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potassium balance in acid-base disorders

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Official reprint from UpToDate www.uptodate.com ©2015 UpToDate Author David B Mount, MD Section Editor Richard H Sterns, MD Deputy Editor John P Forman, MD, MSc Potassium balance in acidbase disorders All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Mar 2015. | This topic last updated: Oct 17, 2013. INTRODUCTION — There are important interactions between potassium and acidbase balance that involve both transcellular cation exchanges and alterations in renal function [1 ]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid base disorders. INTERNAL POTASSIUM BALANCE — Acidbase disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2 ]. An oftenquoted study found that the plasma potassium concentration will rise by 0.6 meq/L for every 0.1 unit reduction of the extracellular pH [3 ]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 meq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4 ]. Metabolic acidosis — In metabolic acidosis, more than onehalf of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid ( figure 1 ). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6 ]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis or ketoacidosis [3,7 ]. The hyperkalemia that is commonly seen in diabetic ketoacidosis, for example, is more closely related to the insulin deficiency and hyperosmolality than to the degree of acidemia. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" .) Why this occurs is not well understood. Two factors that may contribute are the ability of the organic anion to accompany the hydrogen ion into the cell, perhaps as the lipidsoluble, intact acid [8 ], and differential effects on insulin and glucagon secretion [4,9 ]. Just as metabolic acidosis can cause hyperkalemia, a rise in the plasma potassium concentration can induce a mild metabolic acidosis. In patients with hypoaldosteronism, for example, the mild metabolic acidosis is primarily due to the associated hyperkalemia [10 ]. Two factors contribute to this phenomenon: The net effect of these changes in cation distribution and renal function is that metabolic acidosis and relative ® ® A transcellular exchange occurs as the entry of most of the excess potassium into the cells is balanced in part by intracellular hydrogen ions moving into the extracellular fluid [11 ]. The net effect is an extracellular acidosis and an intracellular alkalosis. ● Normally, the kidney increases ammonium excretion after an acid load, an effect that is stimulated in part by a fall in intracellular pH [12 ]. In hyperkalemia, the associated intracellular alkalosis diminishes ammonium generation by the proximal tubule [13 ]. However, the predominant problem is inhibition of ammonium reabsorption by the thick ascending limb resulting from an increased concentration of potassium in the tubular fluid [14 ]. Normally, ammonium exiting the proximal tubule is reabsorbed in the thick ascending limb via the apical Na K /NH 2Cl cotransporter (NKCC2), after which it crosses the interstitium and is excreted into the urine by the collecting duct [1517 ]. Potassium competes with ammonium for reabsorption by NKCC2, and therefore, elevated tubular potassium concentrations can impair normal renal ammonium handling, resulting in acidosis. ● + + 4 +

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  • 19/4/2015 Potassiumbalanceinacidbasedisorders

    http://www.uptodate.com/contents/potassiumbalanceinacidbasedisorders?topicKey=NEPH%2F2353&elapsedTimeMs=0&source=search_result&sea 1/5

    OfficialreprintfromUpToDate www.uptodate.com2015UpToDate

    AuthorDavidBMount,MD

    SectionEditorRichardHSterns,MD

    DeputyEditorJohnPForman,MD,MSc

    Potassiumbalanceinacidbasedisorders

    Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.Literaturereviewcurrentthrough:Mar2015.|Thistopiclastupdated:Oct17,2013.

    INTRODUCTIONThereareimportantinteractionsbetweenpotassiumandacidbasebalancethatinvolvebothtranscellularcationexchangesandalterationsinrenalfunction[1].Thesechangesaremostpronouncedwithmetabolicacidosisbutcanalsooccurwithmetabolicalkalosisand,toalesserdegree,respiratoryacidbasedisorders.

    INTERNALPOTASSIUMBALANCEAcidbasedisturbancescausepotassiumtoshiftintoandoutofcells,aphenomenoncalled"internalpotassiumbalance"[2].Anoftenquotedstudyfoundthattheplasmapotassiumconcentrationwillriseby0.6meq/Lforevery0.1unitreductionoftheextracellularpH[3].However,thisestimatewasbasedupononlyfivepatientswithavarietyofdisturbances,andtherangewasverybroad(0.2to1.7meq/L).ThisvariabilityintheriseorfalloftheplasmapotassiuminresponsetochangesinextracellularpHwasconfirmedinsubsequentstudies[2,4].

