Acute Renal Failure

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Internal Medicine Resident Half-Day Ahsan Alam, MD. Acute Renal Failure. Internal Medicine Resident Half-Day Ahsan Alam, MD. Acute Kidney Injury. What is Acute Kidney Injury. Abrupt decline in GFR Increase in serum creatinine P UF = (P GC - P T ) - ( p GC - p T ) - PowerPoint PPT Presentation

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  • Acute Renal FailureInternal Medicine Resident Half-DayAhsan Alam, MD

  • Acute Kidney InjuryInternal Medicine Resident Half-DayAhsan Alam, MD

  • What is Acute Kidney InjuryAbrupt decline in GFRIncrease in serum creatinine

    PUF = (PGC - PT) - (pGC - pT)

    Varying definitions (RIFLE, AKIN, etc)

  • Rising Prevalence of AKI

  • Why do we care about AKI?Nash K et al. Am J Kidney Dis 2002;39(5):930-936Lassnigg, A. et al. J Am Soc Nephrol 2004;15:1597-1605Mortality post cardiac surgeryMortality with hospital-acquired AKI

    Chart3

    10.6

    22

    30.7

    37.8

    Mortality Rate

    Mortality %

    Sheet1

    CauseEpisodesMortality

    Pre-renal14720

    Medications619

    CIN436

    Sepsis2519

    Obstruction72

    Hepatorenal75

    Sheet1

    00

    00

    00

    00

    00

    00

    Episodes

    Mortality

    N

    Sheet2

    Increase in SCrMortality Rate

    3 mg/dL37.8

    Sheet2

    0

    0

    0

    0

    Mortality Rate

    Mortality %

    Sheet3

  • Case #1A 76 yr old female presents to ED with abdominal pain and dyspneaSerum creatinine is 135 mmol

    Does she have AKI?

  • Diagnostic ApproachTime of onset prior serum creatinineCareful review of history and physical examComorbiditiesMedicationsCurrent illness (vomiting, diarrhea, blood loss, etc)BP, volume status, skin lesions, flank/abdominal signs

  • Case #1DM2, HTN, CAD (CABG 2004), CVA 2000 (right CEA 2009), hypothyroidismMedicationstelmistartan 80 mg, ramipril 10 mg, furosemide 40/80 mg, metoprolol, clonidine, atorvastatin, clopidogrel, insulin, thyroxine

    If this is AKI, what are the most likely diagnoses?

  • Causes of Hospital-Acquired AKI and MortalityNash K et al. Am J Kidney Dis 2002;39(5):930-9364,622 consecutive patients7.3% with AKI

    Chart2

    14720

    619

    436

    2519

    72

    75

    Episodes

    Mortality

    N

    Sheet1

    CauseEpisodesMortality

    Pre-renal14720

    Medications619

    CIN436

    Sepsis2519

    Obstruction72

    Hepatorenal75

    Sheet1

    Episodes

    Mortality

    N

    Sheet2

    Sheet3

  • Case #1The patient undergoes investigations for her symptoms in hospital

    DaySCr01351106211531224172524763377361

  • Case #1* CI-AKI

    DayProcedureRxSCr01351Abdo U/S (ED)CT Abdo/Pelvis (ED)light hydration1062CT Abdo/Pelvis/Ext r/o DVT + PE studyNAC 600 mg bid1153NAC 600 mg bid1224172*52476337

  • Case #1* CI-AKI* Stage 2-3 AKI

    DayProcedureRxSCr01351Abdo U/S (ED)CT Abdo/Pelvis (ED)light hydration1062CT Abdo/Pelvis/Ext r/o DVT + PE studyNAC 600 mg bid1153NAC 600 mg bid1224172*524763377Nephrology consult361*

  • AKI Network (AKIN) ClassificationLopes, J. A. et al. Crit Care 2008;12(4):R110

    StageSCrUOP (ml/kg/hr)1>1.5-2X or >27 mmol/L increase6 h2>2-3X12h3>3x or >360 mmol/Lor RRT

