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MetabolicAlkalosis
GENERALPRINCIPLES
Development of a persistent metabolic alkalosis requires both generation (an inciting cause) and
maintenance(apersistentimpairmentofthecorrectiverenalresponse).
Generationoften occurswitha primary increase in theplasma andmay be due toeither
gainfromalkaliadministrationor,morecommonly,excessiveH+loss.Thelattermayresultfrom the
lossofH+-richfluids,includingupperGIsecretions.Contractionalkalosisreferstothecontractionof
volumearoundafixedcontentofbicarbonate.
Maintenancerequires a concomitantimpairmentinrenal excretionbecausethekidneynormally
hasalargecapacitytoexcrete .Thisoccursasaresultofadecreasedglomerularfiltrationrate
or enhanced tubular reabsorption from chloride depletion, volume contraction, and
hypokalemia. A decrease in filtered chloride is sensed by the macula densa and, as a result of
tubuloglomerular feedback, reduces filtered and stimulates aldosterone release. It also limits
adaptivedistal secretion.Metabolicalkalosisisoftendescribedasbeingchlorideresponsiveor
chlorideunresponsive.
DIAGNOSIS
ClinicalPresentation
Becausekeycausesofmetabolicalkalosisarerelatedtovolumecontraction,patientsmaypresentwith
signsofvolumedepletion.Occasionally,patientsdemonstratehypertensionormildECFexpansionasa
resultofmineralocorticoidexcess.
DiagnosticTesting
Theetiologyofmetabolicalkalosisisoftenobviousfromthehistory.Commoncausesincludelossof
upperGIsecretionsthroughvomitingorexcessiveurinaryH+lossfromdiuretics.
Urine electrolytes are generallyuseful in identifying the etiology of a metabolic alkalosis whenthe
historyandphysicalexaminationareunrevealing.
A urine [Cl−] <20 mEq/L is consistent withchloride-responsive metabolic alkalosis andusually
indicatesvolumedepletion.Aurine[Cl−]>20mEq/Lindicatesachloride-unresponsivecause(see
Table12-3).
Urine[Na+]isnotreliableinpredictingtheeffectivecirculatingvolumeintheseconditionsbecause
bicarbonaturiaobligatesrenalNa+losseveninvolumedepletion.
Serum potassium levels are often low in metabolic alkalosis because of transcellular shifts.
Furthermore,hypokalemiacontributestoalkalosisbyincreasingtubularH+secretionandCl−wasting.
TREATMENT
Chloride-responsive metabolic alkaloses are most effectivelytreated with salineresuscitationuntil
euvolemia is achieved. The increase in filtered chloride leads to improved renal handling of the
bicarbonateload.
Chloride-unresponsive metabolic alkaloses do not respond to saline administration and are often
associatedwithanormalorexpandedECFvolume.
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MineralocorticoidexcesscanbemanagedwithaK+-sparingdiuretic(amilorideorspironolactone)
andrepletionoftheK+deficit.
The alkalosis from excessive alkali administration will quickly resolve once the load is
withdrawn,assumingnormalrenalfunction.
Given that the presence of hypokalemia will continue to perpetuate some degree of alkalosis
regardlessofotherinterventions,potassiummustberepletedinallcasesofmetabolicalkalosis.
Acetazolamide can be used if the alkalosis persists despite the above interventions or if saline
administration is limited by a patient’s volume overload. This therapy promotes bicarbonaturia,
althoughrenalK+lossisenhancedaswell.Acetazolamidecanbedosedat250mgq6h×4orasa
singledoseof500mg.
Severe alkalemia (pH >7.70) with ECF volume excess and/or renal failure can be treated with
isotonic (150 mEq/L) HCl administered via a central vein. The amount of HCl required can be
calculatedasfollows:(0.5×leanweightinkg)×( −24).Correctionshouldoccurover8–24
hours.
