Acute Kidney Injury Mary (tessie) Behrens, MD, FACP, FASN, FNKF - PowerPoint Presentation

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Acute Kidney Injury

Mary (tessie) Behrens, MD, FACP, FASN, FNKFMid-atlantic nephrology associates, P.a.

Annual Meeting of Maryland Chapter of the American College of PhysiciansJanuary 31, 2020

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Agenda

DefinitionStagingBio-Markers

Etiology of AKIClassificationDiagnosisTreatment

Prevention of AKI

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AKI DefinitionOne of the following criteria needs to be metIncrease in Serum Creatinine (

Scr) by ≥ 0.3 mg/dl within 48 hoursIncrease in Scr to ≥ 0.5 times baseline which is known or presumed to have occurred within the 7 prior daysUrine volume < 0.5 ml/kg/hr

for 6 hoursKDIGO: Kidney Disease: Improving Global Outcomes 2012

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Staging of AKI

Stage

Serum CreatinineUrine Output

1

1.5-1.9 times baseline

or

≥

0.3

mg/dl increase

< 0.5 ml/kg/

hr

for 6-12 hours

22 – 2.9 times baseline< 0.5 ml/kg/hr for ≥ 12 hours33 times baselineOrIncrease in serum creatinine to ≥ 4.0 OrInitiation of renal replacement therapy< 0.3 ml/kg/hr for ≥ 24 hours OrAnuria for ≥12 hours

KDIGO 2012

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RIFLE Criteria

R

isk1.5 fold increase in serum creatinine, or 25% reduction in GFR or urine output <0.5 mg/kg/hr for 6 hours

I

njury

2 fold increase in serum creatinine,

or 50% reduction in GFR or urine output < 0.5 ml/kg/

hr

for 12 hours

F

ailure

3 fold increase in serum creatinine or 75% reduction in GFR or urine

output < 0.3 ml/kg/hr for 24 hours or anuric for 12 hoursLossComplete loss of kidney function for > 4 weeksEndEnd Stage Renal Disease - Complete loss of kidney function for > 3 months

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Hospital Survival, Stratified by AKI Stage

Rewa

O., Bagshaw, S. (2014) Nat Rev Neph 2013

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Framework for Progression of AKI

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BiomarkersSerum creatinine is a poor marker for early AKI detectionNumerous biomarkers have been studied

Could be used for early detection of AKIMay help with differential diagnosis of AKICould help with prognosis of AKI

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Some BiomarkersEarly detection: Cystatin C, GST, KIM-1

Differential Diagnosis: IL18, KIM-1, NGALPrognosis (mortality, RRT): NGAL, NAG, LFABP

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Who is at Risk for AKI?

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Exposures

SepsisBurnsShockCritical illness

Cardiac surgeryMajor non-cardiac surgeryNephrotoxic drugs

Radiocontrast agents

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Susceptibilities

Volume depletionAdvanced ageFemaleBlack race

CKDChronic disease: heart, lungs, liverDiabetes

Cancer

Anemia

KDIGO 2012

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AKI Leads to CKD

AKI

CKD

CKD Predisposes to AKI

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Who to Assess for AKIAKI frequently without symptoms in early stagesThose identified as high risk: heart failure, liver failure

Outpatients with acute illness, GI, feverHospital patients on regular basisFrequently if seriously illPeriodically if not

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Assessing for AKIStratify High Risk CohortHigh Risk

Discontinue nephrotoxic drugsOptimize volume statusClose monitoringHemodynamicLabs – creatinine & urine outputAvoid Contrast

KDIGO 2012

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Assessing for AKI – cont’dStage 1 Diagnostic work-upNon-invasive

InvasiveStage 2Adjust drug dosingConsider renal replacement

KDIGO 2012

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DiagnosisHistory

PhysicalCreatinineUrinalysisAssess urine output (hospital setting)UltrasoundUrine electrolytes

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Causes of AKIPre-renal

RenalGlomerularVascular

Tubulo interstialPost renal

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Pre-Renal

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Pre-Renal

Volume DepletionExtrarenal lossRenal lossesIntrarenal VasoconstrictionMedications

