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ACUTE RENAL FAILURE

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CLINICAL PHARMACY IN NEPHROLOGY ACUTE RENAL FAILURE Background Common in Hospitalized patients Associated with high Morbidity and Mortality Often ... – PowerPoint PPT presentation

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Title: ACUTE RENAL FAILURE


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CLINICAL PHARMACY IN NEPHROLOGY
  • ACUTE RENAL FAILURE

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Background
  • Common in Hospitalized patients
  • Associated with high Morbidity and Mortality
  • Often Multifactorial
  • Identifiable risk factors.

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Acute Renal Failure
  • Sudden decrease in function (hours-days)
  • Often multifactorial
  • Pre-renal and intrinsic renal causes 70
  • oliguric UOP lt 400 ml
  • Non-oliguric (up to 65)
  • Associated with high mortality and morbidity

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Acute Renal Failure Diagnosis
  • Laboratory Evaluation
  • Scr, More reliable marker of GFR
  • Falsely elevated with Septra, Cimetidine
  • small change reflects large change in GFR
  • BUN, generally follows Scr increase
  • Elevation may be independent of GFR
  • Steroids, GIB, Catabolic state, hypovolemia
  • BUN/Cr helpful in classifying cause of ARF
  • ratiogt 201 suggests prerenal cause
  • ratio 10-151 suggests intrinsic renal cause

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Acute Renal Failure Diagnosis (contd)
  • Urinalysis
  • Unremarkable in pre and post renal causes
  • Differentiates ATN vs. AIN. vs. AGN
  • Muddy brown casts in ATN
  • WBC casts in AIN
  • Hansel stain for Eosinophils

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Acute Renal Failure Diagnosis (contd)
  • Urinary Indices
  • FE Na (U/P) Na X (P/U)CrX 100
  • FENa lt 1 C/W Pre-renal state
  • May be low in selected intrinsic cause
  • Contrast nephropathy
  • Acute GN
  • Myoglobin induced ATN
  • FENagt 1 C/W intrinsic cause of ARF

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Prerenal Azotemia
  • Nearly as common as ATN (think of as early part
    of the disease spectrum)
  • Diagnose by history and physical exam
  • N/V, Diarrhea, Diuretic use,...
  • low FENa (lt1)
  • high BUN/creat ratio, normal urinary sediment
  • Treat by correction of predisposing factors

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Acute Renal Failure Etiologies
  • Acute Tubular Necrosis
  • Most common cause of intrinsic cause of ARF
  • Often multifactorial
  • Non-oliguria carries better prognosis
  • Ischemic ATN
  • Hypotension, sepsis, prolonged pre-renal state
  • Nephrotoxic ATN
  • Contrast, Antibiotics, Heme proteins

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Acute Tubular Necrosis (ATN) -- 2
  • Diagnose by history, ? FENa (gt2)
  • sediment with coarse granular casts, RTE cells
  • Treatment is supportive care.
  • Maintenance of euvolemia (with judicious use of
    diuretics, IVF, as necessary)
  • Avoidance of hypotension
  • Avoidance of nephrotoxic medications (including
    NSAIDs and ACE-I) when possible
  • Dialysis, if necessary
  • 80 will recover, if initial insult can be
    reversed.

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Contrast nephropathy
  • 12-24 hours post exposure, peaks in 3-5 days
  • Non-oliguric, FE Na lt1 !!
  • RX/Prevention 1/2 NS 1 cc/kg/hr 12 hours
    pre/post
  • Mucomyst 600 BID pre/post (4 doses)
  • Risk Factors CRF, Hypovolemia.

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Rhabdomyolytic ARF
  • Diagnose with ? serum CPK (usu. gt 10,000), urine
    dipstick () for blood, without RBCs on
    microscopy, pigmented granular casts
  • Common after trauma (crush injuries), seizures,
    burns, limb ischemia occasionally after IABP or
    cardiopulmonary bypass
  • Treatment is largely supportive care.
  • Alkalinization of urine .

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Acute Glomerulonephritis
  • Rare in the hospitalized patient
  • Most common types acute post-infectious GN,
    crescentic RPGN
  • Diagnose by history, hematuria, RBC casts,
    proteinuria (usually non-nephrotic range), low
    serum complement in post-infectious GN), RPGN
    often associated with anti-GBM or ANCA
  • Usually will need to perform renal biopsy

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Acute Glomerulonephritis (2)
  • If diagnosis is post-infectious, disease is
    usually self-limited, and supportive care is
    usually all that is necessary.
  • For RPGN, may need immunosuppressive therapy with
    steroids Cytoxan, plasmapheresis (if assoc.
    with anti-GBM)

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Atheroembolic ARF
  • Associated with emboli of fragments of
    atherosclerotic plaque from aorta and other large
    arteries
  • Diagnose by history, physical findings (evidence
    of other embolic phenomena--CVA, ischemic digits,
    blue toe syndrome, etc), low serum C3 and C4,
    peripheral eosinophilia, eosinophiluria, rarely
    WBC casts
  • Commonly occur after intravascular procedures or
    cannulation (cardiac cath, CABG, AAA repair, etc.)

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Acute Interstitial Nephritis
  • Usually drug induced
  • methicillin, rifampin, NSAIDS
  • Develops 3-7 days after exposure
  • Fever, Rash , and eosinophilia common
  • U/A reveals WBC, WBC casts, Hansel stain
  • Often resolves spontaneously
  • Steroids may be beneficial ( if Scrgt2.5 mg/dl)

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Acute Renal Failure Etiologies
  • Post-Renal
  • Bladder outlet obstruction
  • BPH, intrapelvic pathology
  • Crystalluria
  • Acyclovir, Indanivir, Uric Acid
  • Papillary tip necrosis
  • DM with pyelonephritis
  • Analgesic abuse
  • Sickle cell disease

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Prevention
  • What works?
  • Maintenance of euvolemia
  • Avoidance of nephrotoxins when possible
  • NSAIDs, aminoglycoside, Amphotericin, IV contrast
  • BP control--avoidance of excessive hypo- or
    hypertension

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Prevention
  • What doesnt work?
  • Empiric use of
  • Diuretics (i.e., Furosemide, Mannitol)
  • Dopamine (or Dopamine agonists such as
    Fenoldopam)
  • Calcium-channel blockers

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Acute Renal Failure Treatment
  • Water and sodium restriction
  • Protein restriction
  • Potassium and phosphate restriction
  • Adjust medication dosages
  • Avoidance of further insults
  • BP support
  • Nephrotoxins

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Hyperkalemia
  • Highly Arrhythmogenic
  • Usually with progressive EKG changes
  • Peaked T waves ---gt Widened QRS--gt Sinus wave
  • Kgt 5.5 meq/L needs evaluation/intervention
  • Usually in setting of Decrease GFR but
  • medication also a common cause
  • ACEI
  • NSAIDS
  • Septra, Heparin

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Dialysis Indications
  • Refractory hyperkalemia
  • Metabolic acidosis
  • Volume overload
  • Mental status changes

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