RespiratoryAcidosis
GENERALPRINCIPLES
Thecausesofrespiratoryacidosiscanbedividedintohypoventilationfrom(1)respiratorycenter
depression,(2)neuromuscularfailure,(3)decreasedrespiratorysystemcompliance,(4)increased
airwayresistance,and(5)increaseddeadspace(seeTable12-3).
DIAGNOSIS
Symptoms of respiratory acidosis result from changes in the cerebrospinal fluid (CSF) pH. A very
severehypercapniamaybewelltoleratedifitisaccompaniedbyrenalcompensationandarelatively
normalpH.Conversely,amodestriseinpCO2canbeverysymptomaticifacute.
Initialsymptomsandsignsmayincludeheadacheandrestlessness,whichmayprogresstogeneralized
hyperreflexia/asterixisandcoma.
TREATMENT
Treatmentisdirectedatcorrectingtheunderlyingdisorderandimprovingventilation(seeChapter 10,
PulmonaryDiseases).
AdministrationofNaHCO3toimprovetheacidemiamayparadoxicallyworsenthepHinsituationsof
limitedventilation. Theadministered will combine with H+ in the tissues and form pCO2 and
water. If ventilation is fixed, this extra CO2 generated cannot be blown off and worsening of
hypercapniawillresult.Therefore, should,ingeneral,beavoidedinpurerespiratoryacidoses.
RespiratoryAlkalosis
GENERALPRINCIPLES
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ThecommoncausesofhyperventilationresultinginrespiratoryalkalosisaregiveninTable12-3.
DIAGNOSIS
ClinicalPresentation
The rise in CSF pH that occurs with acute respiratory alkalosis is associated with a significant
reduction in cerebral blood flow that may lead to light-headedness and impaired consciousness.
Generalizedmembraneexcitabilitycanresultinseizuresandarrhythmias.Symptomsandsignsofacute
hypocalcemia(see “Calcium,Hypocalcemia,ClinicalPresentation”section)maybeevidentfrom the
abruptfallinionizedcalciumthatcanoccur.
Chronic respiratory alkalosis is usually asymptomatic because a normal pH is well defended by
compensation.
DiagnosticTesting
TheriseinpHfromacuterespiratoryalkalosiscancauseareducedionizedcalcium,aprofound
hypophosphatemia,andhypokalemia.
TREATMENT
Treatmentofrespiratoryalkalosisshouldfocusonidentifyingandtreatingtheunderlyingdisease.
Inintensivecareunitpatients,thismayinvolvechangingtheventilatorsettingstodecreaseventilation
(seeChapter8,CriticalCare).
REFERENCES
1. HillierTA,AbbottRD,BarrettEJ.Hyponatremia:evaluatingthecorrectionfactorfor
hyperglycemia.AmJMed.1999;106:399-403.
2. SternsRH,CappuccioJD,SilverSM,etal.Neurologicsequelaeaftertreatmentofsevere
hyponatremia:amulticenterperspective.JAmSocNephrol.1994;4:1522-1530.
3. BilezikianJP,KhanAA,PottsJTJr,etal.Guidelinesforthemanagementofasymptomaticprimary
hyperparathyroidism:summarystatementfromthethirdinternationalworkshop.JClinEndocrinol
Metab.2009;94:335-339.
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13
RenalDiseases
BlessingOsondu,SethGoldberg
EvaluationofthePatientWithRenalDisease
DIAGNOSIS
ClinicalPresentation
Mostpatientswithrenaldiseaseareasymptomatic.Renaldiseaseisofteninitiallydiscoveredbecause
ofabnormalroutinelaboratorydata,specificallyanelevatedserumcreatinine(Cr)level.Anabnormal
urinalysis or sediment, with proteinuria, hematuria, or pyuria, may also indicate renal disease,
requiringfurtherevaluation.
The presentation of acute kidney injury (AKI) can be quite variable, ranging from constitutional
symptoms of generalized malaise to more concerning symptoms such as worsening hypertension,
dependent or generalized edema, decreasing urine output, foamy urine, weight changes, or poor
appetite. With advanced chronic kidney disease (CKD), patients may start to experience nausea,
vomiting, a metallic taste in the mouth, and lethargy. A wide range of electrolyte abnormalities
includinghyperkalemia,hypocalcemia,hyperphosphatemia,andmetabolicacidosismayalsodevelop.
