overviewofthecausesofchronicdiarrhea
inchildren",sectionon'Congenitalsecretoryandosmoticdiarrheas'.)
EXCESSIVERENALHYDROGENLOSSAninappropriateincreaseinrenalacidlossrequiresenhanceddistal
hydrogensecretion.Thismostoftenoccurswhenadequatesodiumandwaterdeliverytothedistalnephronis
combinedwithincreasedmineralocorticoidactivity.
Mineralocorticoidshavemultipleactionsinthedistalrenaltubulewhichcombinetoenhancehydrogenion
secretion:
TheydirectlystimulatethesecretoryHATPasepump(figure1).
Mineralocorticoidsalsoincreasethenumberofopenepithelialsodiumchannels(ENaC)andsimultaneously
increaseNaKATPase,whichtogetherenhancesthemovementofNafromthedistaltubulelumenacross
thecellandintotheECF(figure2).Sodiumisreabsorbedmorereadilythanluminalanions,andthis
generatesamoreelectronegativetubularlumen.Theelectronegativelumenreducesbackdiffusionof
secretedhydrogenionsfromthelumenintothetubularcellsandincreasesdistalpotassiumsecretion,
resultinginhypokalemiaandtotalbodypotassiumdepletion[14,15].
PrimarymineralocorticoidexcessAnycauseofprimaryhypersecretionofmineralocorticoids(oftendueto
mineralocorticoidsecretionthatisindependentofhypovolemia)canleadtometabolicalkalosis,whichisgenerally
accompaniedbyhypertensionandhypokalemia.(See"Approachtothepatientwithhypertensionand
hypokalemia".)
Incontrast,patientswithsecondaryhyperaldosteronismduetoreducedeffectivearterialbloodvolume(asin
hypovolemia,heartfailure,orcirrhosis)usuallydonotdevelopmetabolicalkalosisorhypokalemiaunlesstheyare
treatedwithdiuretics.Insuchpatients,intheabsenceofdiuretictherapy,theavidproximaltubulesodium
reabsorptionmarkedlyreducesdistalsodiumdelivery.Whendistalsodiumdeliveryisdiminished,thehighlevels
ofaldosteronecannotinducealargeamountofdistalsodiumreabsorptionorpotassiumandprotonsecretion.
Thecombinationofhighmineralocorticoidlevelsandgenerousdistalsodiumdeliveryonlyoccurswithprimary
hypersecretionofmineralocorticoids(oradisorderthatmimicsprimaryhyperaldosteronism,suchasLiddle's
syndrome)orthecombinationofsecondarymineralocorticoidsecretionplusadiureticwhosesiteofactionis
proximaltothesiteofhydrogenionsecretion.(See"Geneticdisordersofthecollectingtubulesodiumchannel:
Liddle'ssyndromeandpseudohypoaldosteronismtype1",sectionon'Liddle'ssyndrome'.)
LooporthiazidediureticsThesediureticsincreasebothdistalsodiumdeliveryandthesecretionof
aldosterone.Althoughthisissecondaryasopposedtoprimaryhyperaldosteronism,thediureticinducedincrease
indistalsodiumdeliveryincreasesurinaryhydrogenandpotassiumsecretion,resultinginmetabolicalkalosisand
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hypokalemia.Ifhypovolemiaisinducedbythediuresis,thisalsocontributestotheelevationofserumbicarbonate
[1618].(See'Contractionalkalosis'below.)
BartterandGitelmansyndromesMetabolicalkalosisandhypokalemiaarepresentinBartterandGitelman
syndromes.ThesedisordersareproducedbygeneticdefectsiniontransportersintheloopofHenleanddistal
tubule,respectively,producingasimilarinhibitoryeffectonsodiumchloridereabsorptionasloopandthiazide
diuretics.(See"BartterandGitelmansyndromes".)