  • Risk Factors for AKILameire et al. NDT. 2008;6:392

  • Consistent Risk FactorsAgeHypovolemiaHypotensionSepsisCKDHepatic dysfunctionCardiac dysfunctionDMExposure to nephrotoxins

  • Differential Diagnosis of AKIPre-renal

    Renal

    Post-renal

  • Pre-renalHypovolemiaDiuretics, trauma, surgery, burns, hemorrhage, pancreatitis, GI loss, etc.Decreased effective circulating volumeNephrotic sydrome, cirrhosis, CHF, tamponade, massive PE, etc.Renovascular obstructionRAS/atherosclerosis/thrombosis/embolism, dissecting aneurysm, vasculitis, compressionImpaired glomerular autoregulationNSAIDs, ACEi/ARB, calcineurin inhibitors

  • Intrinsic RenalGlomerular and small vessel diseasesRapidly progressive GN, endocarditis, post-strep GN, vasculitides, scleroderma/malignant HTN, HUS, PET, DICInterstitial nephritisInfection-related, inlammation, drug-induced, infiltrative (lymphoma, leukemia, sarcoidosis)Tubular LesionsPost-ishemia, nephrotoxic (drugs, contrast, anesthetics, heavy metals), pigment nephropathy, light chain, hypercalcemia

  • Post-renalBladder flow obstructionUrethral, bladder neck (BPH), neurogenic bladderUreteral obstruction (bilateral or single kidney)Stones, clots, tumours, papillary necrosis, retroperitoneal fibrosis, surgical ligation

  • Urine Output and AKIAnuric< 50 cc / 24 hrsOliguric< 500 cc / 24 hrsNon-olguricNormal urine output, but inadequate clearanceGFR 2 ml/min will produce ~3L of urine/day if there is no tubular reabsorption

  • Diagnostic ApproachUrine dipstickUrine microscopyCellular elementsRBC, WBC, Renal tubular epithelial cellsOther (squamous, vaginal)CastsHyaline, granular, waxy, RBC, WBC, tubular cellOrganismsBacteria, yeastCrystalsLipiduria

    Specific gravitypHLeukocytesNitritesProteinGlucoseKetonesUrobilinogenBilirubinBlood

  • Urine FindingsWBC casts - pyelonephritisWBC

  • Urine FindingsCrystalluria uric acidCrystalluria calcium oxalate(ethylene glycol toxicity)

  • Urine FindingsRBC casts - GNDysmorphic RBC - GN

  • Urine FindingsMuddy brown casts acute tubular necrosis

  • Urine FindingsSpecific gravitypHLeukocytesNitritesProteinGlucoseKetonesUrobilinogenBilirubinBlood1.0305.0+++++80 yo female found on the floor of her apartment after 2 days, SCr 400 mol/L, K 6.8 mmol/L, CK 54,000

  • Urine Indices

    Perfusion-relatedATNUna (mEq/L)FeNa (%)Urine Osm (mOsm/L)BUN/PCr ratio

  • Urine Indices

    Perfusion-relatedATNUna (mEq/L)40FeNa (%)1Urine Osm (mOsm/L)>500300-350BUN/PCr ratio>2010

  • FeNaLimitations of FeNaDiuretic usePost-ischemic ATN who have less severe diseaseAKI on chronic pre-renal disease (cirrhosis, CHF)Contrast or pigment nephropathyAcute GN or vasculitisAlternativesFE of urea, lithium, uric acidFeNa = UNa/PNa x 100 UCr/PCr

  • ImagingAssess kidney size/morphologyHydronephrosis

  • Kidney BiopsyIntrinsic renal AKIIndicationsIsolated glomerular hematuria with proteinuria Nephrotic syndrome Acute nephritic syndrome Unexplained acute or rapidly progressive AKI

  • Kidney BiopsyCrescentic GN

  • Principles of AKI ManagementIdentify AKIAvoid further nephrotoxic injuryOptimize renal hemodynamicsTreat complicationsFluid balance, electrolytes, uremiaNutritional supportRenal Support (RRT)Monitoring after AKI