DiagnosticTesting
Duringtheinitialevaluationofapatientwithrenaldisease,itisimportanttodetermineifthereisaneed
foremergentdialysisbyobtainingpertinentlaboratoryandimagingstudies.Additionaltestingisthen
performedtoidentifytheunderlyingetiology.
Basicdiagnostictesting
A basic evaluation includes electrolytes (with calcium and phosphorus), Cr, blood urea nitrogen
(BUN), andalbumin.WhenCr isstableoverdaystoweeks,itcanbeusedtocalculateanestimated
glomerular filtration rate (eGFR). eGFR can be calculated using the Chronic Kidney Disease
Epidemiology Collaboration (CKD-EPI) equation or the Modification of Diet in Renal Disease
(MDRD)formula.Historically,theseequationshaveincorporatedamodifierforrace.However,with
the growing acknowledgment that race is a social construct, and not a biologic one, the American
SocietyofNephrologyandtheNationalKidneyFoundationhaveadvocatedforremovingthisvariable.
With both equations, CKD is not diagnosed when the eGFR is >60 mL/min/1.73 m2 unless other
evidenceofrenaldamage(e.g.,proteinuria)ispresentforatleast3months.
UseofcystatinCtoestimatetheGFRcanmoreaccuratelyclassifypatientsintheeGFRrangeof45–60
mL/min/1.73m2,althoughthishasnotbeenshowntoimproveoutcomesortoprovidebetterpredictions
ofrisk.
1
Unlike the complex formulae described above, the Cockcroft–Gault equation can be calculated
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manually, and yields an estimated creatinine clearance, which is equal to ([140 − age]/[serum
creatinineinmg/dL])×(weightinkg/72).Theequationshouldbemultipliedby0.85forwomen.
Theseequationsarenothelpfulinestimatingrenalfunctionwhenthecreatinineisnotinsteadystate.
Urinestudies
Routineurinestudiesincludeaurinedipstick(forprotein,blood,glucose,leukocyteesterase,nitrites,
pH,andspecific gravity)aswellas afreshly voidedspecimenformicroscopic examinationofurine
sediment(cells, casts,andcrystals). Theurinesample is centrifugedat2100rpmfor5 minutes,and
thenmostofthesupernatantispouredoff.Thepelletisresuspended bygentlytapping thesideofthe
tube.
Proteinuriaandalbuminuriacanbeestimatedfromaspoturineprotein-to-creatinineratiooralbuminto-creatinineratioinpatientswhoseserumcreatininelevelisinthesteadystate.Theratioisexpressed
inmilligramsofproteinoralbuminpergramofcreatinine.The2012KDIGOguidelineshaverevised
the definition for albuminuria based on the urinary albumin-to-creatinine ratio as being normal to
mildly increased (A1,<30 mg/g), moderately increased (A2, 30–300 mg/g), andseverelyincreased
(A3, >300 mg/g).2 These values can serve as a useful prognostic tool for adverse events. Theterm
microalbuminuria is no longer used. A normal ratio for proteinuria is <250 mg/g. A 24-hour urine
collectionforproteincanbeobtainedwhentheserumCrisnotatastablebaseline.
Hematuria,whichis definedas morethanthreered bloodcells(RBCs)perhigh-powerfield onan
unspunspecimen,canrepresentaninfectious,inflammatory,or malignantprocessanywherealongthe
urinarytract.DysmorphicRBCs(withroundedprotuberances)aresuggestiveofaglomerularsourceof
injury.ThesemaybeaccompaniedbyRBCcastsformedwithinthetubules.TheabsenceofRBCsina
patient with a positive dipstick for blood suggests hemolysis or rhabdomyolysis, forms of pigment
nephropathy.
