Acute Kidney Injur

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Acute Kidney Injury Acute Kidney Injury(Acute Renal Failure)(Acute Renal Failure)

2009 GI/GU Core2009 GI/GU Core

March 10, 2009March 10, 2009

Clifford Miles MD, MSClifford Miles MD, MS

Assistant Professor Assistant Professor

Section of NephrologySection of Nephrology



ObjectivesObjectives

Recognize the significance of AKIRecognize the significance of AKI

Know how AKI is currently definedKnow how AKI is currently defined

Know the common etiologiesKnow the common etiologies

Understand the approach to evaluationUnderstand the approach to evaluationand initial management of a patient withand initial management of a patient with

AKI AKI



IncidenceIncidence

AKI complicates ~5% of hospital AKI complicates ~5% of hospital

admissions, but >30% of ICU admissionsadmissions, but >30% of ICU admissions Associated with: Associated with:

– – Higher mortality (21% vs. 2.3%)Higher mortality (21% vs. 2.3%) – – Longer hospital stay (7 vs. 3 days)Longer hospital stay (7 vs. 3 days)

– – Greater likelihood of discharge to shortGreater likelihood of discharge to short-- or or

longlong--term care facility (for survivors)term care facility (for survivors)LiangosLiangos, et al. CJASN 2006, et al. CJASN 2006



Copyright ©2005 American Society of Nephrology

Chertow, G. M. et al. J Am Soc Nephrol 2005;16:3365-3370

Figure 2. Mortality associated with change in serum creatinine



DefinitionDefinition

General: a syndrome characterized by rapid fallGeneral: a syndrome characterized by rapid fall

in GFR with accumulation of nitrogenous wastein GFR with accumulation of nitrogenous wasteand perturbation of ECF, electrolyte, and acidand perturbation of ECF, electrolyte, and acid--

base balancebase balancemodified from Kieran/Brady in Johnson/modified from Kieran/Brady in Johnson/FeehallyFeehally C 2003C 2003

Variable in studies, including:Variable in studies, including:

– – Rise in serum creatinine (e.g., >0.3 mg/Rise in serum creatinine (e.g., >0.3 mg/dLdL increase)increase)

– – Percent rise in creatinine (e.g., >50%)Percent rise in creatinine (e.g., >50%) – – OliguriaOliguria = Urine output <400mL/day (0.5mL/kg/hr)= Urine output <400mL/day (0.5mL/kg/hr)



EtiologyEtiology

Divided intoDivided into prepre--,, postpost--, and, and intraintra--renalrenal

categoriescategoriesVast majority of AKI (>85%) is related toVast majority of AKI (>85%) is related to

prerenal or ischemic ATNprerenal or ischemic ATN



Prerenal AKIPrerenal AKI

Characterized by lowCharacterized by low ““Effective circulatingEffective circulating

volumevolume””PerfusionPerfusion isis adequate to meet metabolicadequate to meet metabolic

needs of parenchymaneeds of parenchymaBy definition, reversible upon correction of By definition, reversible upon correction of

hypoperfusionhypoperfusion



Comprehensive Clinical Nephrology, 2nd Ed.

© 2003, Elsevier Limited. All rights reserved.



PostrenalPostrenal AKI AKI

Incidence depends on populationIncidence depends on population

– – Uncommon to develop during hospital stayUncommon to develop during hospital stay(<5%)(<5%)

– – Female > male during midFemale > male during mid--lifelife

– – Male > female above ~60 yearsMale > female above ~60 years

Must involve entireMust involve entire nephronnephron mass tomass to

cause AKI:cause AKI:

– – Solitary kidney, bladder outlet, bothSolitary kidney, bladder outlet, both uretersureters……




AKI

No AKI




IntrinsicIntrinsic

– – Crystals/stonesCrystals/stones – – Blood clotBlood clot

– – Papillary necrosisPapillary necrosis

– – Intratubular Intratubular precipitation (precipitation (egeg,,

BenceBence Jones)Jones)

– – Tumor Tumor – – StrictureStricture

– – FunctionalFunctional

ExtrinsicExtrinsic

– – Mass effect (prostate,Mass effect (prostate,pregnancy, tumor)pregnancy, tumor)

– – InflammationInflammation

(diverticulitis,(diverticulitis,appendicitisappendicitis……))

– – Vascular (aneurysm)Vascular (aneurysm)

