肌酐清除率与体内钙离子及骨质关系.docx
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肌酐清除率与体内钙离子及骨质关系.docx
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肌酐清除率与体内钙离子及骨质关系
KDOQIClinicalPracticeGuidelinesforChronicKidneyDisease:
Evaluation,Classification,andStratification
PART6.ASSOCIATIONOFLEVELOFGFRWITHCOMPLICATIONSINADULTS
GUIDELINE10.ASSOCIATIONOFLEVELOFGFRWITHBONEDISEASEANDDISORDERSOFCALCIUMANDPHOSPHORUSMETABOLISM
Bonediseaseanddisordersofcalciumandphosphorusmetabolismdevelopduringthecourseofchronickidneydiseaseandareassociatedwithadverseoutcomes.
∙PatientswithGFR<60mL/min/1.73m2shouldbeevaluatedforbonediseaseanddisordersofcalciumandphosphorusmetabolism.
∙Patientswithbonediseaseanddisordersofbonemetabolismshouldbeevaluatedandtreated—seeforthcomingKDOQIClinicalPracticeGuidelinesonBoneMetabolismandDiseaseinChronicKidneyDisease.
BACKGROUND
Chronickidneydiseaseisassociatedwithavarietyofbonedisordersanddisordersofcalciumandphosphorusmetabolism.Themajordisordersofbonecanbeclassifiedintothoseassociatedwithhighparathyroidhormone(PTH)levels(osteitisfibrosacystica)andthosewithlowornormalPTHlevels(adynamicbonedisease).Thehallmarklesionofchronickidneydiseaseisosteitisfibrosa,duetosecondaryhyperparathyroidism.However,withtheadventofintensivetreatmentsforsecondaryhyperparathyroidism,theprevalenceofdisordersassociatedwithlowornormalPTHlevelshasincreased.
Irrespectiveofthecause,bonediseasecanleadtopainandanincreasedincidenceoffractures.Abnormalcalcium-phosphorusmetabolismandhyperparathyroidismcanalsoleadtocalcificationofbloodvesselsandpotentiallyanincreasedriskofcardiovascularevents.
Thestageofchronickidneydiseaseatwhichbonediseasebeginstodevelophasnotbeenwelldocumented,norhasaconsensusbeendevelopedregardingthebestscreeningmeasuresfordetectingearlyabnormalitiesofcalcium-phosphorusmetabolismandbonedisease.TheaimofthisguidelineistoprovideevidenceontheassociationoflevelofGFRwithdisordersofcalcium-phosphorusmetabolismandbonediseaseandtoproviderecommendationsonhowtoapproachthiscomplicationofchronickidneydisease.
RATIONALE
BoneDiseaseinChronicKidneyDisease
Bonediseaseassociatedwithchronickidneydiseaseiscomposedofanumberofabnormalitiesofbonemineralization.ThemajordisorderscanbeclassifiedintothoseassociatedwithhighboneturnoverandhighPTHlevels(includingosteitisfibrosa,thehallmarklesionofsecondaryhyperparathyroidism,andmixedlesion)andlowboneturnoverandlowornormalPTHlevels(osteomalaciaandadynamicbonedisease).372OsteomalaciamayberelatedtovitaminDdeficiency,excessaluminum,ormetabolicacidosis;whereasadynamicbonediseasemayberelatedtoover-suppressionofPTHwithcalcitriol.372-374
Thepathophysiologyofbonediseaseduetosecondaryhyperparathyroidismisrelatedtoabnormalmineralmetabolism:
(1)decreasedkidneyfunctionleadstoreducedphosphorusexcretionandconsequentphosphorusretention;
(2)elevatedserumphosphoruscandirectlysuppresscalcitriol(dihydroxyvitaminD3)production;(3)reducedkidneymassleadstodecreasedcalcitriolproduction;(4)decreasedcalcitriolproductionwithconsequentreducedcalciumabsorptionfromthegastrointestinaltractcontributestohypocalcemia,asdoesabnormalcalcium-phosphorusbalanceleadingtoanelevatedcalcium-phosphorusproduct.375,376Hypocalcemia,reducedcalcitriolsynthesis,andelevatedserumphosphoruslevelsstimulatetheproductionofPTHandtheproliferationofparathyroidcells,377-379resultinginsecondaryhyperparathyroidism.HighPTHlevelsstimulateosteoblastsandresultinhighboneturnover.Thehallmarklesionofsecondaryhyperparathyroidismisosteitisfibrosacystica.Highboneturnoverleadstoirregularlywovenabnormalosteoid,fibrosis,andcystformation,whichresultindecreasedcorticalboneandbonestrengthandanincreasedriskoffracture.
Lowturnoverbonediseasehastwosubgroups,osteomalaciaandadynamicbonedisease.Bothlesionsarecharacterizedbyadecreaseinboneturnoverorremodeling,withareducednumberofosteoclastsandosteoblasts,anddecreasedosteoblasticactivity.Inosteomalaciathereisanaccumulationofunmineralizedbonematrix,orincreasedosteoidvolume,whichmaybecausedbyvitaminDdeficiencyorexcessaluminum.AdynamicbonediseaseischaracterizedbyreducedbonevolumeandmineralizationandmaybeduetoexcessaluminumoroversuppressionofPTHproductionwithcalcitriol.372
OtherComplicationsofAbnormalCalcium-PhosphorusMetabolism
Inadditiontoabnormalitiesinbonemetabolism,abnormalcalcium-phosphorusmetabolismmayleadtocalciphylaxisorextraosseouscalcificationofsofttissueandvasculartissue.Thiscomplicationinitsfullmanifestationhasbeenreportedtoaffectapproximately1%ofdialysispatients.380However,instudiesofcoronaryarterycalcificationusingelectronbeamcomputedtomography,dialysispatientshadcoronarycalcificationscoresthatwereseveral-foldhigherthanthoseofpatientswithknowncoronaryarterydisease.381Thepathogenesisremainsunclear,buthyperphosphatemia,hypercalcemia,elevatedcalcium-phosphorusproduct,andincreasedPTHlevelsareprobablecontributors.