Whitebloodcells(WBCs)intheurinerepresent aninfectiousorinflammatoryprocess.Thismaybe
seen with urinary tract infection (UTI), kidney parenchymal infections such as pyelonephritis or
abscess,or acuteinterstitialnephritis (AIN).WBCcastscanaccompanyWBCsintheurineandare
suggestiveofAINandpyelonephritisbutcanalsobeseenaspartofanactivesedimentininflammatory
glomerulardiseases.
Additionalbiochemistrytestscanbeorderedtoevaluateforspecificetiologiesandwillbediscussed
intheindividualsectionsbelow.
Imaging
Renal ultrasonography can be helpful in acute and chronic kidney diseases. It can document the
presenceoftwokidneys,assessorgansizeanddistributionofrenalcysts,andidentifyhydronephrosis
in the setting of obstruction. Small kidneys (<9 cm) generally reflect chronic disease. Diseases
includingdiabetes,HIV,depositiondisorders,andpolycystickidneydiseaseareassociatedwithlarge
kidneys (generally >13 cm). A discrepancy in kidney size of >2 cm suggests chronic disease in a
unilateral kidney, such as that seen in renal artery stenosis with atrophy of the affected kidney.
Retroperitoneal fibrosis can encase the ureters and prevent dilation despite the presence of an
obstruction.
CTwithcontrasthaslessutilityintheevaluationofkidneydiseasebecausetheiodinatedcontrastdye
can be nephrotoxic. However, noncontrast helical CT scanning has become the test of choice in
evaluatingnephrolithiasis.
MRI and magnetic resonance angiography (MRA) can be helpful in evaluating renal masses,
detecting renal arterystenosis, anddiagnosing renal veinthrombosis. Unlikestandard arteriography,
MRA doesnot requiretheadministrationofnephrotoxiccontrastagentsbut doesemploygadolinium-
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based contrast agents, which are associated with the development of nephrogenic systemic fibrosis
(NSF)inpatientswithadvancedkidneydiseaseordialysisdependence.3Guidelinesthatlimittheuse
ofgadoliniuminat-riskpatientshavedecreasedtheincidenceofNSF.
Radionuclidescanningusestechnetiumisotopestoassessthecontributionofeachkidneytotheoverall
renal function, providing important information if unilateral nephrectomy is being considered for
malignancyorforlivingdonation.Renalscanningisalsousefulintransplantation,whererenaluptake
andexcretionofthetracercanbefollowed.
Diagnosticprocedures
Kidney biopsy should be considered in adults with unexplained proteinuria, hematuria, or renal
dysfunction. It can determine diagnosis, classify disease, guide therapy, and provide prognostic
relevanceinmanysettings,particularlyintheevaluationofglomerularordepositiondiseases.Biopsy
of a renal transplant allograft may be necessary to distinguish allograft rejection from medication
toxicity and other causes of renal dysfunction. Biopsy is unlikely to provide useful diagnostic
informationwhen thekidneysareverysmall,suggestiveofadvancedchronicityandfibrotic kidneys.
This scenario alsocarries anincreasedriskofpostproceduralbleeding,andbiopsyshouldgenerally
beavoidedinthesecases.
Preparative measures for native kidney biopsy include avoiding aspirin, NSAIDs, and antiplatelet
agentsfor5–7days.Blood pressuremustbecontrolled,andanticoagulation mustbereversedbefore
theprocedure.Ultrasonography(todocumentthepresenceoftwokidneysandassesssizeandlocation)
andurinalysisorurineculturetoexcludeinfectionshouldalsobeperformedpriortotheprocedure.If
uremicplateletdysfunctionissuspectedbyabnormalplateletfunctionassays,IVdesmopressinacetate
(DDAVPat0.3μg/kg)canbeinfused30minutesbeforebiopsy.Patientsondialysisshouldnotreceive
heparinimmediatelyafterthebiopsy.Ifbodyhabitusprecludesapercutaneousapproach,atransjugular
renalbiopsycanbeperformed.