    MetabolicacidosisInmetabolicacidosis,morethanonehalfoftheexcesshydrogenionsarebufferedinthecells.Inthissetting,electroneutralityismaintainedinpartbythemovementofintracellularpotassiumintotheextracellularfluid(figure1).Thus,metabolicacidosisresultsinaplasmapotassiumconcentrationthatiselevatedinrelationtototalbodystores.Theneteffectinsomecasesisoverthyperkalemiainotherpatientswhoarepotassiumdepletedduetourinaryorgastrointestinallosses,theplasmapotassiumconcentrationisnormalorevenreduced[5,6].Thereisstillarelativeincreaseintheplasmapotassiumconcentration,however,asevidencedbyafurtherfallintheplasmapotassiumconcentrationiftheacidemiaiscorrected.

    AfallinpHismuchlesslikelytoraisetheplasmapotassiumconcentrationinpatientswithlacticacidosisorketoacidosis[3,7].Thehyperkalemiathatiscommonlyseenindiabeticketoacidosis,forexample,ismorecloselyrelatedtotheinsulindeficiencyandhyperosmolalitythantothedegreeofacidemia.(See"Diabeticketoacidosisandhyperosmolarhyperglycemicstateinadults:Clinicalfeatures,evaluation,anddiagnosis".)

    Whythisoccursisnotwellunderstood.Twofactorsthatmaycontributearetheabilityoftheorganicaniontoaccompanythehydrogenionintothecell,perhapsasthelipidsoluble,intactacid[8],anddifferentialeffectsoninsulinandglucagonsecretion[4,9].

    Justasmetabolicacidosiscancausehyperkalemia,ariseintheplasmapotassiumconcentrationcaninduceamildmetabolicacidosis.Inpatientswithhypoaldosteronism,forexample,themildmetabolicacidosisisprimarilyduetotheassociatedhyperkalemia[10].Twofactorscontributetothisphenomenon:

    Theneteffectofthesechangesincationdistributionandrenalfunctionisthatmetabolicacidosisandrelative

    Atranscellularexchangeoccursastheentryofmostoftheexcesspotassiumintothecellsisbalancedinpartbyintracellularhydrogenionsmovingintotheextracellularfluid[11].Theneteffectisanextracellularacidosisandanintracellularalkalosis.

    Normally,thekidneyincreasesammoniumexcretionafteranacidload,aneffectthatisstimulatedinpartbyafallinintracellularpH[12].Inhyperkalemia,theassociatedintracellularalkalosisdiminishesammoniumgenerationbytheproximaltubule[13].However,thepredominantproblemisinhibitionofammoniumreabsorptionbythethickascendinglimbresultingfromanincreasedconcentrationofpotassiuminthetubularfluid[14].Normally,ammoniumexitingtheproximaltubuleisreabsorbedinthethickascendinglimbviatheapicalNa K /NH 2Cl cotransporter(NKCC2),afterwhichitcrossestheinterstitiumandisexcretedintotheurinebythecollectingduct[1517].PotassiumcompeteswithammoniumforreabsorptionbyNKCC2,andtherefore,elevatedtubularpotassiumconcentrationscanimpairnormalrenalammoniumhandling,resultinginacidosis.

    + +4+

  • 19/4/2015 Potassiumbalanceinacidbasedisorders

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    hyperkalemiaareoftenseentogether.

    MetabolicalkalosisForsimilarreasonsinwhichtheaboveionicchangesarereversed,metabolicalkalosisandhypokalemiaarecommonlyassociated.Metabolicalkalosiscausespotassiummovementintothecells,andhypokalemiacauseshydrogenmovementintothecells[18,19].Withmetabolicalkalosis,theplasmapotassiumconcentrationfallslessthan0.4meq/Lper0.1unitincreaseinsystemicpH[3].

    RespiratoryacidbasedisordersRespiratoryacidosisandalkalosisinducerelativelysmallchangesinpotassiumbalance[3].Thereasonforthisminoreffectisnotwellunderstood.

    CONCURRENTDISORDERSOFPOTASSIUMBALANCETheprecedingdiscussionhasemphasizedtheeffectofpHonpotassiumdistributionbetweenthecellsandextracellularfluid.However,patientswithacidbasedisturbancescommonlyhaveconcurrentdisordersofexternalpotassiumbalancethatcanaffectthisrelationship.