MarkersofBoneDiseaseandAbnormalCalcium-PhosphorusMetabolisminChronicKidneyDisease
Bonebiopsyfollowingdouble-tetracyclinelabelingisthegoldstandardforthediagnosisofbonediseaseinchronickidneydiseaseandistheonlymeansofdefinitivelydifferentiatingthem.Fivebonelesionsassociatedwithchronickidneydiseasehavebeenclassifiedbasedonboneformationrate,osteoidarea,andfibrosisonbonebiopsyofpatientswithkidneyfailure372,382(Table92).
Bonebiopsyisnoteasy,nornecessaryinroutineclinicalpractice.Classically,boneresorptioncanbeseenonplainradiographsincasesofadvancedosteitisfibrosa,butradiologicalstudies,includingdensitometry,havenotbeenconclusivelyshowntodifferentiatethevarioustypesofbonediseaseassociatedwithkidneyfailure.Bonebiopsyiscurrentlyrecommendedonlyforpatientswithsymptomaticdiseaseinwhominterventionsarebeingcontemplated(suchasparathyroidectomyordesferoxaminetreatmentforelevatedaluminumlevels)383orforresearchoftheeffectivenessoftherapiesoralternativediagnostictests.384Intheabsenceofdirectpathologicstudies,clinicianshavereliedonbiochemicaldatatodeterminetheprobablepresenceof,orassesstheriskfor,boneabnormalities.Lowcalcitriol(dihydroxyvitaminD3)andcalciumlevels,andhighphosphorusandPTHlevels,aretheclassicabnormalitieswhichdevelopwithdecreasedGFR.385Thebiochemicalstudiesincommonuseareserumphosphorus,calcium,andPTHlevels.Calcitriollevelscanalsobemeasured,butthisisnotcommonlydoneinclinicalpractice.SerumphosphorusandcalciumlevelsareusedinscreeningforabnormalitiesofmineralmetabolismthatmayleadtoPTHexcess;however,PTHlevelsmaybegintoriseevenbeforethereisappreciablehyperphosphatemia.379Hence,therecommendationtoobtainPTHlevelsintheassessmentofbonediseaseinchronickidneydisease.
Anidealserologicmarkerwouldbeuniquetoboneandwouldbewellcorrelatedtohistologicfindingsonbiopsy.TwomarkersstudiedmoreextensivelyincludePTHandbonealkalinephosphatase(bAP).PTHsecretionisdirectlycorrelatedwithboneturnover,butPTHlevelsarenotreliablycorrelatedwithboneturnoveramongdialysispatients,especiallyinthemiddleranges.386,387PTHlevels<65pg/mLwerefoundtobepredictiveofnormalboneorlowturnoverlesions,andPTHlevels>450pg/mLwerepredictiveofhighturnoverlesions,butlevelsinbetweendidnothavegoodpredictivevalue.Overallboneturnovercouldnotbepredictedin30%ofHDand50%ofPDpatients.387Inanotherstudy,lowturnoverlesionswerenotedinthemajorityofpatientswithPTHlevels<100pg/mLandhighturnoverlesionsinthemajorityofpatientswithPTHlevels>200to300pg/mL.386HighbAPlevelshavebeenassociatedwithhighboneturnoverandlowlevelswithadynamicbonediseaseindialysispatients.Inonestudy,thecombinationofhighbonealkalinephosphataselevelswithhighPTHlevelsincreasedthesensitivityofdiagnosisofhighturnoverlesions;conversely,lowlevelsofbothofthesemarkersresultinincreasedsensitivityfordiagnosisoflowturnoverlesions.However,specificcut-offlevelsforbAPhavevariedinthefewstudiesexaminingtherelationshiptobonehistology.383
Othermarkersofbonediseasenotyetfullyinvestigatednorinwidespreadclinicaluseincludeosteocalcin,�2microglobulin,procollagentypeIcarboxy-terminalpropeptides(PICP),andtypeIcollagencrosslinkedtelopeptides(ICTP),amongothers.PICPhasbeencorrelatedwithboneformation,andICTPandosteocalcinbeencorrelatedwithboneresorption.However,levelsofmanyofthesemarkersareaffectedbyage,diet,liverfunction,andkidneyfunction;thus,interpretationoflevelsisdifficult.383
Thus,abnormalitiesofbonemineralmetabolismarepresentifthereisanelevatedserumphosphorusorPTHlevelorreducedserumcalciumorcalcitriollevel.GiventhepossibilityofanelevatedPTHlevelinthefaceofnormalserumcalciumandphosphoruslevels,thediagnosisofearlyabnormalityofmineralmetabolismrequiresmeasurementofPTHlevels.ExtremeelevationsofserumPTHlevelsaremoreconvincinglyassociatedwithhighturnoverlesionsthanlowlevelswithlowturnoverlesions.Definitivediagnosisoftypeofbonediseaserequiresbonebiopsy.
StrengthofEvidence
Bonediseaseanddisordersofcalciumandphosphorusmetabolismdevelopduringthecourseofchronickidneydisease(R).Radiologicandhistologicchangesofb
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- 清除 体内 离子 骨质 关系
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