Ahemoglobindropofapproximately10%iscommonaftertheprocedure.Difficultyvoidingafterthe
proceduremayrepresenturethralclotobstructingtheflowofurine.
AcuteKidneyInjury
GENERALPRINCIPLES
Definition
AccordingtotheKDIGO2012guidelines,AKIisdefinedandcategorizedbyvaryingCrelevationsor
decreasesinurineoutput.
4
Stage1AKIisdefinedasaCr1.5–1.9timesbaseline(knownorpresumedtohaveoccurredwithinthe
prior7days),anincreaseinCr≥0.3mg/dLwithin48hours,oraurineoutput<0.5mL/kg/hfor6–12
hours.
Stage 2 AKIis definedas a Cr 2–2.9 times baseline or a urine output <0.5 mL/kg/h for at least 12
hours.
Stage 3 AKI is defined as a Cr ≥ 3 times baseline, a Cr increase of ≥4 mg/dL, initiation of renal
replacementtherapy,urineoutput<0.3mL/kg/hforatleast24hours,oranuriaforatleast12hours.
Classification
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Renalfailurecanbeclassifiedasoliguricornonoliguricbasedontheamountofurineoutput.Cutoffsof
approximately500mL/dor25mL/hfor6–12hoursarefrequentlyusedinclinicalpractice.
Etiology
TheetiologyofAKIshouldbedeterminedwhenpossible.Itcanbeclassifiedbasedontheanatomic
locationofthephysiologicdefect.Prerenaldiseaseinvolvesadisturbanceofrenalperfusion,whereas
postrenaldiseaseinvolvesobstructionalongtheurinarycollectingsystem.Intrinsicrenaldisease
involvesthetubules,glomeruli,microvasculature,orinterstitiumofthekidneys.Table13-1listssomeof
thecommoncausesofAKI.
TABLE13-1
CAUSESOFACUTERENALFAILURE
Prerenal Intrinsic Postrenal
Hypovolemia
Hypotension
(includingsepsis)
Lossof
autoregulation
(NSAIDs,RAAS
blockers)
Abdominal
compartment
syndrome
Renalartery
stenosis
Heartfailure
Hepaticcirrhosis
Tubular:IschemicATN,toxicATN(contrast,
pigment,uricacid)
Vascular:Glomerulonephritis,dysproteinemia,
thromboticmicroangiopathy(HUS,TTP),
atheroembolicdisease
Interstitial:Acuteinterstitialnephritis,
pyelonephritis
Urethralobstruction
Ureteralobstruction
(bilateral,orunilateralif
solitarykidney)
ATN,acutetubularnecrosis;HUS,hemolyticuremicsyndrome;RAAS,renin–angiotensin–aldosteronesystem;TTP,thrombotic
thrombocytopenicpurpura.
PRERENAL
Thetermprerenalazotemiaimpliesthattheinherentfunctionofthekidneysispreserved,inthesetting
of renal hypoperfusion and reduced GFR. States of decreased effective circulating blood volume,
resultingfromintravascularvolumedepletion,lowcardiacoutput,ordisorderedvasodilation(hepatic
cirrhosis),mayalsoresultinprerenalazotemia.
Whenthecauseistruevolumedepletion,presentationinvolvesahistoryofexcessivevolumelossor
reduced intake. The physical examinationmay reveal drymucous membranes, poor skinturgor,and
orthostaticvitalsigns(dropinbloodpressurebyatleast20/10mmHgoranincreaseinheartrateby
10bpmafterstandingfromaseatedorlyingposition).Thecentralvenouspressureistypically<8cm
H2O.