  • MedicationsPre-renalCalcineurin inhibitors, radiocontrast, ACEi/ ARB, NSAIDS, amphotericin BIntra-renalaminoglycosides, amphotericin B, cisplatin, cephalosporins, sulfa, rifampin, NSAIDS, interferonPost-renalacyclovir, MTX, indinavir, sulfadiazine

    Review renal dosing of medications

  • Fluid ManagementCorrect fluid deficitWill not guarantee AKI preventionStudies of PA catheters did not reduce AKIHigh urine flow in specific conditionsMyoglobinuria, tumour lysis, contrast media, etc.Little evidence on fluid choiceCrystalloidsHypooncotic colloids (4% albumin) Hyperoncotic solutions (HES, dextrans) carry risk of renal dysfunction

  • Renal Perfusion and Vasoactive AgentsNo support forLoop diureticsDopamineSelected use ofMannitol (Rhabdomyolysis, post-cardiac surgery)Unclear support forNatriuretic peptides (ANP, BNP)Fenoldopam (DA agonist)Theophylline (adenosine antagonist)

  • Renal PerfusionVasopressorsInotropes to improve low cardiac functionTarget MAP needs to be individualizedCommonly 65 mmHgHigher in elderly where autoregulation impaired

  • Nutrition in AKIAKI is a catabolic stateInadequate nutritional support can delay renal recovery

    Cochrane review 2010:There is not enough evidence to support the effectiveness of nutritional support for AKI

    Adequate calorie delivery in anuric patient will necessitate RRT

  • Treat ComplicationsMonitor and correct electrolytes, acidosisRenal replacement therapyIf indicated, do not withhold until patient is anuric

  • Indications for DialysisA E I O UAcidosisElectrolyte disturbanceIngestionsOverload (volume)Uremia

  • New Paradigm for AKIAKD CKDAKI

  • Natural history of AKICerda et al. cJASN. 2008;

  • Follow up after AKI

  • Questions?

  • Case #1* CI-AKI* Stage 2-3 AKI

    DayProcedureRxSCr01351Abdo U/S (ED)CT Abdo/Pelvis (ED)light hydration1062CT Abdo/Pelvis/Ext r/o DVT + PE studyNAC 600 mg bid1153NAC 600 mg bid1224172*524763377Nephrology consult361*

  • Fluids Isotonic vs. HypotonicIsotonic saline (0.9%) more protective than half normal (0.45%)1,620 pts undergoing cardiac catheterization

    Goal is to achieve good urine flowMueller C et al. Arch Intern Med. 162: 329-336, 2002

  • FluidsOptimal rate and duration is not clear

    IV rate >1-1.5 ml/kg/hr to achieve urine flow >150 ml/hr

    At least 1hr (3-12hr) prior and 3-6hr (6-12hr) after contrast

  • Zoungas S et al. Ann Intern Med 2009;151:631-638Bicarbonate vs Saline

  • Zoungas S et al. Ann Intern Med 2009;151:631-638Bicarbonate vs Saline

  • Zoungas S et al. Ann Intern Med 2009;151:631-638Bicarbonate vs Saline Adverse EventsDialysis(15/1552)MortalityCHF

  • BicarbonateEffectiveness is uncertain

    Evidence that it should be preferred over isotonic saline is weak and inconsistent

  • N-Acetylcysteine RationaleScavenger of free radicals

    Vasodilatory properties; enhanced NO availability

    Attenuates ischemic injury in animals

  • N-AcetylcysteineKelly AM et al. Ann Intern Med 2008;148:284-294

  • Standard vs. High Dose NACMarenzi G et al. N Engl J Med 2006;354:2773-2782In-hopsital mortality: 11% placebo 4% low-dose 3% high doseN=354,
  • N-AcetylcysteineActual benefit is debatable, but safe* and inexpensive

    Appropriate to give IV or h