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    Acute Kidney Injury

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    Lecture for Internal Medicine Residents about Acute Kidney injury, focusing on general aspects of etiology, diagnosis and treatment.

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    Acute Kidney Injury

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    medpedshospitalist
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    Lecture for Internal Medicine Residents about Acute Kidney injury, focusing on general aspects of etiology, diagnosis and treatment.

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    Lecture for Internal Medicine Residents about Acute Kidney injury, focusing on general aspects of etiology, diagnosis and treatment.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    2K views42 pages

    Acute Kidney Injury

    Uploaded by

    medpedshospitalist
    Lecture for Internal Medicine Residents about Acute Kidney injury, focusing on general aspects of etiology, diagnosis and treatment.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 42

    Acute Kidney Injury

    Moises Auron MD, FAAP FACP


    Assistant Professor of Medicine and Pediatrics

    January 28, 2010


    Outline
    • Definition
    • Etiology and Clinical Presentation
    • Diagnosis
    • Treatment
    Definition
    • Acute Kidney Injury Network (AKIN)
    – AKI - represent the entire spectrum of acute
    renal failure
    • RIFLE Classification
    – three levels of injury (Risk, Injury, and Failure)
    – two outcome measures (Loss and ESRD)

    Critical Care. 2007, 11(2):R31


    RIFLE Criteria

    Limitations:
    • Change in creatinine may not
    correlate with change in GFR
    • Need to know baseline
    creatinine.
    • No correlation between U/O
    and Screat levels
    •Should exclude U obstruction

    (Acute Dialysis Quality Initiative (ADQI) Group). Critical Care. 2004;8(4):R204-12.


    • Abrupt (< 48 h) absolute increase in the
    serum creatinine concentration of ≥0.3
    mg/dL from baseline
    • Increase in the serum creatinine ≥ 50 %
    • Oliguria < 0.5 mL/kg per hour for > 6 hrs.

    Critical Care. 2007, 11(2):R31


    GFR and Creatinine

    Dennen P. Crit Care Med 2010; 38(1):261–275


    Epidemiology
    • Upon admission to hospital – 1%
    • During hospitalization – 2-5%
    • After Cardiopulmonary bypass. – 5-15%

    Thadhani R. NEJM. 1996;334(22):1448-60


    Etiology
    • Prerenal (40-80% cases)
    – Volume depletion
    • Blood loss: surgery, trauma, gastrointestinal or
    genitourinary bleeding
    • Gastrointestinal: vomiting, diarrhea
    • Urinary (diuretics, diabetes insipidus)
    • Cutaneous losses (burns, fever)
    – Decreased Arterial Blood Pressure
    • Low Cardiac output
    • Cardio renal syndrome type 1
    • Sepsis/shock
    • Hepatorenal syndrome
    • Drugs: ACEI, NSAIDS

    Thadhani R. NEJM. 1996; 334:1448–1460


    Etiology of low perfusion states

    Abuelo JG. NEJM. 2007;357(8):797-805.


    Hepatorenal Syndrome

    Garcia-Tsao G. HEPATOLOGY 2008;48:2064-2077.


    Gines P. N Engl J Med 2009;361(13):1279-90.
    AKI in Cirrhosis

    Garcia-Tsao G. HEPATOLOGY 2008;48:2064-2077.


    Gines P. N Engl J Med 2009;361(13):1279-90.
    Cardiorenal Syndrome Type 1

    Shamseddin MK. Nat Rev Nephrol. 2009;5:641–649.


    Ronco C. European Heart Journal e-pub Dec 25, 2009. doi:10.1093/eurheartj/ehp507
    Sepsis and AKI

    Schrier RW. NEJM 2004;351(2):159-69.


    Etiology
    • Renal (5-15%)
    – Vascular
    • Thrombosis (arterial and venous)
    – Cholesterol emboli (post-intervention)
    • Renal artery stenosis
    • Hemolytic-uremic syndrome
    • Malignant hypertension
    • Vasculitis (Wegener’s, SLE, PAN, MPA).
    • Scleroderma
    – Glomerular
    • Acute glomerulonephritis: vasculitis, post-infectious (Streptococcus).
    – Tubular and interstitial disease
    • Acute tubular necrosis (ATN) – ischemia or injury from tubular nephrotoxins
    • Nephrotoxic agents: aminoglycosides, amphotericin B, contrast agents
    • Rhabdomyolysis
    • Tumor lysis syndrome
    • Acute interstitial mephritis – Eosinophiluria, drug hypersensitivity
    • Nephrolithiasis

    Thadhani R. NEJM. 1996; 334:1448–1460


    http://path.upmc.edu/cases/case51/dx.html
    Ischemic Acute Tubular Necrosis

    Abuelo JG. NEJM. 2007;357(8):797-805.


