醫(yī)學(xué)資料 Renal Main腎病學(xué)習(xí)課件

RenalMain51-60Q1A52-year-oldmanwithalcoholismcomestotheemergencydepartmentduetogeneralizedweakness,anxiety,andtremors.Hislastdrinkwas2daysago.Hehasnosignificantmedicalhistoryandnomedicalfollow-up.ThepatientsmokescigarettesbutdoesnotuseIllicitdrugs.Hetakesnomedications.Onexamination,heappearsdisheveledandmalnourished.Hisinitialelectrolytepanelresultsareasfollows:Heistreatedforalcoholwithdrawalandgivenaggressiveintravenouspotassiumaswellasoralpotassiumsupplementation.Threedayslater,hiselectrolytepanelresultsareasfollows:Whichofthefollowingbestexplainswhythispatient'spotassiumlevelisverydifficulttocorrect?A.AlcoholwithdrawalB.HypoalbuminemiaC.HypomagnesemiaD.HypophosphatemiaE.PoororalabsorptionF,RenaltubularacidosisG.ThiaminedeficiencyA1

Correctanswer:CChronicalcoholismisassociatedwithahighincidenceofseveralelectrolyteabnormalities,ofwhichhypomagnesemiaisthemostcommon(likelyduetopoornutritionalintake,alcohol-inducedrenallosses,anddiarrhea).Hypomagnesemiacommonlyoccurstogetherwithhypokalemiaandisawell-knowncauseofrefractoryhypokalemia(hypokalemiathatcannotbecorrectedwithpotassiumreplacement).intracellularmagnesiumisthoughttoinhibitpotassiumsecretionbyrenaloutermedullarypotassium(ROMK)channelsinthecollectingtubulesofthekidney.Therefore,lowintracellularmagnesiumconcentrationsresultinexcessiverenalpotassiumlossandrefractoryhypokalemia.NormalizationofmagnesiumlevelsrestoresROMKchannelpotassiumtransportregulation,decreasesrenalpotassiumlosses,andailowsforsuccessfulcorrectionofhypokalemiawithoral(preferred)orintravenouspotassiumrepiacement.(ChoiceA)AcutealcoholwithdrawalmayinitiallycontributetohypokalemiathroughanincreaseInsympatheticnervoussystemactivity,whichshiftspotassiumintocells.However,itisunlikelytoplayasignificantroleinthispatient'shypokalemia,whichhaspersistedthroughout3daysoftreatment.(ChoiceB)Hypoaibuminemiaiscommonlyseeninpatientswithalcoholismduetopoornutritionorhepaticsyntheticdysfunction,itisacommoncauseoftotalhypocalcemia(duetoahighproportionofserumcalciumbeingprotein-bound)butisnotasignificantcauseofhypokalemia.(ChoiceD)Hypophosphatemiaiscommoninpatientswithalcoholismand,whensevere,canresultinweakness,rhabdomyolysis,paresthesias,andrespiratoryfailure.Itdoesnotdirectlycontributetohypokalemia.(ChoiceE)Poororalabsorptionmayresultinhypokalemiarefractorytooralreplacement,butitisunlikelyinthispatientwithhypokalemiathathasalsobeenrefractorytoaggressiveintravenousreplacement.(ChoiceF)TypeIorIIrenaltubularacidosiscancausehypokalemiabutisusuallyassociatedwithmetabolicacidosis.Thispatienthasarelativelynormalserumbicarbonatelevel,andhishistoryofalcohoiismmakeshypomagnesemiaamorelikelycauseofhisrefractoryhypokalemia.(ChoiceG)ThiaminedeficiencyiscommonInpatientswithalcoholismduetopoornutrition,butItdoesnotcauserefractoryhypokalemia.Educationalobjective:Patientswithchronicalcoholismoftenpresentwithmultipleelectrolyteabnormalities(eg,hypokaiemia,hypomagnesemia,hypophosphatemia).Hypomagnesemiacanleadtorefractoryhypokaiemiaduetoremovalofinhibitionofrenalpotassiumexcretionandshouldbesuspectedinpatientswithhypokalemiathatisdifficulttocorrectwithpotassiumreplacement.Q2A55-year-oldmancomestotheemergencydepartmentduetoprogressivelyworseningshortnessofbreathforthepast3days.Healsoreportswheezingandproductivecoughwithpurulentsputum.Thepatient'smedicalhistoryincludeschronicbronchitisandbenignprostatichyperplasia.Hesmokesapackofcigarettesdaily.Temperatureis37.2℃(99℉);bloodpressureis150/90mmHg,pulseis114/min，andrespirationsare26/min.Thepatient'spulseoximetryshows84%onroomair.Heisalertandansweringquestionscoherently.Examinationshowsdecreasedbreathsoundsanddiffusewheezingoveralllungfields.Thepatientisadmittedtothehospitalandstartedonantibiotics,systemiccorticosteroids,andnebulizedalbuterolandipratropium.Thefollowingday,laboratoryresultsareasfollows:Serumchemistry2daysagowasnormal.Whichofthefollowingisthemostlikelycauseofthispatient'slowserumpotassium?A.DecreaseinavaiiabiiityofinsulinB.DecreaseinextracellularpHC.DecreaseinmineralocorticoidactivityD.Increasedbeta-adrenergicactivityE.IncreasedbloodcellproductionF.IncreasedgastrointestinallossA2Correctanswer:DLowserumpotassiummayresultfromIncreasedpotassiumentryintocells,renalpotassiumwasting,orgastrointestinalfluidloss.Thispatientwithanacuteexacerbationofchronicobstructivepulmonarydisease(CORD)istreatedwithanInhaledbeta-2adrenergicagent(albuterol).Exogenousandendogenous(eg,epinephrine)beta-adrenergicagonistscauseapotassiumshiftintotheintracellularspacebystimulatingthesodium-potassiumATPasepumpandthesodium-potassium-2chloridecotransporter.Adrenergicagentsalsostimulatereleaseofinsulin,whichfurtherpromotesintracellularpotassiumshift,causinghypokalemia.(ChoiceA)insulinpromotespotassiumshiftintotheintracellularspaceandisusedinthemanagementofhyperkalemia.Decreasedinsulinavailabilitywouldexacerbatehyperkalemia.(ChoiceB)DecreasedpH(acidosis)withCOPDexacerbationmaybeseeninpatientswithCO,retention.However,thiswouldresultinhyperkalemia.(ChoiceC)Renalpotassiumwastingwithhypertensionisafeatureofprimaryhyperaldosteronism.Decreaseinmineralocorticoidactivitywillleadtohyperkalemia.Diureticsalsocauserenalpotassiumloss.(ChoiceE)Increasedpotassiumuptakebycellsduringacceleratedhematopoiesis(eg,administrationofgranulocytecolony-stimulatingfactors)maycausehypokalemia.ThispatienthasnoevidenceofIncreasedhematopoiesis.(ChoiceF)Lowergastrointestinalfluidlevelshaveahighpotassiumconcentration;therefore,diarrheaisadirectcauseofhypokalemia.Vomitingcausesmetabolicalkalosis,whichleadstorenalpotassiumwasting.Thispatientdoesnothaveanygastrointestinalfluidlosses.Educationalobjective:Hypokalemiamaybecausedbyincreasedintracellularentryofpotassium(eg,withinsulin,beta-adrenergicagents,hematopoiesis),gastrointestinallosses,andrenalpotassiumwasting(eg,hyperaidosteronism,diuretics).Q3A67-year-oldmanwithmildchronicobstructivepulmonarydiseaseisbroughttotheemergencydepartmentbyhisdaughterwiththechiefcomplaintofseizure.Thepatienthashadepisodesofconfusionandlethargyoverthepastweek.Hecomplainsofsomeexertionalshortnessofbreathandnonproductivecough.Hisdaughterbelievesthatheislosingweightandhasdecreasedappetite.Histemperatureis37.2℃(99℉);bloodpressureis134/33mmHg:andpulseis104/minandirregular.Themucousmembranesaremoistandthereisnoperipheraledema.Neurologicexaminationisunremarkable.Laboratoryresultsareasfollows:Rapidcorrectionofthispatient'smetabolicabnormalitiesputshimathighestriskofwhichofthefollowing?A.CerebraledemaB.EmbolicstrokeC.HydrocephalusD.OsmoticdemyelinationE.VentriculararrhythmiasA3Correctanswer:DThispatientpresentswithaprovokedseizureinthesettingofseverehyponatremia.Thisisconsideredamedicalemergencyandrequirespromptcorrectionoftheserumsodiumconcentrationwith3%salinesolution.However,correctionoftheserumsodiumshouldnotexceed0.5mEq/L/hrtoavoidcausingirreversiblebraindamagefromosmoticdemyeiinationorcentralpontinemyelinolysis.Rapidcorrectionofserumsodiuminthesettingofhyponatremiaresultsinexcesswaterbeingmovedbyosmosisfromtheintracellularcompartment(neuronsandglia)intotheextracellularcompartment.Thisinturnleadstodisruptionofcellularmetabolicactivityandsubsequentcelldamage.Theoppositeistruewhenrapidlycorrectingapatientwithhypernatremia,whencerebraledemacanoccur(ChoiceA).Thispatient'shyponatremiacouldbefromlungcancer-associatedsyndromeofinappropriateantidiuretichormonegivenhiseuvoiemicstatus,recentweightloss,andsmokinghistory.(ChoiceB)Thispatienthasanirregularheartrhythm,whichmaybesecondarytoatrialfibrillation,andthereforeisatincreasedriskofanembolicstroke.However,rapidcorrectionofhishyponatremiawillnotcontributetothatrisk.(ChoiceC)RapidcorrectionofhyponatremiaresultsInIncreasedwatermovementoutofbraintissueandsowouldnotcontributetotheformationofhydrocephalus.Hydrocephaluscanbeeitherobstructive(noncommunicating)ornonobstructive(communicating),resultingfromexcesscerebrospinalfluidproductionorimpairedcerebrospinalfluidabsorption.(ChoiceE)Electrolyteabnormalitiescanresultincardiacarrhythmias.However,rapidcorrectionofhyponatremiaismorelikelytoresultinosmoticdemyeiinationinthecentralnervoussystemthantocauseaventriculararrhythmia.Educationalobjective:Acute,symptomatichyponatremia(impairedmentalstatus/seizures)Isamedicalemergency.Itrequiresapromptincreaseintheserumsodiumconcentrationwith3%orhypertonicsalineatarateofnomorethan0.5mEq/L/hrtoavoidcausingcentralnervoussystemosmoticdemyeiinationsyndrome.Q4An83-year-oldwomanisbroughttotheemergencydepartmentfromhernursinghomeduetopoorappetite,fatigue,diarrhea,andconfusion.Thepatienthasahistoryofmoderatedementia,hypertension,mildintermittentasthma,andbilateralkneeosteoarthritis.Shewasrecentlyhospitalizedwithpneumoniaforwhichshewastreatedwithbroad-spectrumantibiotics.Thepatientwasdischargedtothenursinghomeinstableconditionandhadnormallaboratoryvalues2weeksago.Sincethattime,shehashadworseningdiarrhea.Thediarrheaisfoul-smellingbutdoesnotcontainanyblood.Shehasmildabdominaldiscomfort.Temperatureis37.6℃(99.7℉),bloodpressureis96/54mmHg,pulseis112/min,andrespirationsare14/min.Shehaspoorskinturgor.Thereisnoperipheraledema.Thepatient'slungsarecleartoauscultation.Theabdomenissoft,butshehasmildgeneralizedtendernesswithoutreboundorguarding.Laboratoryresultsareasfollows:AstoolspecimentestspositiveforClostridiumdifficiletoxin.Whichofthefollowingscenariosmostaccuratelydescribesthepathophysiologyresponsibleforthehyponatremiainthispatient?A.Highantidiuretichormone,highurinesodiumB.Highrenin,highaldosterone,highantidiuretichormoneC.Highrenin,highaldosterone,lowantidiuretichormoneD.Lowantidiuretichormone,lowurinesodiumE.Lowrenin,lowaldosterone,highantidiuretichormoneA4Correctanswer:BAnassessmentofvolumestatusisessentialindiagnosingandtreatinghyponatremia(serumsodium<135mEq/L).Thispatient'srecenthistoryofpoororalintakeanddiarrheaduetoClostridiumdifficileinfectionlaboratoryevidenceofprerenalazotemia(eg;bloodureanitrogen/creatinineratio>20),andexaminationfindingsoftachycardia,hypotension,decreasedskinturgor,andabsenceofperipheraledemastronglysuggesthypovolemia(depletionofsaltandwater).Hypovolemichyponatremiaoccursduetoamultiple-pathwaymechanismthatillustratesthebody'sprioritytorestoreeuvolemiaattheriskofdevelopinghypotonicity:Decreasedrenaiperfusionleadstodecreasedrenaltubularsodiumdelivery,whichstimulatestherenin-angiotensin-aldosteronesystemandincreasessodiumreabsorption.