PosthypercapnicalkalosisChronicrespiratoryacidosiscausesanappropriatecompensatoryincreaseinrenal
hydrogensecretion.TheensuingriseintheplasmabicarbonateconcentrationwillraisethepHtowardnormal[19].
Theelevationintheserumbicarbonateconcentrationisassociatedwithammoniumchloridelossand
hypochloremia[20].
IfthechronicallyelevatedPCO2israpidlylowered,usuallybymechanicalventilation,theplasmabicarbonate
concentrationmayremainelevated,especiallyifthepatienthasaloweffectivearterialbloodvolume,areduced
glomerularfiltrationrate(GFR),andischloridedeficient.Restorationofanormal,orreduced,PCO2witha
persistentlyelevatedbicarbonateconcentrationresultsinametabolicalkalosisthatiscalled"posthypercapnic"
metabolicalkalosis.Thisalkalosiswillpersistuntilenoughsodiumchlorideisingestedorinfusedtorepletethe
extracellularfluidvolumeandchloridedeficit[20].
ArapidfallinPCO2leadingtoaposthypercapnicalkalosismayacutelyraisethecerebralintracellularpH.
Althoughthiseffecthasbeenreportedtoproduceseriousneurologicabnormalitiesanddeath,thereareinsufficient
datatoconfirmthatthealkalosisisthepathophysiologicmechanism[21].Mostexperts,nonetheless,recommend
thatthePCO2begraduallyreducedinpatientswithchronichypercapnia.
HypercalcemiaandthemilkalkalisyndromeThemilkalkalisyndromeisanimportantcauseofmetabolic
alkalosisandisusuallyassociatedwithhypercalcemia.(See"Themilkalkalisyndrome".)
Themilkalkalisyndromemostcommonlyresultsfromtheingestionoflargeamountsofcalciumcarbonate
togetherwithvitaminD.Ifpresent,vomitingleadstohypovolemiaandreducedrenalfunction,andhypercalcemia
impairsrenalfunctionhypovolemiaandreducedrenalfunctioninturnmaintainthealkalosis[2225].Alkalosisalso
enhancesrenalcalciumreabsorption,therebyexacerbatingthehypercalcemia[25].(See"Themilkalkali
syndrome".)
INTRACELLULARSHIFTOFHYDROGENMetabolicalkalosiscanalsobegeneratedbyashiftofhydrogen
ionsintothecells.Thismostoftenoccursinpatientswithmarkedpotassiumdeficitsandhypokalemia.Thismay
beanimportantpathophysiologicmechanisminpatientswithmetabolicalkalosisduetovomitingornasogastric
suction[26].(See"Potassiumbalanceinacidbasedisorders".)
HypokalemiaHypokalemiaisafrequentfindinginpatientswithmetabolicalkalosis.Itisanimportant
contributortoboththedevelopmentandmaintenanceofthealkalosis.Thepotassiumlossandhypokalemia
interactwithmetabolicalkalosisinmultipleways[1]:
Manymajorcausesofmetabolicalkalosis(vomiting,diuretics,mineralocorticoidexcess)directlyorindirectly
inducerenalpotassiumloss.(See"Causesofhypokalemiainadults".)
Hypokalemiacausespotassiumtomovefromcellsintotheextracellularfluid,andthistranscellular
potassiumfluxcausesextracellularhydrogenionstomoveintocellstomaintainelectroneutrality[1].These
ionfluxessimultaneouslyincreasetheplasmabicarbonateconcentrationandlowertheintracellularpH.To
theextentthatthisoccursinrenaltubularcells,theensuingintracellularacidosispromoteshydrogen
secretionintothelumen,andtherefore,bicarbonatereabsorption[27].(See"Potassiumbalanceinacidbase
disorders"and"Pathogenesisofmetabolicalkalosis".)
Hypokalemiaalsoincreasesrenalammoniagenesisandammoniumexcretion,whichcanbothgenerateand
helptomaintainmetabolicalkalosis.