    Contrast Induced AKI

    Abu Jawdeh BJ. J Hosp Med. 2009;4:500–506.


    Solomon R. Radiol Clin N Am. 2009;47:783–788
    Rhabdomyolysis

    Bosch X. NEJM. 2009;361(1):62-72.


    Etiology of AKI in the ICU

    Dennen P. Crit Care Med 2010; 38(1):261–275


    Acute interstitial nephritis

    Needham E. Am Fam Physician 2005;72:1739-46.


    AKI and Metabolic Acidosis
    • Anion Gap Metabolic Acidosis
    – Normal osmolal gap: salicylate and
    paraldehyde
    – Increased osmolal gap: methanol,
    ethanol, isopropyl alcohol and ethylene
    glycol
    • Ethylene-glycol: calcium oxalate crystals

    http://www1.nasa.gov/centers/marshall/news/background/facts/renal.html
    Etiology
    • Postrenal (10-30%)
    – Bilateral urinary tract obstruction
    • PUV (children)
    • BPH
    • Retroperitoneal malignancies
    • Urethral strictures
    • Nephrolithiasis
    • Catheters
    • Neurogenic bladder

    Thadhani R. NEJM. 1996; 334:1448–1460


    British Journal of Radiology.2002;75:177-179
    Anderson RJ. Best Pract Res Clinical Anaesth. 2004;18(1):1–20.
    Luyckx VA. Nat Clin Pract Nephrol. 2008;4(12): 664-71.
    Diagnosis

    Anderson RJ. Best Pract Res Clinical Anaesth. 2004;18(1):1–20.


    Creatinine and drugs
    • Inhibition of secretion of creatinine by the proximal tubule
    – Cimetidine
    – Trimethoprim
    – Pyrimethamine
    – Salicylates

    • Modification of the production rate and the release of


    creatinine:
    – Corticosteroids
    – Vitamin D metabolites

    • Unclear:
    – phenacemide

    Andreev E. J Int Med 1999; 246: 247-52.


    Diagnosis: Urinary Indices

    Fe Urea % <35 50 – 65
    Fe Uric Acid % <7 >15
    Fe Lithium % <7 >20

    Esson ML. Ann Intern Med. 2002;137:744-752.


    Anderson RJ. Best Pract Res Clinical Anaesth. 2004;18(1):1–20.
    Calculation of FENa

                          UNa   x   PCr
    FENa (%) =            x    100
                          PNa   x   UCr
    Diagnosis: Urinary sediment
    x400 x400

    Perazella, MA. CJASN ePress. Jan 14 2010 as doi: 10.2215/CJN.06960909


    Esson ML. Ann Intern Med. 2002;137:744-752.
    Diagnosis: Urinary sediment

    Hansel stain

    http://missinglink.ucsf.edu/lm/IDS_102_cases_glomerular/Nephritic_syndrome.htm
    Kaye M. Kidney International (2008) 73, 980.
    Diagnosis – Urinary microscopy

    Perazella, MA. CJASN ePress. Jan 14 2010. DOI 10.2215/CJN.06960909


    Kanbay M. Int Urol Nephrol. Nov 17 2009. DOI 10.1007/s11255-009-9673-3
    Diagnosis: Ultrasound
    • R/O obstruction
    • Assess renal size and
    parenchyma
    • Doppler (renal flow and
    resistive index)
    – Normal < 0.7
    – High: intrarenal vascular
    disease or arteriosclerosis,
    ATN, urinary obstruction
    and acute graft rejection.
    Ikee R. Am J Kidney Dis 2005 Oct;46(4):603-9.
    http://radiology.med.sc.edu/renalultrasound.htm
    Diagnosis: CT scan/MRI
    • Nephrolithiasis (non-contrast)
    • Pyelonephritis
    • Renal vein thrombosis
    • Assessment of renal arteries
    – Avoid gadolinium in GFR < 30 ml/min/1.73m2
    Biomarkers of AKI