(AngiotensinIIalsostimulatesthirst,whichleadstoincreasedwaterintake.)aNonosmoticstimulationofantidiuretichormone(ADH)occursinresponsetoangiotensinII,hypovoiemia(stimulatesstretchreceptorsintheleftatrium),andhypotension(stimulatesbaroreceptorsinthecarotidarteries).Consequentsaltandwaterretentionhelpcorrectthehypovolemia.However,inthesettingofongoingADHsecretion,hypotonichypovolemichyponatremiacandevelopduetoretentionofarelativeexcessoftotalbodywater.ADHlevelswillremainhigh(notlow)untilhypovolemiaiscorrected(ChoiceC).Infusionofnormalsalineisthetreatmentofchoiceforhypovolemichyponatremiaasitreplenishesthebody'sdepletedsaltstores,restoreseuvolemia,andshutsoffnonosmoticstimuliforADHrelease.(ChoicesAandE)HighADHandhighurinesodiumarecharacteristicofthesyndromeofinappropriateADHsecretion,whichIsacommoncauseofeuvolemichyponatremia.Lowreninandlowaldosteronewouldalsobeexpected.Thispatienthashypovolemic,ratherthaneuvolemic,hyponatremia.(ChoiceD)LowADHandlowurinesodiummaybeobservedinapatientwithcentraldiabetesinsipidus,whichtypicallypresentswithpolyuria,polydipsia,andnormaltohighserumsodiumlevels.Educationalobjective:Hypovolemichyponatremiaoccursduetononosmoticstimulationofantidiuretichormone(ADH)secretioninresponsetohypovolemia,hypotension,anddecreasedrenalperfusion(viaangiotensinII).RestorationofbloodvolumeshutsoffnonosmoticstimulationofADHandcorrectsthehyponatremia.Q

5A24-year-oldwomanisbroughttotheemergencydepartmentduetofeelinglightheadedeverytimeshestandsup.Thepatienthasnosignificantmedicalproblems.Sheleftherboyfriend4monthsagoashewas"eatingtoomuch"andhassincehaddecreasedappetiteandlost5kg(11lb).Thepatienthasalsomissedherlast2menstrualperiods.Shedoesnotusetobacco,alcohol,orillicitdrugs.Familyhistoryissignificantforcoronaryarterydiseaseandcongestiveheartfailure.Hertemperatureis36.7℃(93℉):bloodpressureis100/70mmHg,andpulseis88/minwhilesupine.Onstanding,bloodpressureis80/55mmHgandpulseis120/min.Otherthandryskinandmucousmembranes,thepatient'sphysicalexaminationisunremarkable.Initiallaboratoryresultsareasfollows:Whichofthefollowingisthemostlikelyunderlyingetiologyforthispatient'ssymptoms?A.CerebralsaltwastingB.DiureticabuseC.LaxativeabuseD.LowcaloricintakeE.MineralocorticoiddeficiencyF.Self-inducedvomitingA5Correctanswer:BThisyoungwomanhasdizzinessduetoorthostatichypotension.Inaddition,shehasabnormalserumandurineelectrolytes,includinghyponatremia,hypokalemia,hypochloremia,andincreasedurinarysodiumandpotassium.Diureticabuse,whichleadstohypovolemia,bestexplainsthelaboratoryfindingsinthispatientasfollows:Normally,dehydratedpatientswithhyponatremiaareexpectedtohavelowurinesodium(<20mEq/L);however,thispatienthaselevatedurinesodium,whichsuggestssaltwasting(eg,diureticuse,cerebralsaltwasting[CSW],adrenalinsufficiency).Normally,patientswithhypokalemiarespondbyreducingurinepotassiumexcretion,exceptincasesofrenalpotassiumwasting(eg,diureticuse,hyperaldosteronismrrenaltubularacidosis).HypochloremiaIslikelyaresultofdiuresisandcontractionalkalosis;urinechloridelevelscanvary.SurreptitiousdiureticuseIssometimesemployedasameanstoloseweight.Patientsmaygainaccesstothesemedicationsfromfamilymemberswhohavebeenappropriatelyprescribedthesemedications.