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ALKALIADMINISTRATIONItisdifficulttoproducemorethanamodestincreaseinplasmabicarbonatewith
chronicalkalitherapyinnormalindividuals.Theshorttermadministrationofevenlargeamountsofsodium
bicarbonatetonormalindividualsusuallyresultsinveryrapidrenalexcretionoftheentirealkaliloadwithminimal
increaseinthebicarbonateconcentration.Asanexample,administrationofenormousamountsofsodium
bicarbonate,between1000to1400meqperdayina70kgindividual,foraslongastwotothreeweeksonly
raisedtheserumbicarbonateconcentrationtoamaximumof36meq/Lbecausemostoftheingestedsodium
bicarbonatewasrapidlyeliminatedintheurine[28].
Morepronouncedmetabolicalkalosiscanoccuriflargequantitiesofsodiumbicarbonate(oranysodiumsaltsof
organicanionsthataremetabolizedtobicarbonatesuchaslactate,citrate,oracetate)aregivenoverashort
periodoftime.However,hypovolemia,reducedeffectivearterialbloodvolume,orrenalimpairmentispresentin
mostofthefollowingexamples:
Theadministrationofsodiumbicarbonatetotreatlacticacidosisorketoacidosismayproduceapost
correctionmetabolicalkalosis.Inthesesettings,theadministeredbicarbonaterepresents"excess"alkali
sincereversaloftheunderlyingdisorderwillregeneratebicarbonatefromthemetabolismoflactateorbeta
hydroxybutyrate,bothofwhichrepresent"potentialbicarbonate"[29].(See"Pathogenesisofmetabolic
alkalosis"and"Diabeticketoacidosisandhyperosmolarhyperglycemicstateinadults:Treatment",section
on'Bicarbonateandmetabolicacidosis'and"Bicarbonatetherapyinlacticacidosis".)
Administrationoflargequantitiesofcitratesaltscanproduceametabolicalkalosis.Thisbecomeslikely
whenmorethaneightunitsofbloodaretransfused.Citricacidandsodiumcitrate,whichareusedto
anticoagulatetheblood,arelatermetabolizedtosodiumbicarbonate.Infusionoflargeamountsoffresh
frozenplasma,forexampleduringplasmapheresis,generatesthesametypeofalkalosisasaresultof
sodiumcitrateanticoagulant.Theuseofcitratesaltsratherthanheparinasananticoagulantinhemodialysis
patientsorduringcontinuousrenalreplacementtherapyalsorepresentsanalkaliload.
Freebaseandcrackcocaineareproducedwithsodiumbicarbonate,andextensiveusecangenerate
metabolicalkalosisespeciallywhenrenalfunctionisverypoor[1,3034].
Theintentionalinductionofmetabolicalkalosisinathleteshasbeenstudiedasamethodtoimproveexercise
performance[35,36].Thepresumptivemechanismofactionmayberelatedtoenhancedhydrogenionefflux
outofmuscleanddecreasedinterstitialpotassiumaccumulationinmuscle,resultinginimprovedATP
resynthesisandanaerobicglycolysis.
CONTRACTIONALKALOSISAcontractionalkalosisoccurswhenthereislossofrelativelylargevolumesof
lowbicarbonate,sodiumcontainingfluid[17,18].Theplasmabicarbonateconcentrationrisesinthissetting
becausethereiscontractionoftheextracellularvolumearoundarelativelyconstantquantityofextracellular
bicarbonate.Thedegreetowhichthisoccursisoffsetbyintracellularbuffering,whichresultsinthereleaseof
hydrogenionsfromcellbufferstolowertheplasmabicarbonateconcentrationtowardthebaselinevalue[18].
Administrationofintravenousloopdiureticstoinducerapidfluidremovalinamarkedlyedematouspatientisthe
mostcommoncauseofacontractionalkalosis[17,37].Othercausesincludesweatlossesincysticfibrosis,
congenitalchloridediarrhea,andpossiblythelossofgastricsecretionsinpatientswithachlorhydria[8,3840].