– – RetroperitonealRetroperitonealfibrosisfibrosis

CongenitalCongenital



IntrarenalIntrarenal AKI AKI

Vascular Vascular

– – Arterial or venous Arterial or venous

thrombosisthrombosis

– – SclerodermaScleroderma

– – Malignant hypertensionMalignant hypertension

– – Atheroemboli Atheroemboli

Tubular Tubular

– – Ischemia (prolongedIschemia (prolongedprerenal state)prerenal state)

– – Toxin: pigment, medication,Toxin: pigment, medication,

contrastcontrast

Glomerular Glomerular

– – Acute Acute GlomerulonephritisGlomerulonephritis

– – VasculitisVasculitis

– – ThromboticThrombotic

microangiopathymicroangiopathy

InterstitialInterstitial

– – Allergic interstitial nephritis Allergic interstitial nephritis(NSAID,(NSAID, β β--lactamlactam))

– – Infiltration (Infiltration (sarcoidsarcoid, tumor), tumor)



Evaluation of AKIEvaluation of AKI

HistoryHistory

– – Is it really acute? Clues to chronic kidney disease:Is it really acute? Clues to chronic kidney disease: Anemia Anemia

HyperphosphatemiaHyperphosphatemia

Small kidney size (Ultrasound)Small kidney size (Ultrasound)

Knowledge of past kidney functionKnowledge of past kidney function

– – Risk factorsRisk factors

Advanced age Advanced age

DiabetesDiabetes

Congestive heart failureCongestive heart failure

Underlying chronic kidney diseaseUnderlying chronic kidney disease



EvaluationEvaluation

More historyMore history

– – Volume status:Volume status:Vomiting, diarrhea, fever, burns,Vomiting, diarrhea, fever, burns, diuresisdiuresis

Review I/O, weights, BP/Review I/O, weights, BP/orthostaticsorthostatics

– – Exposures:Exposures:

NSAIDsNSAIDs, contrast,, contrast, aminoglycosidesaminoglycosides, ACE inhibitors, ACE inhibitors

Procedures, trauma, seizureProcedures, trauma, seizure

– – Other ROS keys:Other ROS keys:

Rash,Rash, purpurapurpura, arthritis, arthritisCough/Cough/hemoptysishemoptysis, sinus disease, sinus disease

Urinary retention,Urinary retention, dysuriadysuria,, hematuriahematuria, previous stones, previous stones

Flank painFlank pain



ExamExam

Volume assessment:Volume assessment:

– – Hypotension, tachycardia,Hypotension, tachycardia, orthostasisorthostasis, dry mucous, dry mucousmembranes, flat neck veins suggest volume depletionmembranes, flat neck veins suggest volume depletion

– – Crackles, S3, edema suggest fluid overloadCrackles, S3, edema suggest fluid overload

Clues to systemic disease:Clues to systemic disease: – – Rash, oral ulcers, arthritis, murmur,Rash, oral ulcers, arthritis, murmur,

neurologic deficitsneurologic deficits

Concern for obstruction:Concern for obstruction: – – Pelvic mass, enlarged lymph nodes,Pelvic mass, enlarged lymph nodes,

prostateprostate



UltrasoundUltrasound



Selected syndromesSelected syndromes

Allergic interstitial nephritis Allergic interstitial nephritis

– – Begins 2Begins 2--3 weeks after starting drug3 weeks after starting drug – – AKI (rising creatinine) AKI (rising creatinine)

– – Fever Fever – – EosinophiliaEosinophilia

– – RashRash

– – AIN 2 AIN 2°° NSAIDsNSAIDs: months after drug started,: months after drug started,

develop proteinuria, find minimal changedevelop proteinuria, find minimal change

disease on kidney biopsydisease on kidney biopsy



Selected syndromesSelected syndromes

Acute Acute glomerulonephritisglomerulonephritis (GN)(GN)

– – Rapid onset of edema, hypertension, andRapid onset of edema, hypertension, andoliguriaoliguria

– – Proteinuria,Proteinuria, hematuriahematuria (micro or macro)(micro or macro)

– – Low urine sodiumLow urine sodium

– – Serum complement (C3, C4) low or normalSerum complement (C3, C4) low or normal



Major Causes of Acute Nephritis

Low Serum ComplementLow Serum Complement Normal Serum ComplementNormal Serum Complement