    ConcurrentmetabolicacidosisInmetabolicacidosiscausedbydiarrhea,fecallossofalkaliisaccompaniedbygastrointestinallossofpotassium.Thenetresultisanormalaniongapmetabolicacidosiswithpotassiumdepletionandhypokalemia.(See"Causesofhypokalemiainadults",sectionon'Lowergastrointestinallosses'.)

    Inseveralorganicacidoses,theacidanionisexcretedintheurinewithsodiumorpotassiumastheaccompanyingcation.Hypokalemiamayresultdespitetheconcurrentshiftofpotassiumoutofcellsinresponsetoacidemia.Themetabolicacidosiscausedbygluesniffingisthemostdramaticexampleofthisphenomenon.Inhaledtolueneismetabolizedtohippuricacid,andtheacidanion(hippurate)iseliminatedintheurinebybothfiltrationandsecretion,commonlyresultinginhypokalemia[20].(See"Theaniongap/HCO3ratioinpatientswithahighaniongapmetabolicacidosis".)

    Renalpotassiumwastingalsooccursindiabeticketoacidosis.However,incontrasttotolueneinhalation,manypatientsmaydevelophyperkalemia.Hyperkalemiainsuchpatientsresultsfromprofoundpotassiumshiftoutofcellscausedbyhyperosmolalityandinsulindeficiency,andnot,asnotedabove,bythemetabolicacidosis.Theadministrationofinsulintypicallyleadstohypokalemia,unmaskingthetruestateofpotassiumbalance.(See"Diabeticketoacidosisandhyperosmolarhyperglycemicstateinadults:Treatment".)

    Renalpotassiumwastingcanresultinseverehypokalemiainuntreateddistalrenaltubularacidosis(RTA)andinpatientswithproximalRTAwhoaretreatedwithsodiumbicarbonate.Ontheotherhand,truehyperkalemia(ie,increasedbodypotassiumstores)ispresentinpatientswithhypoaldosteronism(type4RTA)duetoimpairedurinarypotassiumexcretion.(See"Overviewandpathophysiologyofrenaltubularacidosisandtheeffectonpotassiumbalance".)

    ConcurrentmetabolicalkalosisRenalpotassiumwastingresultinginpotassiumdepletionandhypokalemiaisafeatureofmostcausesofmetabolicalkalosis(eg,vomiting,diuretics,BartterandGitelmansyndromes).

    SUMMARY

    Inmetabolicacidosis,morethanonehalfoftheexcesshydrogenionsarebufferedinthecells.Inthissetting,electroneutralityismaintainedinpartbythemovementofintracellularpotassiumintotheextracellularfluid(figure1).Thus,metabolicacidosisresultsinaplasmapotassiumconcentrationthatiselevatedinrelationtototalbodystores.Theneteffectinsomecasesisoverthyperkalemia.(See'Metabolicacidosis'above.)

    Justasmetabolicacidosiscancausehyperkalemia,ariseintheplasmapotassiumconcentrationcaninduceamildmetabolicacidosis.Thisisduetotranscellularexchangeasmostoftheexcesspotassiumentersthecellswithintracellularhydrogenionsmovingintotheextracellularfluid.Theneteffectisanextracellularacidosisandanintracellularalkalosis.Inthekidney,hyperkalemiadiminishesammoniumexcretion,therebypreventingexcretionofthedailyacidloadandcontributingtothemetabolicacidosis.(See'Metabolicacidosis'above.)

    Forreasonsthataresimilarbutreciprocal,metabolicalkalosisandhypokalemiaarecommonly

  • 19/4/2015 Potassiumbalanceinacidbasedisorders

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    REFERENCES

    1. AronsonPS,GiebischG.EffectsofpHonpotassium:newexplanationsforoldobservations.JAmSocNephrol201122:1981.

    2. SternsRH,CoxM,FeigPU,SingerI.Internalpotassiumbalanceandthecontroloftheplasmapotassiumconcentration.Medicine(Baltimore)198160:339.

    3. AdroguHJ,MadiasNE.Changesinplasmapotassiumconcentrationduringacuteacidbasedisturbances.AmJMed198171:456.

    4. AdroguHJ,MadiasNE.PCO2and[K+]pinmetabolicacidosis:certaintyforthefirstanduncertaintyfortheother.JAmSocNephrol200415:1667.

    5. MagnerPO,RobinsonL,HalperinRM,etal.Theplasmapotassiumconcentrationinmetabolicacidosis:areevaluation.AmJKidneyDis198811:220.