Low cardiac output causes prerenal azotemia via a drop in the effective circulating volume despite
being inastateoftotalbodyvolumeoverload.Sympathetic andneurohormonalactivationstimulates
the renin–angiotensin–aldosterone system (RAAS) for sodium reclamation, as well as driving
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antidiuretic hormone (ADH), promoting further water retention. This can lead to an increased
reabsorptionofureanitrogeninrelationtocreatinine,andpatientspresentwitha prerenalpatternon
laboratoryinvestigations(BUN:Crratio>20,urinesodium<20mEq/L,fractionalexcretionofsodium
<1%). In heart failure, diuresis may paradoxically improve the prerenal azotemia by unloading the
ventricles and improving cardiac function and renal perfusion (see Chapter 5, Heart Failure and
Cardiomyopathy). The use of ultrafiltration (UF) was evaluated and found to be inferior to
pharmacologic therapies, resulting in more adverse events in the treatment of acute decompensated
heartfailure.
5
Hepatic failure with splanchnic vasodilation, venous pooling, and ascites formation diminishes the
effective circulating volume. RAAS activation along with ADH secretion will produce a prerenal
patternonlaboratoryinvestigations,despitebeinginastateoftotalbodyvolumeoverload.This can
progresstohepatorenalsyndrome(HRS),whichischaracterizedbyariseinserumcreatinineof>1.5
mg/dLthatisnotreducedwithadministrationofalbumin(1g/kgofbodyweight)andafteraminimum
of2 daysoffdiuretics. Thediagnosis of HRSshould be made inthe absence ofshock, nephrotoxic
agents,or findingsofrenalparenchymal disease(e.g.,activeurinarysedimentonurinemicroscopy).
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Spontaneous bacterial peritonitis, aggressive diuresis, gastrointestinal bleeding, or large-volume
paracentesiscanprecipitateHRSinpatientswithliver cirrhosis. Managementoftherenal disease is
supportive, and if definitive treatment of the liver disorder (either through recovery or via
transplantation)canoccur,renalrecoveryis common.Temporizing measuresincludetreatmentofthe
underlyingprecipitatingfactor(e.g.,peritonitis,gastrointestinalbleeding,hypotension)andwithholding
diuretics or other offending agents. Dialytic support can be used as a bridge to transplantation in
appropriate candidates, with anticipation of renal recovery if the period of dialysis dependence is
shorterthan6weeks.
Simultaneous liver kidney (SLK) transplant should be considered if the candidate meets specific
criteria published in 2016 by the US Organ Procurement and Transplant Network (OPTN) and the
United Networkfor Organ Sharing (UNOS). TheseincludeCKD witha GFR ≤35 mL/min/1.73 m2,
sustainedAKIwithaGFR≤25mL/min/1.73m2,ordialysisdependenceforatleast6weeks.Patients
withthe diagnosisofametabolicdiseasethatwouldplacearenalallograftatriskoffailing,suchas
primaryhyperoxaluria,atypicalhemolyticuremicsyndrome(HUS)frommutationsinfactorHorfactor
I,familialnon-neuropathicsystemicamyloidosis,ormethylmalonicaciduria,wouldalsobecandidates
forSLK.7AdditionaltreatmentoptionsarediscussedfurtherinChapter19,LiverDiseases.
Inthe volume-depletedpatient,certainmedicationscanaffecttheabilityofthekidneytoautoregulate
blood flow and maintain GFR. NSAIDs inhibit the counterbalancing vasodilatory effects of
prostaglandinsattheafferent arteriole andcaninduceAKIinvolume-depletedpatients.Angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) can cause efferent
arteriolarvasodilationandadropintheGFR.
Abdominal compartment syndrome from intestinal ischemia, obstruction, or massive ascites can
compromiseflowthroughtherenalvasculatureviaincreasedintra-abdominalpressure(IAP).AnIAP
>20mmHg,measuredvia a pressuretransducerattached tothebladdercatheterina patientwhois
sedated,supportsthediagnosis.
POSTRENAL
Postrenal injury occurs when the flow of urineis obstructed within the collecting system. Common
causes include prostatic enlargement, bilateral kidney stones, or malignancy (e.g., extrinsic
compressionbyamass,retroperitonealfibrosis).Theincreasedintratubularhydrostaticpressureleads
to the diminished GFR. Bilateral involvement (or unilateral obstruction to a solitary functioning
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kidney) isgenerallyrequired to producea significantchangeintheCr level. Whenthis diagnosis is
suspected, a renal ultrasound should be obtained early to evaluate for hydronephrosis. Note that
hydronephrosis may be less pronounced when there is concomitant volume depletion or if
retroperitonealfibrosishasencasedtheureters,preventingtheirdilation.Therefore,ifthisdiagnosisis
still suspected, renal ultrasound should be repeated after the patient has received adequate volume
repletion.