(ChoiceA)CSWpresentswithhypovolemiaandhyponatremiawithhighurinesodium(>20mEq/L).However,CSWalwaysoccursduetoaneurologicinsult(injuryorsurgery).(ChoiceC)Laxativeabusewillalsoleadtohypotensionandhypovolemia.However,elevatedurinesodiumindicatesthatsodiumlossisthroughtheurinarytract(eg,diureticuse)ratherthanthegastrointestinaltract(eg,laxativeuse).(ChoiceD)Lowcaloricintakecausesweightlosssecondarytowastingofmusclemassandfatandcouldalsoleadtoelectrolyteabnormalities.However,elevatedurinesodiumandpotassiumarenotexpected.(ChoiceE)Mineralocorticoiddeficiencycanleadtowastingofsodiumandwater,butserumpotassiumlevelsareincreasedinsuchpatients.(ChoiceF)Self-inducedvomitingmayleadtohypovolemia,hypokalemia,andhyponatremia.However,urinarysodiumwillbelowasthekidneystrytoconservewaterbvmaximallyresorbingsodiumandwater.Educationalobjective:Diureticabuseleadstoincreasedexcretionofwaterandelectrolytesbythekidneys,resultingindehydration,weightloss,orthostatichypotension,hyponatremia,andhypokalemia.Urinarysodiumandpotassiumwillbeelevated.PatientssometimesabusediureticstoInduceweightloss.Q6A47-year-oldwoman,gravida4:para4,comestothephysicianwithlowerabdominalpainthatisrelievedwithurination.Thepainhasbeenpresentforover2months.Thepatienthasalsobeenvoidingmorefrequentlythanusual.Sheisoccasionallysexuallyactivewithherhusband,butintercourseispainful.Thewomanhasahistoryof4uncomplicatedvaginaldeliveriesduringher30s.Shehasnofeverorchilis.Onexamination,thepatienthasmildlowerabdominalpainwithnoreboundorguarding.Herexternalgenitaliaappearnormal.Onbimanualexamination,palpationoftheanteriorvaginalwallelicitsseverepain.MocervicalmotiontendernessIspresent.Therestoftheexaminationisnormal.Urinalysisresultsareasfollows:Whichofthefollowingisthemostlikelydiagnosis?A.CystoceleB.InterstitialcystitisC.PelvicinflammatorydiseaseD.StressincontinenceE.UrinarytractinfectionA6Correctanswer:BInterstitialcystitis(alsoknownaspainfulbladdersyndrome)isachronic,painfulbladderconditionofuncertainetiology.Thepelvicpainininterstitialcystitisisclassicallyexacerbatedbybladderfillingandrelievedbyvoiding.Theonsetofthesymptomsistypicallygradual,andthesymptomsworsenoveraperiodofmonths.Othercharacteristicsymptomsincludeurinaryurgencyandfrequency,andchronicpelvicpain.Thepaincanbeexacerbatedbyexercise,sexualIntercourse(dyspareunia),andalcoholconsumption.Thediagnosisofinterstitialcystitisisprimarilyclinical.Urinalysisisobtainedtoexcludeothercausesofbladderpain(eg,urinarytractInfection,sexuallytransmitteddisease,cancer);resultsarenormalininterstitialcystitis.Treatmentispalliativeandincludestriggeravoidance,amitriptyline,andanalgesicsforpainflares.(ChoiceA)AcystoceSereferstobladderprolapseintotheanteriorvaginalwall,whichcancausevaginalpressure,dyspareunia,urinaryfrequencyandurgency,andincontinence.Thispatienthasnoevidenceofaprolapseonexamination.(ChoiceC)Pelvicinflammatorydiseaseischaracterizedbypelvicpain,cervicalmotiontenderness,andfever.Urinarysymptomsareusuallynotpresent.(ChoiceD)Stressincontinencereferstoinvoluntaryleakageofurinewithexertion,sneezing,orcoughing.Painistypicallynotasymptomofstressincontinence.(ChoiceE)Urinalysis(andurineculture,ifurinalysisisabnormal)isperformedtoruleouturinarytractinfection.Thenormalurinalysisinthispatientexcludesaurinarytractinfection.Educationalobjective:Interstitialcystitis(painfulbladdersyndrome)isanidiopathic,chronicconditioncharacterizedbybladderpainthatisworsenedbyfillingandrelievedbyvoiding.Dyspareunia,urinaryfrequencyandurgencycanalsobepresent.Q

