A CUTE K IDNEY I NJURY Pamela Pride, MD, FHM Cathryn Caton, MD, MS June 5, 2012 MUSC.

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Presentation transcript:

A CUTE K IDNEY I NJURY Pamela Pride, MD, FHM Cathryn Caton, MD, MS June 5, 2012 MUSC

O BJECTIVES Define Acute Kidney Injury (AKI) Define the significance of AKI in a hospitalized patient Differentiate pre/intra/post renal injury Utilize history, physical exam and appropriate diagnostic tests to determine etiology of AKI

A CUTE K IDNEY I NJURY – W HAT IS IT ? An abrupt or rapid decline in renal filtration function Marked by rise in serum creatinine azotemia Patients may be Oliguric Non - oliguric

I MPORTANCE OF AKI Green bars unadjusted Blue Bars age and gender adjusted Gray bars are multivariable adjusted OR 1.7; 95% CI, 1.2 to 2.6

C OMMON C AUSES OF AKI ACE-I when vomiting ACE-I + NSAID BPH Stones ATN Sepsis Drugs Contrast Rhabdomyolysis OUTPATIENTINPATIENT

A PPROACH TO A P ATIENT WITH AKI Think three broad categories Pre-renal Intrinsic renal Post-renal

E VALUATION OF AKI HPI Past Medical History – ?CKD ?DM ?Proteinuria ?HTN Family History Social History – IVDA Hepatitis HIV risks Medications – review all medications Physical Exam

P HYSICAL E XAM Pre-Renal Orthostatic hypotension Tachycardia Decreased skin turgor Signs of heart failure Post-renal Palpable bladder

P HYSICAL E XAM Intrinsic renal ATN – volume overload Glomerulonephritis – variable Vasculitis – purpura Atheroembolic disease – livedo reticularis, blue toes Interstitial nephritis – rash, fever, +/- eos

L ABORATORY D ATA BMP CBC UA Urine sediment – look for muddy brown casts FeNa Renal Ultrasound or Computed tomography

I NTERPRETING F E N A Non-pre-renal with low FeNa Contrast Rhabdo Early sepsis Obstruction Acute glomerulonephritis Pre-renal with high FeNa Diuretic use Pre-existing CKD

P RE -R ENAL Hypoperfusion Hypovolemia Decreased cardiac output Decreased effective circulatory volume CHF Cirrhosis Impaired renal hemodynamics NSAIDs ACE ARB

I NTRINSIC AKI Essentially ruled out pre-renal, post-renal No good reason for ATN Check complement levels – C3, C4 ANCA, antiGBM ANA LDH, haptoglobin – hemolysis, thrombotic microangiopathy

P OST -R ENAL AKI Obstruction BPH Stone

I NTERPRETING URINARY SEDIMENT Granular castRBC cast

I NTERPRETING URINARY SEDIMENT Tubular Epithelial CellsWBC vs Epithelial Cell

I NTERPRETING URINARY SEDIMENT Oval Fat BodiesWBC Cast

R EFERENCES Chertow GM, Burdick E, Honour M, et. Al. Acute Kidney Injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol, 16: , Wald R, Quinn RR, Luo J et. al. Chronic dialysis and death among survivors of acute kidney injury requiring dialysis. JAMA, 302: , Blantz RC. Pathophysiology of pre-renal azotemia. Kidney Int, 53: , Friedrich JO, Adhikari N, Herridge MS, et. al. Meta-analysis: low dose dopamine increases urine output but does not prevent renal dysfunction or death. Ann Intern Med, 142: , 2005 Steiner RW: Interpreting the fractional excretion of sodium. Am J Med, 77: , 1984