    Soni SS. Blood Purif 2009;28:165–174


    Biomarkers of AKI
    • Cystatin C - cysteine protease inhibitor
    synthesized by all nucleated cells. It is freely
    filtered by the glomerulus, reabsorbed
    completely by PCT and not secreted.
    – Levels of cystatin C are not affected by gender, age,
    race or muscle mass.
    • IL-18 - proinflammatory cytokine induced in PCT
    and is detected in urine following AKI.
    – Early predictor of AKI in ARDS (AUC) 0.73.
    – More specific for ischemic AKI and its levels are not
    deranged in CKD, UTI or nephrotoxic AKI
    Soni SS. Blood Purif 2009;28:165–174
    Biomarkers of AKI
    • Kidney Injury Molecule-1 (KIM-1) - transmembrane
    protein markedly overexpressed in PCT in response
    to ischemic or toxic AKI.
    – Urinary KIM-1 helped to distinguish ischemic AKI from
    prerenal azotemia and CKD
    • Neutrophil gelatinase-associated lipocalin (NGAL)
    - 25-kD protein massively released from renal tubular
    cells after injury
    – Higher baseline NGAL - increased risk of worsening
    residual renal function w/n 1 yr
    Ronco C. Critical Care 2007, 11:173.
    Bolignano D. Clin J Am Soc Nephrol. 2009;4: 337–344.
    Soni SS. Blood Purif 2009;28:165–174.
    NGAL as biomarker for AKI

    Soni SS. Blood Purif 2009;28:165–174


    Prevention of CIN
    • Minimize radiocontrast dose
    • Isoosmolar radiocontrast media preferred
    • I.V. NaHCO3 at 3 mL/kg/hr for 1 hour prior to
    radiocontrast exposure, then 1 mL/kg/hr for 6 hours after
    • I.V. N-acetylcysteine 1200 mg before procedure, then
    1200 mg po bid for total 4 doses.
    • If I.V. N-acetylcysteine not available, then P.O. N-
    acetylcysteine 600-1200 mg po for 2 doses before and 2
    doses after the procedure.
    • If already on acute hemodialysis, consider CVVH 6
    hours before and for 24 hours after the procedure

    Abu Jawdeh BJ. J Hosp Med. 2009;4:500–506.


    General management of AKI
    • Exclude prerenal causes
    • Exclude postrenal causes (US; bladder scan; postvoid residual).
    • Review urinary sediment
    – muddy brown casts: ATN
    – red blood cell casts: glomerulonephritis or vasculitis
    – pyuria: acute interstitial nephritis
    – Clear sediment or hyaline cast: prerenal or postrenal azotemia
    • Evaluate urinary indices
    • After confirmation of ATN notify nephrologist when serum creatinine
    level is 2.0 mg/dL
    • Anticipate dialysis
    – oliguric ATN (urine volume < 400 mL/24 hr) - 85% of patients
    – nonoliguric ATN (urine volume > 400mL/24 hr) - 30% to 40% of patients.
    • Assess for differential diagnoses (ANCA, ANA, ESR, etc.)

    Esson ML. Ann Intern Med. 2002;137:744-752.


    General management of AKI
    • Avoid excessive fluid overload leading to
    pulmonary edema.
    • Avoid hypotension and maintain euvolemia.
    • Treat hyperkalemia.
    • Review patient’s medications - necessary dose
    adjustments.
    • Use enteral alimentation if possible
    • Discuss timing for initiation and mode of renal
    replacement with nephrologists

    Esson ML. Ann Intern Med. 2002;137:744-752.


    Vasoactive drugs and AKI
    • Norepinephrine - in hypotensive vasodilated
    patients with AKI, restoration of BP within
    autoregulatory values should occur promptly
    with NE.
    • Dopamine has no advantages over
    norepinephrine.
    • Epinephrine and phenylephrine may be similar in
    efficacy to noradrenaline – limited data
    – Epinephrine: associated with hyperglycemia,
    hyperlactatemia, acidosis, and hypokalemia.
    • Terlipressin - useful in hepatorenal syndrome

    Bellomo R. Crit Care Med 2008; 36(Suppl):S179–S186


    Indication for dialysis

    Needham E. Am Fam Physician 2005;72:1739-46.


    Hepatorenal Syndrome: Treatment

    Garcia-Tsao G. HEPATOLOGY 2008;48:2064-2077.


    Gines P. N Engl J Med 2009;361(13):1279-90.

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