Treatment depends on the level of obstruction. When urethral flow is impeded (often by prostatic
enlargement in men), placement of a bladder catheter can be both diagnostic and therapeutic; a
postvoid residual urine volume >300 mL suggests the diagnosis. When the upper urinary tract is
involved, urologic or radiologic decompression may be necessary, with stenting or placement of
percutaneousnephrostomytubes.
Reliefofbilateralobstructionisfrequentlyfollowedbyapostobstructivediuresis.Serumelectrolytes
needtobecloselymonitoredifpolyuriaensues,andreplacementofapproximatelyhalfoftheurinary
volumewith0.45%salineisrecommended.
Crystals may cause micro-obstructive uropathy within the tubules. IV acyclovir and the protease
inhibitor indinavir can induce AKI by this mechanism. The urine may show evidence of crystals,
althoughsometimes notuntil urineflow is re-established.Treatmentis typicallysupportive after the
offending agentis discontinued. Aswithresolutionofotherformsofobstructiveuropathy,apolyuric
phasemayoccur.
INTRINSICRENAL
Causesofintrinsicrenalfailurecanbedividedanatomicallyintotubular,glomerular/vascular,and
interstitialcategories.Diseasecanbeprimarilyrenalinnatureorpartofasystemicprocess.
Tubular
Ischemic acutetubularnecrosis(ATN)is themostcommon causeofrenalfailureinthehospital
setting, especially in the intensive care unit, and is the end result of any process that leads to
significant hypoperfusionofthe kidneys,including sepsis, hemorrhage, or any prolonged prerenal
insult.
Theinjuryresultsinthesloughingofrenaltubularcells,withthiscellulardebriscongealingina
matrix of Tamm–Horsfall protein to form granular casts. The casts have a “muddy brown”
appearanceandarestronglysuggestiveofATNintheappropriateclinicalcontext.Thefractional
excretionofsodium(FENa)(>1%)andfractionalexcretionofurea(FE
Urea
)(>35%) aretypically
elevatedasthetubuleslosetheirabilitytoconcentratetheurine.However,thesecalculationsare
notspecifictoATN.
Management of ATN is supportive, with avoidance of further nephrotoxic insults. Fluid
managementisaimedatmaintainingeuvolemia.Volumedeficits,ifpresent,shouldbecorrected.If
therearesignsofvolumeoverloadandoliguria,afurosemidestresstestmaypredicttheseverity
ofAKI.Asinglefurosemidedoseof1.0or1.5mg/kg(dependingonpriorfurosemideexposure)
isadministered,andtheurineoutputinthefirst2hoursismeasured.A2-hoururineoutputofless
than200mL offersthebestcombinationofsensitivity andspecificityandhasagoodpredictive
capacitytoidentifythosepatientswhowillprogresstoadvancedstagesofAKI.Patientsmustbe
euvolemic or hypervolemic to qualify for this test and should not be on pressor support.
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Continuing diuretictherapyifa responseisseenhasnotbeenshown tohastenrecoverybutcan
simplifyoverallmanagement.
Recoveryfrom ATNmaytakedaystoweekstooccurbutcanbe expectedin>85% of patients
withpreviouslynormalrenalfunction.Dialysismaybenecessarytobridgethetimetorecovery.
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Toxic ATN can result from endogenous chemicals (e.g., hemoglobin, myoglobin pigments) or
medications (e.g., iodinated contrast, aminoglycosides, combination of vancomycin and
piperacillin/tazobactam).TheseformssharemanyofthediagnosticfeaturesofischemicATN.