Systemic DiseasesSystemic Diseases •• Systemic DiseasesSystemic Diseases

systemic lupus erythematosissystemic lupus erythematosis Polyarteritis nodosaPolyarteritis nodosasubacute bacterial endocarditissubacute bacterial endocarditis Hypersensitivity vasculitisHypersensitivity vasculitis

shunt nephritisshunt nephritis Wegener Wegener ’’s granulomatosiss granulomatosis

cryoglobulinemiacryoglobulinemia HenochHenoch--SchSchöönleinnlein purpurapurpura

GoodpastureGoodpasture’’s syndromes syndrome

Renal DiseasesRenal Diseases •• Renal DiseasesRenal Diseases

Acute PSGN Acute PSGN IgAIgA NephropathyNephropathy

MPGNMPGN idiopathic RPGNidiopathic RPGN

Type IType I antianti--GBM diseaseGBM disease

Type IIType II immune complex diseaseimmune complex disease



DrugDrug--related AKIrelated AKI

Reduced renal perfusionReduced renal perfusion

– – NSAIDsNSAIDs, ACE inhibitors,, ACE inhibitors,

cyclosporine, tacrolimus,cyclosporine, tacrolimus,

radiocontrastradiocontrast,, amphotericinamphotericin

BB

Direct tubular toxicityDirect tubular toxicity – – Aminoglycosides Aminoglycosides,, cisplatincisplatin,,

cyclosporine, tacrolimus,cyclosporine, tacrolimus,

IVIG,IVIG, radiocontrastradiocontrast

RhabdomyolysisRhabdomyolysis

– – Cocaine, ethanol,Cocaine, ethanol,

lovastatinlovastatin

Intratubular Intratubular precipitationprecipitation

– – Acyclovir, Acyclovir,-- sufonamidessufonamides,,

ethylene glycol,ethylene glycol, methotrexatemethotrexate

Allergic interstitial nephritis Allergic interstitial nephritis

– – PenicillinsPenicillins,, cephalosporinscephalosporins,,

sulfonamides,sulfonamides, rifampinrifampin,,NSAIDsNSAIDs,, furosemidefurosemide,,

thiazidesthiazides,, allopurinolallopurinol……

HemolyticHemolytic

--uremicuremic

syndromesyndrome

– – Cyclosporine, tacrolimus,Cyclosporine, tacrolimus,

mitomycinmitomycin, quinine, quinine



Urine indicesUrine indices

>50>50<35<35FE urea (%)FE urea (%)

>1>1<1<1FE Na (%)FE Na (%)

((Una/Pna)/(Ucr/Pcr Una/Pna)/(Ucr/Pcr ) * 100) * 100

>40>40<20<20UNa (UNa (mEqmEq/L)/L)<350<350>500>500UosmUosm ((mOsmmOsm/kg)/kg)

IntrinsicIntrinsicPrerenalPrerenalMeasureMeasure

Measures of renal solute and water avidityMeasures of renal solute and water avidity – – Most helpful in setting of Most helpful in setting of oliguriaoliguria

– – Affected by other factors: HF, cirrhosis, drugs, age Affected by other factors: HF, cirrhosis, drugs, age

– – ““PrerenalPrerenal”” indices seen in early obstruction, acuteindices seen in early obstruction, acuteGN, HRS, and postGN, HRS, and post--contrastcontrast



CALCULATINGCALCULATING THE FRACTIONALFRACTIONALEXCRETION OFEXCRETION OF SODIUM ((FeNaFeNa))

The fractional excretion of sodium (FENa) is the most useful parameter by whichto distinguish prerenal acute renal failure from acute tubular necrosis. The FENais calculated as follows:

Amount of sodium excretedThe FENa = X 100Amount of sodium filtered

The amount of sodium excreted is the product of the urinary sodiumconcentration (UNa) multiplied by the urinary volume (V). The amount of sodium

filtered is the product of the plasma sodium concentration (PNa) multiplied by theglomerular filtration rate (GFR). In turn, the GFR can be defined as:

(UCr /PCR) x V

Where UCr is the urinary creatinine level and PCr is the plasma creatinine value.

Thus, the FENa can be calculated as:

FENA = UNa x VX 100 = (U/P)Na x100

PNa x (UCr /PCr ) x V (U/P)Cr



FeNaFeNa in AKIin AKI

<1%<1%

– – PrerenalPrerenal azotemiaazotemia – – Renal vasoconstrictionRenal vasoconstriction

HepatorenalHepatorenal syndromesyndrome

NSAID useNSAID useSepsisSepsis

Early Early myoglobinuricmyoglobinuric AKI AKI

RadiocontrastRadiocontrast

– – Acute GN Acute GN

– – Early ObstructionEarly Obstruction

>1%>1%

– – Diuretic use**Diuretic use** – – ATN ATN

– – NonreabsorbableNonreabsorbable

solute (bicarbonate,solute (bicarbonate,glucose)glucose)