7A22-year-oldmancomestotheurgentcarecliniccomplainingofdarkurinehenoticedearlierthismorning.Heisrecoveringfromanupperrespiratorytractinfectionthatstarted4daysago.Thepatient'stemperatureis37.1℃(98.9℉)tbloodpressureis145/92mmHg;pulseis80/min,andrespirationsare14/min,Physicalexaminationshowsnoskinrashandnojointabnormalities.Laboratoryresultsareasfollows:UrinalysisSerumcomplementlevels(C3andC4)arewithinnormallimits,andotherserologicalworkupispending.Whichofthefollowingisthemostlikelydiagnosis?A.AcuteinterstitialnephritisB.AcutepostinfectiousglomerulonephritisC.AiportsyndromeD.Anti-glomerularbasementmembranediseaseE.BenignrecurrenthematuriaF.Goodpasture'ssyndromeG.Henoch-SchonleinpurpuraH.lgAnephropathyI.LupusnephritisA7Correctanswer:HThispatient'sgrosshematuriaisassociatedwithanupperrespiratorytractinfection(URI),hypertension,proteinuria,redbloodcellcasts,andacutekidneyinjury.Thissuggestsglomerulonephritis(GN).AfteraURLGNcanoccurduetoIgAnephropathyandpostinfectiousGN.PostinfectiousGNtypicallyoccurs10-21daysafteraURI(post-pharyngitic)andIsmorecommoninchildren.Adultscanbeasymptomaticordevelopacutenephriticsyndrome.LaboratorystudiesusuallyshowlowC3complementandelevatedanti-streptolysinOand/oranti-DNAseB.Thispatient'snormalserumcomplementsandhematuriatimecourse(4daysafterURI)arenotconsistentwithpostinfectiousGN(ChoiceB).IgAnephropathyisthemostcommoncauseofGNinadults.Patientscanhaverecurrentepisodesofhematuriausuallywithin5daysofaURI(synpharyngitic).IgAnephropathyismorecommoninyoungadultmen.SerumcomplementlevelstendtobenormalwithmesangialIgAdepositsseeninkidneybiopsy.PatientscanhaveabenigncourseordeveloprapidlyprogressiveGNornephroticsyndrome.(ChoiceA)Acuteinterstitialnephritisisanacuteinflammatoryprocessinvolvingtherenaltubulesandinterstitiumfollowingexposuretoadrug(eg,antibiotics,nonsteroidalanti-inflammatorydrugs,proton-pumpInhibitors).Otherfindingscanincludefever,skinrasheosinophilia,eosinophiluria,orwhitebloodcellcasts.However,thispatientlacksotherfindings(eg,fever,skinrash)andhasnohistoryofdrugexposure;thismakesacuteinterstitialnephritisiessiikely.(ChoiceC)AlportsyndromeisanX-linkeddefectincollagen-IVformationandpresentswithhearingloss,ocularabnormalities,hematuria,andprogressiverenalinsufficiency.Kidneybiopsyusuallyshowsthinningoftheglomerularbasementmembrane.However,post-URlgrosshematuriaisnottypicallyseeninAlportsyndrome.(ChoicesDandF)Anti-glomerularbasementmembrane(anti-GBM)diseaseisduetoanti-GBMantibodiesagainstcollagenIV(alpha-5chain)damagingtheglomeruliandalveolarlining.Anti-GBMdiseasemanifestsaseitherarenallimitedprocess(rapidlyprogressiveGN)oralveolarhemorrhage(pulmonaryrenalsyndrome).Goodpasture'ssyndromereferstoapulmonary-renalsyndromethatisamanifestationofanti-GBMdisease.Thispatient'sabsenceofsignificantlyelevatedcreatininemakesthislesslikely.(ChoiceE)Benignrecurrenthematuria,alsoknownasthinbasementmembranenephropathy,isabenignfamilialconditionthatpresentsasisolatedmicroscopichematuria.However,itdoesnotworsenkidneyfunctionorpresentasgrosshematuriaafteraURI.