Iodinatedcontrast is a potent renal vasoconstrictor and is toxic to renal tubules. When renal
injury occurs, the Cr typically rises 24–48 hours after exposure and peaks in 3–5 days. Risk
factors for contrast nephropathy include underlying CKD, age >75 years, diabetes, volume
depletion,heartfailure,highercontrastvolumes, anduseofhyperosmolarcontrast.Preventative
measuresincludeperiproceduralIVvolumeexpansionanddiscontinuationofdiureticswithin24
hoursoftheprocedure.Normalsalineat150mEq/Lcanbegivenat3mL/kg/hfor1hourbefore
exposure,thenat1mL/kg/hfor6hoursaftertheprocedure.Inalargerandomizedcontrolledtrial,
sodium bicarbonatewas notfoundtobe superior tonormal saline,whereas acetylcysteinewas
equivocaltoplaceboandthereforeisnotrecommended.
9
Aminoglycoside nephrotoxicity is typically nonoliguric, occurs from direct toxicity to the
proximaltubules, andresultsintherenalwastingofpotassium andmagnesium. Replacementof
theseelectrolytesmaybecomenecessary. Asimilar patternofpotassium andmagnesium loss is
seen in cisplatin toxicity. A prolonged exposure to the aminoglycoside of at least 5 days is
required. Peakandtroughlevels correlatepoorlywiththe riskofdeveloping renal injury. Risk
maybeminimizedbyavoidingvolumedepletionandbyusingtheextended-intervaldosingmethod
(seeChapter15,Antimicrobials).
Pigment nephropathy results from direct tubular toxicity by hemoglobin and myoglobin.
Vasoconstriction may also play a role. The diagnosis may be suspected by a positive urine
dipsticktestforbloodbutanabsenceofRBCsonmicroscopicexamination.Inrhabdomyolysis,
the creatine kinase level is elevated to at least 10 times the upper limit of normal with a
disproportionate rise in the serum Cr. Potassium and phosphorus may also be elevated in the
setting of muscle breakdown. Aggressive IV fluid administrationwith normal saline should be
initiatedimmediately,andlargevolumesarerequiredtoreplacethefluidlostintonecroticmuscle
tissue.Urinaryalkalinizationwithintravenoussodiumbicarbonateisnotgenerallyrecommended
asitmayworsenthehypocalcemia.
Intumorlysissyndrome,thereisrapiddeathofcancercellseitherspontaneouslyorinresponse
totreatment. In additiontotheelevatedCr,thereistypicallyhyperuricemia,hyperphosphatemia,
andhypocalcemia. Aratio ofurineuric acid tourineCr thatis >1 isconsistent withacuteuric
acid nephropathy, as is the findingofuric acid crystals intheurinesediment. Prophylaxis with
allopurinol 600 mg can decrease uric acid production. Rasburicase (15 mg/kg IV) is highly
effective at depleting uric acid levels and can be given as prophylaxis or as treatment.
Alkalinizationoftheurineshouldbeavoidedifhyperphosphatemiaispresentbecausethiscould
increasetheriskofcalciumphosphateprecipitationintheurine.
Glomerular/vascular
ThefindingofdysmorphicurinaryRBCs,RBCcasts,orproteinuriainthenephroticrange(>3.5
g/d) would strongly suggest the presence of a glomerular disease. Glomerular diseases are
describedindividuallyinfurtherdetailinlatersectionsofthischapter.
Asubsetofglomerulardiseasescanpresentwithrapidlydeterioratingrenalfunction,termedrapidly
progressive glomerulonephritis. This describes a type of presentation rather than a specific
disease. A nephritic picture is common, with RBC casts, edema, and hypertension. Crescent
formation is seen in >50% of glomeruli, suggesting inflammation and cellular proliferation. For
those deemed to have salvageable renal function, management typically consists of high-dose
corticosteroidsandcyclophosphamideorotherpotentimmunosuppressiveagents.
Thromboticmicroangiopathy(TMA)isageneraltermencompassingabroadspectrumofdisease
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