    6. WiederseinerJM,MuserJ,LutzT,etal.Acutemetabolicacidosis:characterizationanddiagnosisofthedisorderandtheplasmapotassiumresponse.JAmSocNephrol200415:1589.

    7. FulopM.Serumpotassiuminlacticacidosisandketoacidosis.NEnglJMed1979300:1087.8. GraberM.Amodelofthehyperkalemiaproducedbymetabolicacidosis.AmJKidneyDis199322:436.9. AdroguHJ,ChapZ,IshidaT,FieldJB.Roleoftheendocrinepancreasinthekalemicresponseto

    acutemetabolicacidosisinconsciousdogs.JClinInvest198575:798.10. SzylmanP,BetterOS,ChaimowitzC,RoslerA.Roleofhyperkalemiainthemetabolicacidosisof

    isolatedhypoaldosteronism.NEnglJMed1976294:361.11. AltenbergGA,AristimuoPC,AmorenaCE,TaquiniAC.Amiloridepreventsthemetabolicacidosisofa

    KClloadinnephrectomizedrats.ClinSci(Lond)198976:649.12. RoseBD,PostTW.ClinicalPhysiologyofAcidBaseandElectrolyteDisorders,5thed,McGrawHill,

    NewYork2001.p.347.13. DuBoseTDJr,GoodDW.Effectsofchronichyperkalemiaonrenalproductionandproximaltubule

    transportofammoniuminrats.AmJPhysiol1991260:F680.14. DuBoseTDJr,GoodDW.Chronichyperkalemiaimpairsammoniumtransportandaccumulationinthe

    innermedullaoftherat.JClinInvest199290:1443.15. GoodDW.AmmoniumtransportbythethickascendinglimbofHenle'sloop.AnnuRevPhysiol1994

    56:623.16. AttmaneElakebA,MountDB,SibellaV,etal.Stimulationbyinvivoandinvitrometabolicacidosisof

    expressionofrBSC1,theNa+K+(NH4+)2Clcotransporteroftheratmedullarythickascendinglimb.JBiolChem1998273:33681.

    17. BourgeoisS,MeerLV,WootlaB,etal.NHE4iscriticalfortherenalhandlingofammoniainrodents.JClinInvest2010120:1895.

    18. SabatiniS,KurtzmanNA.Themaintenanceofmetabolicalkalosis:factorswhichdecreasebicarbonateexcretion.KidneyInt198425:357.

    19. COOKERE,SEGARWE,CHEEKDB,etal.Theextrarenalcorrectionofalkalosisassociatedwithpotassiumdeficiency.JClinInvest195231:798.

    20. CarlisleEJ,DonnellySM,VasuvattakulS,etal.Gluesniffinganddistalrenaltubularacidosis:stickingtothefacts.JAmSocNephrol19911:1019.

    Topic2353Version10.0

    associated.Metabolicalkalosiscausespotassiummovementintothecells,andhypokalemiacauseshydrogenmovementintothecells.(See'Metabolicalkalosis'above.)

    Somepatientswithmetabolicacidbasedisorderhaveconcurrentdisordersofpotassiumbalancewhichcanproducehypokalemiaorhyperkalemiathroughmechanismsotherthanthosedependentuponcellularexchange.Examplesincludediarrhea,renaltubularacidosis,anddiabeticketoacidosis.(See'Concurrentdisordersofpotassiumbalance'above.)

  • 19/4/2015 Potassiumbalanceinacidbasedisorders

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    GRAPHICS

    Ionredistributionafteracidload

    EffectofanHClloadonthedistributionofCl,Na,andK.AsHentersthecellstobebuffered,intracellularNaandKleavethecellsandmoveintotheextracellularfluid,tendingtoraisetheplasmapotassiumconcentration.TheseionshiftsarereversedwhenHionsareremovedfromtheextracellularfluid.

    Graphic68866Version2.0

  • 19/4/2015 Potassiumbalanceinacidbasedisorders

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    Disclosures:DavidBMount,MDConsultant/AdvisoryBoards:ZSPharma[Potassiumbinders(ZS9,preclinical)].RichardHSterns,MDNothingtodisclose.JohnPForman,MD,MScNothingtodisclose.Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,theseareaddressedbyvettingthroughamultilevelreviewprocess,andthroughrequirementsforreferencestobeprovidedtosupportthecontent.AppropriatelyreferencedcontentisrequiredofallauthorsandmustconformtoUpToDatestandardsofevidence.Conflictofinterestpolicy

    Disclosures


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