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  1. Elevated levels of urea and nitrogenous wastes in the blood (eg: elevated BUN)
  2. Symptoms associated with accumulation of metabolic by-products and endogenous toxins in the blood
  3. What are common symptoms of uremia?
    • N/V
    • Loss of appetite
    • Weakness
    • Mental confusion
  4. What is the normal 24 hr range of urine output?
    1-1.5 L
  5. What two things affect urine output?
    • Blood Volume Status
    • Diuretic Use
  6. Non-oliguria
    > 500 mL of urine/day in patients with renal insufficiency
  7. Oliguria
    Less than 400-500 mL of urine/day
  8. Anuria
    < 50-100 mL urine/day
  9. What is "a complex disorder used to describe abrupt changes or reductions in golmerular function"?
    • Acute Kidney Injury
    • (formerly known asAcute Renal Failure)
  10. What two factors are associated with AKI?
    • Increased length of hospital staty
    • Increased ventilator days
  11. Define pre-renal disease
    Damage caused by hypoperfusion of the renal cells
  12. Give two examples of intravascular volume depletion that can cause pre-renal disease
    • Hemorrhage
    • Dehydration
  13. Give two examples of reduced effective circulating volume that can cause pre-renal disease
    • Sepsis
    • Heart Failute
    • Ascites
  14. How do ACEi and NSAIDs cause pre-renal disease?
    Alter the hemodynamic state to the kidney
  15. Give an example of occlusion of pre-renal vasculature
    Bilateral renal artery stenosis
  16. What type of renal disease is classified by direcct damage to the renal cells?
    Intrisinc renal disease
  17. What causes 85% of intrinsic AKI?
    Acute tubular necrosis
  18. Describe the etiology of intrinsic renal failure.
    • Vasculature damage: small vessel emboli or vasculitis
    • Glomerular damage: glomerulonephritis
    • ATN
    • Acute, allergic interstitial nephritis (2nd most common)
  19. What is a result of extending pre-renal states or exposure to direct toxins (i.e. uric acid, contrast media, aminglycosides)?
    Acute tubular necrosis
  20. What is an inflammatory, immunologic reaction within the renal interstitium that can result from drugs, infections, or autoimmune disorders?
    Acute, allergic interstitial nephritis (AIN)
  21. What is another name for post-renal disease?
  22. What are the three types of obstruction?
    • Bladder outlet (prostate hypertrophy or prostate cancer)
    • Urethral
    • Tubular (crystal deposition from medications)
  23. What does RIFLE stand for?
    • Risk of renal dysfunction
    • Injury to the kidney
    • Failure of kidney function
    • Loss of kidney function
    • End Stage Renal Disease
  24. What does RIFLE consist of?
    • Renal dysfunction (1st 3)
    • Clinical outcomes (Last 2)
  25. What can the diagnosis and classification criteria for RIFLE be based on?
    Change in SCr and U/O
  26. In the RIFLE classification how long must signs be present for the classification of ESRD?
    > 3 months
  27. What is the time constraint of AKIN?
    48 hours
  28. What are the SCr criteria for Stage 1 based on AKIN?
    > 0.3 mg/dL or > 1.5-2.0 x baseline
  29. What is the U/O output criteria for Stage 1 based on AKIN?
    < 0.5 ml/kg/hr x 6 hr
  30. What is the SCr criteria for Stage 2 based on AKIN?
    > 2-3 x baseline
  31. What is the U/O criteria for Stage 2 based on AKIN?
    < 0.5 ml/kg/hr x 12 hr
  32. What is the SCr criteria for Stage 3 based on AKIN?
    • > 3 x baseline
    • > 4.0 mg/dL with an acute rise > 0.5 mg/dL
  33. What is the U/O criteria for Stage 3 based on AKIN?
    < 0.3 ml/kg/hr x 24 hr or anuria x 12 hr
  34. AKI is abrupt reduction in kidney function manifested by a ___ increase in SCr, a ___% increase in SCr, or a reduction in urinary output ___________