CardiorenalHepatorenalAbdominal Compartment SyndromeSystemic VasodilationSepsis

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Pre-renal: Diagnosis and TreatmentUrine may show H

igh specific gravityLow UnaFena

< 1%Treat the CauseFluidsDiscontinue medsImprove cardiac outputTreat low BP

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Renal Renal

GlomerularVascularTubulo

interstial

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Renal CausesGlomerularGlomerulonephritis

VasculitisThrombotic microangiopathy

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Renal Diagnosis & Treatment- GlomerularUrine sediment is active

Dysmorphic RBCCellular castsProteinuriaDiagnose with:SerologiesBiopsy

Treatment: immunosuppressants

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Renal CausesVascular Macrovascular

Progressive renal artery stenosisRenal vein thrombosisRenal infarctionMicrovascularAtheroemboli

Malignant hypertensionScleroderma

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Renal Diagnosis & Treatment- VascularUrinanalysis

May see hematuriaOr unremarkableRenal duplexTreatment is dependent on diagnosis

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Vignette

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Case78 yo with DM, HTN, hyperlipidemia comes to the ER with chest pain. Gets

cath and stent in LAD and circumflex artery. Sees you in office 2 weeks post with nausea, fatigue, new skin rash. Labs reveal Cr 4.0 (was 1.2)

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Dx

:

Atheroembolic Disease

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Atheroembolic DiseaseMay see:

Low C3Eosinophiluria HematuriaSupportive treatment plusRisk factor modifications – statinsRAS blockage

Avoid AC & further vascular interventions

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Renal Causes – Tubulo-interstitial

TubularIschemiaProlonged pre-renal hypotensionSepsisNephrotoxic agentsContrastMyoglobin/Hemoglobin

AminoglycosidesEthylene Glycol

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Ischemic AKI

COMPR PHYSIOL 2012

; 2:1303-1353

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Tubular Diagnosis & TreatmentUrinalysis

High urine sodiumGranular CastsContrast – see within 48 hoursRhabdomyolysis – after falls, statinsMuscle achesTreatment

Stop drugsSupportiveOptimize volume

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Renal Causes – InterstitialAcute Interstitial NephritisMedications

AntibioticsProton Pump InhibitorsChemotherapeutic agentsInfectionsVirusesBacterial

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Interstitial Diagnosis & TreatmentTriad – Fever, Rash, EosinophiliaUrinalysis

Una > 40Urine eosinophilsTreatmentStop drugTreat infection

Steroids if no response

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Post Renal CausesExtrarenal ObstructionProstate

Cervical cancerRetroperitoneal fibrosisIntrarenal ObstructionStonesCrystals

Clots

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Post Renal Diagnosis & TreatmentRenal ultrasoundTreatmentFoley catheter

Nephrostomy tubesLithotripsy

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Indications for Renal ReplacementVolume overload not manageable with diureticsPersistent hyperkalemia

Metabolic acidosisUremic symptomsToxic removal

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Renal Replacement OptionsContinuous Renal Replacement Therapy (CRRT)

Hemodynamic instabilityICU statusHemodialysisPeritoneal DialysisRarely used in AKI setting

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Outcomes of AKIRecoveryChronic Kidney DiseaseEnd Stage Renal Disease

Death

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General ManagementEvaluate AKI promptly to determine causes – especially if reversible causes

Monitor patients closely with serum creatinine and urine outputManage them according to severity and causes of AKIEvaluate them 3 months after AKIIf left with CKD – need to manageIf recover need to consider them as high risk for future AKI

KDIGO 2012

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Preventing AKIAvoid nephrotoxic agents in patients with CKDIf CKD and need contrast :

Use isotonic fluids before, during and afterUse low osmolar contrastCorrect volume depletionIf patients have acute illnesses or significant GI symptoms consider holding:

DiureticsACEI/ARBMetformin

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When to Call the NephrologistTo identify etiology of AKI (especially if no rapid improvement)

To manage electrolyte abnormalitiesFor worsening renal functionIf renal replacement therapy is neededWhenever you have a renal question

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SummaryAKI is a complicated and serious problemIt is important to know who to screen

The differential diagnosis of AKI is large and broadUse your history and physical skills with urinalysis and ultrasound to guide youThe best outcomes occur if we can prevent AKINephrologist is frequently needed and always available for assistance

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The End

Thank you for your attention