Acute Renal Failure

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jannabogie
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47875
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Acute Renal Failure
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2010-11-07 12:03:52
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Acute Renal Failure
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Therapeutics Week 9 - Acute Renal Failure
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  1. Define acute renal failure
    An abrupt decrease in GFR occurring over hours to days (sometimes weeks). Assoc with acumulation of waste products including urea and creatinine.
  2. What is normal urine output?
    Greater than or equal to 1200 ml/day
  3. What is anuric?
    Urine output < 50 ml/day
  4. What is oliguric?
    UO < 500 ml/d
  5. What is nonoliguric?
    UO > 500 ml/day
  6. Define the RIFLE characteristics
    • R: Risk of dysfunction. SCr up 50% or GFR down 25% and UO < 0.5 ml/kg/h x 6h
    • I: Injury. SCr up 100% or GFR down 50% and UO < 0.5 ml/kg/hr x 12 h
    • F: Failure. SCr up 200% or > 4 mg/dl or GFR down 75% and UO < 0.3 ml/kg/h x 24 h or anuria x 12 h
    • L: Loss. ARF > 4 weeks
    • E: End Stage Renal Disease. ESRD > 3 months
  7. Define Prerenal renal failure
    ARF caused by decreased renal perfusion in the absence of damage to parenchymal tissue. Often assoc with volume depletion or poor cardiac function. (Blood loss, dehydration)
  8. Define Intrinsic renal failure
    Structural damage to the kidney - usually the tubule - d/t ischemia or toxicity. (contrast induced nephropathy)
  9. Define Postrenal failure
    D/T obstruction of urine flow downstream from the kidney. Usually not drug-induced. (Prostate, foley)
  10. What cause of ARF is the most common in the hospital setting?
    Prerenal ischemia d/t decreased renal perfusion secondary to sepsis, reduced CO, or surgery
  11. 4 causes of decline in intravascular blood volume, leading to prerenal azotemia
    • 1. acute blood loss
    • 2. dehydration
    • 3. hypoalbuminemia
    • 4. diuretic therapy
  12. What is prerenal azotemia?
    Elevated blood levels of urea in the serum
  13. What typically causes renal vasculature damage? (it is rare)
    Atherothrombi dislodged during a procedure or thromboemboli from pts with severe HF or AFib
  14. Glomerular damage can occur d/t emboli and . . .
    Severe inflammatory processes as seen in SLE and poststreptococcal glomerulonephritis
  15. What is the cause of 85% of all ARF?
    Tubule Damage (acute tubular necrosis)
  16. Of the 85% of ARF attributed to ATN, 50% is due to _________ and 35% is due to _____________
    • 50% to renal ischemia
    • 35% to exposure to direct tubule toxins
  17. Tubular injury leads to:
    • 1. Inability to concentrate urine
    • 2. Defective distal sodium reabsorption
    • 3. Decreased GFR
  18. What is the time frame for the maintenance phase and the recovery phase of ATN?
    2-3 weeks per phase
  19. Interstitial damage is most commonly caused by:
    • medications
    • bacterial or viral infections
  20. List the most common causes of Postrenal ARF
    • 1. Bladder outlet obstruction due to a prostatic process (enlarged prostate)
    • 2. Improperly placed urinary catheter
    • 3. Neurogenic bladder
    • 4. Anticholinergic meds
  21. Give the lab values that indicate Prerenal ARF for urine sodium, FENa, Urine/serum osmolality, Urine/Scr, BUN/Scr
    • Urine sodium: < 20
    • FENa %: < 1
    • Urine/serum osmolality: > 1.5
    • Urine/SCr: > 40:1
    • BUN/SCr: >20
  22. Give the lab values that indicate Intrinsic ARF for urine sodium, FENa, Urine/serum osmolality, Urine/Scr, BUN/Scr
    • Urine Sodium: > 40
    • FENa %: > 2
    • Urine/serum osmolality: < 1.3
    • Urine/SCr: < 20:1
    • BUN/SCr: approx 15
  23. Give the lab values that indicate Postrenal ARF for urine sodium, FENa, Urine/serum osmolality, Urine/Scr, BUN/Scr
    • Urine Sodium: > 40
    • FENa %: variable
    • Urine/serum osmolality: < 1.5
    • Urine/SCr: < 20:1
    • BUN/SCr: approx 15
  24. What meds can disrupt the usefulness of FENa in diagnosing ARF?
    Diuretics (mainly loops)
  25. At what potassium concentrations is immediate treatment of hyperkalemia required?
    > 7 OR 6.1 - 6.9 if there are EKG changes
  26. Does calcium affect potassium?
    no
  27. What is the initial treatment of hyperkalemia and how does it work?
    Calcium to protect/stabilize the heart. It antagonizes the action of K+ on cardiac membranes.