    • 0.3 mg/dL
    • 50
    • < 0.5 ml/kg/hr x 6 hr
  35. What are some limitations of RIFLE and AKIN?
    • Need baseline SCr levels
    • May be 1-2 delay in SCr increase after injury
    • U/O Variable based on fluid status and diuretic use
    • Primarily studied/validated in the critically ill population
  36. What are three diagnostic procedures for AKI?
    • Renal ultrasound
    • Kidney-ureter-bladder (KUB) X-ray
    • Cystoscopy with retrograde pyelography
  37. How does a patient with pre-renal AKI present on the physical exam?
    • Hypotension
    • Dry mucus membranes
    • Decrease CO
    • Edema
    • Ascites
  38. What will a patient's urine sediment look like in pre-renal disease?
  39. Fill in the following values for a patient with pre-renal AKI: Urine Na, FEna, BUN/SCr ratio
    • < 20 mEq/L
    • < 1 %
    • > 20:1
  40. What does a patient's urine sediment look like in intrinsic renal disease?
    • Granular and epithelial casts
    • RBCs
    • WBCs may be present in AIN
  41. Fill in the following values for a patient with intrinsic AKI: Urine Na, FEna, BUN/SCr ratio
    • > 40 mEq/L
    • > 2%
    • < 20:1
  42. Fill in the following values for a patient with post-renal AKI: Urine Na, FEna, BUN/SCr ratio
    • > 40 mEq/L
    • Variable
    • 15:1
  43. How does a patient with post-renal AKI appear on physical exam?
    • Prostatic enlargment
    • Bladder distension
  44. What will a patient's urine sediment look like in a patient with post-renal disease?
    • Variable
    • Cellular debris
    • RBCs
    • Crystals possible
  45. What are some non-pharmacologic strategies for preventing AKI?
    • Avoidance of nephrotoxic drugs in high risk patients
    • Maintain hemodynamic stability to avoid hypotension, hypovolemia (i.e. hydration patients in shock, dehydration, adminstration of contrast dye; maintain CO in patients with CHF)
  46. What are risk-factors for AKI?
    • Pre-existing renal dysfunction
    • Age > 75 y/o
    • Volume depletion or decreased circulating volume
    • Serious infections (i.e. sepsis)
    • Comorbidities (i.e. DM)
    • Exposure to nephrotoxins (i.e. contrast dye)
  47. What are two methods to prevent contrast dye induced nephropathy?
    • Sodium bicarbonate + hydration
    • N-acetylcysteine (NAC) + hydration
  48. What are some possible medications that can be used to treat AKI?
    • Dopamine- Increase renal blood flow and U/O
    • Fenoldopam- Increase renal blood flow and U/O--may be useful in critically ill
    • Loop diuretics- increased urine flow, decrease renal ischemia
    • Calcium Channel blockers- reduce renal vasoconstriction--may have some benefit in renal transplant population
    • N-acteylcysteine- antioxidant effect--may be useful in contrast dye induced AKI if given + hydration
    • Ascorbic acid- antioxidant effect
    • Erythropoietin- may protect against ischemic injury
    • Natriuretic peptides- increase renal vasodilation and perfusion--may decrease the need for dialysis
  49. Is the use of loop diuretics in AKI supported at this time?
  50. What are typical indications for renal replacement therapy?
    • Acid-base abnormalities
    • Elecrtolyte imbalance
    • Intoxications
    • Overload of fluid
    • Uremia
  51. What are two types of renal replacement therapy?
    • Intermittent hemodialysis (IHD)
    • Continuous renal replacement therapy (CRRT)
  52. What is the most commonly used agent in fluid overload?
  53. What is a risk of using high dosed loop diuretics?
    Increased risk of ototoxicity
  54. What type of administration should be used to overcome diuretic resistance and avoid adverse reactions associated with high serum concentrations?
    Continuous Infusion
  55. What are three common strategies to reduce diuretic resistance?
    • Lower sodium intake
    • Increase dose or use continuous infusion
    • Combine diuretics with different sites of action
  56. What is the most common complication of AKI?
  57. What is the first sign of hyperkalemia?
    Peaked T waves
  58. When should hyperkalemia be treated?
    If the patient is symptomatic or ECG changes present
  59. What is the K+ goal when treating hyperkalemia?
    < 5 mmol/L
  60. What drugs are used to treat hyperkalemia in AKI?
    • Calcium gluconate
    • Insulin (plus glucose)
    • B-adrenergic agonists
    • Sodium polystyrene sulfonate (Kayexalate)
  61. What is the purpose of using calcium gluconate in Hyperkalemia?
    Cardioprotection: stabilizes membrane voltage
  62. What is the onset of calcium gluconate?
    1-3 minutes
  63. Why are insulin (plus glucose) and B-adrenergic agonists used in hyperkalemia?
    Redistribution of K+ into the cells
  64. What is the onset of action for insulin (plus glucose) and beta adrenergic agonists?
    10-30 minutes
  65. What is the purpose of using Kayexalate in hyperkalemia?
    Removal: eliminates K+ from the gut in exchange for Na+
  66. What is the onset of action for Kayexalate?
    1-3 hours
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