(See"Overviewofthecausesofchronicdiarrheainchildren",sectionon'Congenitalchloridediarrhea'.)
However,useoftheterm"contractionalkalosis"tocharacterizethemetabolicalkalosesassociatedwithvomiting,
nasogastricsuction,anddiureticuseisconfusing.Intheseconditions,theexternallossofhydrogenions
generatedbythestomachorkidneysplaysacrucialroleinthedevelopmentofthesemetabolicalkaloses.
Althoughcontractionoftheextracellularfluidspacedoesalsoelevatethebicarbonateconcentration,amore
importanteffectofthecontractionisenhancedrenalbicarbonatereabsorption,whichmaintainsthealkalosis.
SUMMARY
Metabolicalkalosis,whichproducesanelevationoftheserumbicarbonate,isarelativelyfrequentclinical
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problemthatismostcommonlyduetotheexcesslossofhydrogenionsfromthegastrointestinaltractorin
theurine(table1).Increasedserumbicarbonatemayalsoresultfromhydrogenmovementintothecells,
alkaliadministration,orvolumecontractionaroundarelativelyconstantamountofextracellularbicarbonate
(calledacontractionalkalosis).Patientswithpreservedrenalfunctionwillrapidlyexcreteexcessbicarbonate
intheurine.Thus,formetabolicalkalosistopersist,theremustbeareductionintheabilitytoexcretethe
excessbicarbonateintheurine.(See'Introduction'above.)
Gastrointestinalhydrogenlosscanresultfromtheremovalofgastricsecretions(vomitingornasogastric
suction)orrectallossofintestinalsecretions(someunusualcausesofdiarrhea,suchasvillousadenoma).
(See'Gastrointestinalhydrogenloss'above.)
Anincreaseinrenalacidlossisusuallyduetoadequateorincreasedsodiumandwaterdeliverytothedistal
nephroncombinedwithincreasedmineralocorticoidactivity.Thiscombinationoccurswithprimary
mineralocorticoidexcess,useoflooporthiazidediuretics,BartterandGitelmansyndromes,and
hypercalcemiawiththemilkalkalisyndrome.(See'Excessiverenalhydrogenloss'aboveand'Primary
mineralocorticoidexcess'aboveand'Looporthiazidediuretics'aboveand'BartterandGitelmansyndromes'
aboveand'Hypercalcemiaandthemilkalkalisyndrome'above.)
Chronicrespiratoryacidosisleadstoanappropriateincreaseinrenalhydrogensecretion,andtheensuing
riseintheplasmabicarbonateconcentrationwillraisethearterialpHtowardnormal.Ifthechronically
elevatedPCO2israpidlylowered,usuallybymechanicalventilation,theplasmabicarbonateconcentration
mayremainelevated,producingaposthypercapnicalkalosis.(See'Posthypercapnicalkalosis'above.)
Inadditiontohydrogenlossfromthebody,metabolicalkalosiscanalsobeduetotheshiftofhydrogenions
intothecells.Thismostoftenoccursinpatientswithhypokalemia.(See'Intracellularshiftofhydrogen'
above.)
Alkaliloadsadministeredtoapatientwithanimpairedrenalcapacitytoexcretethebicarbonate(duetolow
effectivearterialbloodvolume,chloridedepletion,hypokalemia,orintrinsicrenaldisease)mayproduce
metabolicalkalosis.Therapidadministrationofalkaliloadscancauseshorttermmetabolicalkalosis.(See
'Alkaliadministration'above.)
Acontractionalkalosisoccurswhenthereislossofrelativelylargevolumesofbicarbonatefreefluid.The
plasmabicarbonateconcentrationrisesinthissettingbecausethereiscontractionoftheextracellularvolume
aroundarelativelyconstantquantityofextracellularbicarbonate.(See'Contractionalkalosis'above.)
UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.