  28. What is the secondary treatment for hyperkalemia?
    Decrease extracellular K+ by promoting its movement into cells using glucose, insulin, B2 receptor agonists, sodium bicarb), or enhance its removal using dialysis or exchange resins.
  29. MOA of furosemide
    Inhibit renal Na+ reabsorption (incr K+ out in urine)
  30. MOA of sodium polystyrene sulfonate (kayexelate)
    Resin exchanges Na+ for K+ (incr K+ elimination)
  31. MOA of calcium
    Raises cardiac threshold potential (reverses electrocardiographic effects)
  32. MOA of sodium bicarb
    Raises serum pH. (intracellular K+ redistribution - back into cell)
  33. Insulin and Glucose MOA
    Insulin stimulates intracellular K+ uptake
  34. Beta Agonists MOA
    Stimulate intracellular K+ uptake
  35. Dialysis MOA
    Removal from serum (incr K+ elimination)
  36. Why do we stop metformin in patients with ARF?
    It puts pt at higher risk for lactic acidosis
  37. Which medications can cause ARF?
    • Vancomycin
    • Aminoglycosides
    • NSAIDS
    • ACE inhibitors
    • ARBs
    • Amphotericin B
    • Lithium
    • Contrast dye
    • COX inhibitors
    • Acyclovir
    • Loop diuretics
    • Bactrim (can incr SCr without causing ARF, or can cause ARF)
  38. MOA of renal failure secondary to aminoglycosides
    • (e.g. gentamicin, tobramycin, amikacin, netilmicin)
    • Progressive rise in SCr and decrease in CrCl after 6-10 days of therapy. Result of proximal tubular epithelial cell damage leading to obstruction of the tubular lumen.
  39. MOA of renal failure secondary to contrast dye
    Direct tubular toxicity and/or renal ischemia
  40. MOA of renal failure secondary to Vancomycin
    Oxidative stress and renal tubular toxicity
  41. Discuss the meta-analysis of the relative efficacy and toxicity of SDD vs. MDD of Aminoglycosides
    • Patient Population: Not pregnant, Not children, No renal dysfunction, Normal weight, undergoing AG for any G- infection
    • Clinical Outcomes: (resolution of s/s) Trend favoring SDD
    • Microbiology Outcomes: No difference - indeterminant
    • Nephrotoxicity: No significant difference, but a trend for SDD to be used - less toxic
    • Other issues: Easy to clear infx were looked at - more serious might have been better.
  42. Discuss the meta-analysis about effectiveness of drugs for preventing contrast-induced nephropathy
    • Is N-acetylcystine effective? Yes, but only with NS, not alone
    • Theophylline? Not statistically. Yes, but very narrow therapeutic window
    • Ascorbic acid? Yes
    • Bicarbonate? Yes
    • Furosemide? No, increased the risk
    • Fenoldopam? No, increased the risk
    • Mannitol? No, increased the risk
    • Dopamine? Not really any benefit seen
    • Issues with the meta-analysis - Some of the studies had low quality scores. Not all had the same risk factors. Volume and type of contrast makes a difference and this was not always controlled for.
  43. Discuss the journal article about the relationship between initial vancomycin concentration-time profile and nephrotoxicity among hospitalized patients
    • Definition of SCr change (nephrotoxicity): 0.05 increase of 50% on at least 2 consecutive days
    • Important baseline characteristics: Pt weight > 101 kg. Trough value. Residents in ICU at time of onset.
    • Rate of renal toxicity: if trough value was > 20, up to 33%
    • Other issues: Need 7 days to see renal tox to vanco. If creatinine goes up the next day, it's probably d/t something else.
  44. MOA of renal failure d/t interaction of ACE-I, ARBs and NSAIDS
    • Hemodynamically mediated.
    • NSAIDs constrict the afferent arterioles into kidney.
    • ACEs, ARBs dilate the efferent arterioles out of the kidney.
    • No pressure inside kidney. Kidney needs pressure to work, so ARF.

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