– – MineralocorticoidMineralocorticoid

deficiencydeficiency – – Late obstructionLate obstruction



Urine sedimentUrine sediment

Crystals,Crystals, RBCsRBCs,, WBCsWBCs

possiblepossibleTraceTrace--mild proteinuria,mild proteinuria,

+/+/-- leukocytesleukocytesPostrenalPostrenal

RBCsRBCs

((dysmorphicdysmorphic

),),

RBC castsRBC castsModerateModerate

--severesevere

proteinuria, hemoglobinproteinuria, hemoglobin Acute Acute

GlomerulonephritisGlomerulonephritis

WBCsWBCs,, EosinophilsEosinophils,,

WBC castsWBC castsmildmild--moderatemoderate

proteinuria, leukocytesproteinuria, leukocytes Allergic Interstitial Allergic Interstitial

nephritisnephritis

Pigmented granular Pigmented granular

castscasts

Mild proteinuriaMild proteinuriaIschemic or Toxic ATNIschemic or Toxic ATN

NegativeNegativeNegative, high SGNegative, high SGPrerenalPrerenal

SedimentSedimentDipstickDipstickConditionCondition



Pigmented granular castsPigmented granular casts



RBC casts,RBC casts, dysmorphicdysmorphic RBCsRBCs



Role of biopsyRole of biopsy

Can quickly yield diagnosis in obscureCan quickly yield diagnosis in obscure

casescasesConfirm clinical suspicion of Confirm clinical suspicion of vasculitisvasculitis

Determine degree of inflammation, as wellDetermine degree of inflammation, as wellasas chronicitychronicity/reversibility/reversibility



ManagementManagement

Etiology dependentEtiology dependent……butbut

1.1. Restore intravascular volume/improveRestore intravascular volume/improvecirculationcirculation

2.2. Consider diuretic trial if stillConsider diuretic trial if still oliguricoliguric3.3. Correct underlying disorder Correct underlying disorder

4.4. Assess need for renal replacement Assess need for renal replacementtherapytherapy

(intermittent or continuous(intermittent or continuous hemodialysishemodialysis, peritoneal), peritoneal)



ComplicationsComplications

MetabolicMetabolic – – HypocalcemiaHypocalcemia,, hyperphosphatemiahyperphosphatemia,, hyponatremiahyponatremia,,

hyperkalemiahyperkalemia,, hypermagnesemiahypermagnesemia, acidosis, acidosisCardiovascular Cardiovascular – – Fluid overload, arrhythmia, hypertension,Fluid overload, arrhythmia, hypertension, pericarditispericarditis

NeurologicNeurologic

– – Somnolence,Somnolence, asterixisasterixis, seizures,, seizures, myoclonicmyoclonic jerks, coma jerks, coma

HematologicHematologic – – Anemia, platelet dysfunction Anemia, platelet dysfunction

GastrointestinalGastrointestinal – – Nausea, vomiting, anorexiaNausea, vomiting, anorexia

InfectiousInfectious – – UTI, wound, pneumonia, sepsisUTI, wound, pneumonia, sepsis……



Indications for dialysisIndications for dialysis

Uremic symptomsUremic symptoms

UremicUremic pericarditispericarditisVolume overloadVolume overload

HyperkalemiaHyperkalemia

Metabolic acidosisMetabolic acidosis

Selected toxins (ethylene glycol, lithiumSelected toxins (ethylene glycol, lithium……))



Clinical course of AKIClinical course of AKI

1.1. Initiating phaseInitiating phaseOften occult (not recognized until too late)Often occult (not recognized until too late)

Early correction may reverse courseEarly correction may reverse course

2.2. Maintenance phaseMaintenance phaseOliguricOliguric or nonor non--oliguricoliguric

Average 10 Average 10--14 days14 daysPoorer prognosis if prolongedPoorer prognosis if prolonged

3.3. Recovery phaseRecovery phase

Often heralded by increase in urine outputOften heralded by increase in urine outputGFR may increase while tubular dysfunctionGFR may increase while tubular dysfunctionpersistspersists

Fluid/electrolyte replacement may be necessaryFluid/electrolyte replacement may be necessary



SummarySummary

AKI is common and associated with high AKI is common and associated with high

morbidity and mortalitymorbidity and mortalityEtiologies are best classified as preEtiologies are best classified as pre--, post, post--

or intraor intra--renalrenalClinical scenario, ultrasound and urineClinical scenario, ultrasound and urine

studies (indices/sediment) are oftenstudies (indices/sediment) are often

sufficient to make diagnosissufficient to make diagnosis

Management tends to be supportiveManagement tends to be supportive

Acute Kidney Injur

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