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GRAPHICS
Majorcausesofmetabolicalkalosis
Gastrointestinalhydrogenloss
Vomitingornasogastricsuction
Antacidsinadvancedrenalfailure
Congenitalchloridediarrhea

Renalhydrogenloss
Primarymineralocorticoidexcess
Looporthiazidediuretics
BartterorGitelmansyndrome
Posthypercapnicalkalosis
Hypercalcemiaandthemilkalkalisyndrome

Intracellularshiftofhydrogen
Hypokalemia

Alkaliadministration
Contractionalkalosis
Massivediuresis
Vomitingornasogastricsuctioninachlorhydria
Sweatlossesincysticfibrosis
Villousadenomaorfactitiousdiarrhea(includinglaxativeabuse)
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AcidsecretingtypeAintercalatedcells

TransportmechanismsinvolvedinhydrogensecretionandHCO 3 andK +
reabsorptionintypeAintercalatedcells,whicharepresentfromthelate
distalconvolutedtubuletotheinitialportionoftheinnermedullarycollecting
duct.WaterwithinthecelldissociatesintoH +andOH ions.Theformerare
secretedintothelumenbyHATPasepumpsintheluminalmembrane,where
theycombinewithurinarybufferstogeneratetitratableacid(eg,convert
HPO 4 2 toH 2 PO 4 )andconvertNH 3 toNH 4 +.TheOH ionsinthecell
combinewithCO 2 toformHCO 3 inareactioncatalyzedbycarbonic
anhydrase(CA).Drivenbytheirelectrochemicalconcentrationgradients,
cellularbicarbonateenterstheperitubularcapillariesinexchangefor
extracellularchlorideviaClHCO 3 exchangersonthebasolateralmembrane.
HKATPasepumps,whichsecreteH +andreabsorbK +,arealsopresentin
theluminalmembraneofthetypeAintercalatedcells.Thenumberand
activityofthesepumpsareincreasedbyK +depletion,suggestingthatthey
maybeimportantforK +conservation.
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Iontransportincollectingtubuleprincipalcells

Schematicrepresentationofsodiumandpotassiumtransportinthe
sodiumreabsorbingprincipalcellsinthecollectingtubules.Theentry
offilteredNaintothesecellsismediatedbyselectivesodium
channelsintheapical(luminal)membrane(ENaC)theenergyforthis
processisprovidedbythefavorableelectrochemicalgradientforNa
(cellinteriorelectronegativeandlowcellNaconcentration).
ReabsorbedNaispumpedoutofthecellbytheNaKATPasepumpin
thebasolateral(peritubular)membrane.Thereabsorptionofcationic
Namakesthelumenelectronegative,therebycreatingafavorable
gradientforthesecretionofKintothelumenviaKchannels(ROMK
andBK)intheapicalmembrane.Aldosterone,aftercombiningwith
thecytosolicmineralocorticoidreceptor(AldoR),leadstoenhanced
Nareabsorptionandpotassiumsecretionbyincreasingboththe
numberofopenNachannelsandthenumberofNaKATPasepumps.
Thepotassiumsparingdiuretics(amilorideandtriamterene)actby
directlyinhibitingtheepithelialsodiumchannelspironolactoneacts
bycompetingwithaldosteroneforbindingtothemineralocorticoid
receptor.
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Disclosures
Disclosures:MichaelEmmett,MDConsultant/AdvisoryBoards:ZSPharma[treatmentofhyperkalemia
(potassiumbinder,zirconiumsilicate)].RichardHSterns,MDNothingtodisclose.JohnPForman,MD,
MScNothingtodisclose.
Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,theseare
addressedbyvettingthroughamultilevelreviewprocess,andthroughrequirementsforreferencestobe
providedtosupportthecontent.Appropriatelyreferencedcontentisrequiredofallauthorsandmust
conformtoUpToDatestandardsofevidence.
Conflictofinterestpolicy

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