(ChoiceG)Henoch-SchonleinpurpuraisasystemicformofIgAinvolvementoftheglomeruli,skin,joints,andintestines.Henoch-SchonleinpurpuraismorecommonInchildrenandpresentsasanerythematousandpapularskinrashinvolvingthedorsalaspectoflowerextremities,abdominalpain,arthralgia/arthritis,andmicroscopichematuria/proteinuria.(ChoiceI)Lupusnephritiscanpresentasnephriticsyndrome,nephroticsyndrome,rapidlyprogressiveGN,orpulmonary-renalsyndrome.Patientsusuallyhavelowcomplementlevels(C3andG4)andpositivelupusantibodies(anti-nuclearantibodies,anti-dsDNA,anti-Smithantibodies).Thispatient'snormalserumcomplementlevelsmakethisunlikely.Educationalobjective:IgAnephropathyisthemostcommoncauseofglomerulonephritisinadults.Patientshaverecurrentepisodesofgrosshematuria,usuallywithin5daysafteranupperrespiratorytractinfection(synpharyngiticpresentation).IgAnephropathyisdifferentiatedfrompostinfectiousglomerulonephritisbasedonearlieronsetofupperrespiratorytractinfection-relatedglomerulonephritisandnormalserumcomplementlevels.Kidneybiopsycanalsohelpdifferentiatethese2processes.Q8A50-year-oldmancomestothephysicianbecauseofaskinrash:jointpalns;malaiseandfatigue.Hehasahistoryofintravenousdrugabuse.Histemperatureis37.1°C(98.9°F),bloodpressureis140/90mmHg,pulseis80/min,andrespirationsare14/min.Examinationshowspalpablepurpuraandhepatosplenomegaly.Urinalysisshowshematuria:redbloodceilcastsandproteinuria.Theresultsofthelaboratorystudiesareasfollows:Whichofthefollowingisthemostlikelydiagnosis?A.Alport'ssyndromeB.AcuteInterstitialnephritisC.AcutepostinfectiousglomerulonephritisD.Anti-glomerularbasementmembranediseaseE.BenignrecurrenthematuriaF.Goodpasture'ssyndromeG.Henoch-SchonleinpurpuraH.Idiopathicanti-GBMantibodymediatedglomerulonephritisI.IgAnephropathyJ.MixedessentialcryoglobulinemiaK.MicroscopicpolyangiitisL.SystemiclupuserythematosusM.ThinbasementmembranediseaseN.Wegener'sgranulomatosisA8Correctanswer:jThispatientmostlikelyhasbenignnephrosclerosissecondarytohypertension.HypertensionisthesecondleadingcauseofendstagerenaldiseaseintheUnitedStates.It;sInter-relatedwithkidneydisease;hypertensioncausesnephropathy,andviceversa.Inparticular,itistherenalvasculaturethatisexquisitelysensitivetodamagesincurredbysystemichypertension.Arterioscleroticlesionsofafferentandefferentrenalarteriolesandglomerularcapillarytuftsarethemostcommonrenalvascularlesionsseen.Asthehypertensionprogresses,thereIsaprogressivedecreaseInrenalbloodflowandglomerularfiltrationrate.Thesequenceofkidneydamageevolvesfromnephrosclerosistoglomerulosclerosis.NephrosclerosisIscharacterizedbyhypertrophyandintimalmedialfibrosisofrenalarterioles;whereas,glomerulosclerosisischaracterizedbyprogressivelossoftheglomerularcapillarysurfaceareawithglomerularandperitubularfibrosis.Microscopichematuriaandproteinuriaoccurduetotheseglomerularlesions.Thekidneysgenerallydecreaseinsize.(ChoiceB)DiabeticnephropathyistheleadingcauseofendstagerenaldiseaseintheUnitedStates.Increasedextracellularmatrix,basementmembranethickening,mesangialexpansion,andfibrosischaracterizediabetesmellitusnephropathy.Thesequenceofpathologicalchangesinthekidneysofapatientwithdiabetesmellitusisasfollows:1.Withinthefirstyearofdiabetesmellitus-Glomerularhyperperfusionandrenalhypertrophywithincreaseinglomerularfiltrationrate.2.Firstfivey