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CRRAB II Week 5 - WLB > Acute Renal Failure - Pathoma > Flashcards

Acute Renal Failure - Pathoma Flashcards

1
Q

What is Acute Renal Failure?

A
  • Acute
  • Severe decrease in renal function
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2
Q

What is the hallmark of acute renal failure?

A
  • Azotemia
    • increase in nitrogenous waste products in the blood
    • causes increased BUN and Creatinine
  • Often have oliguria
    • low production of urine
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3
Q

What are the three types of acute renal failure?

A
  • Pre-renal
    • decreased blood flow
  • Intra-renal
    • problem within kidney
  • Post-renal
    • ureteral blockage (block outflow)
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4
Q

What happens in pre-renal azotemia?

A
  • Decreased Blood Flow →
    • decrease GFR
    • azotemia
    • oliguria
    • reabsorption of fluid and BUN ensues
      • serum BUN:Cr > 20
    • tubular function remains intact
      • FeNa <1%
      • urine osm >500
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5
Q

What happens in post-renal azotemia?

A
  • Obstruction of the urinary tract downstream from the kidney →
    • back up in pressure
    • decreased GFR
    • azotemia
    • oliguria
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6
Q

How do the early stages of post-renal azotemia compare to late stages?

A
  • Early:
    • increased tubular pressure “forces” BUN into the blood stream
      • serum BUN:Cr >15
    • tubular function remains intact
      • FeNa <1%
      • urine osm <350
  • Late:
    • tubular damage
    • decreased reabsorption of BUN
      • serum BUN:Cr <15
    • Decreased reabsorption of sodium​ ​
      • FeNa >2%
    • Inability to concentrate urine
      • ​urine osm <500
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7
Q

What are the causes of Intra-renal azotemia?

A
  • Acute renal necrosis
  • Acute interstitial nephritis
  • Renal papillary necrosis
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8
Q

What is the most common cause of Acute Renal Failure?

A
  • Acute Tubular Necrosis
    • injury and necrosis of tubular epithelial cells
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9
Q

How does Acute Tubular Necrosis cause problems?

A
  • Necrotic cells plug tubules
  • Obstruction decreases GFR
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10
Q

What are the urine findings on UA in Acute Tubular Necrosis?

A
  • Brown, granular casts
  • Decreased reabsorption of BUN
    • serum BUN:Cr <15
  • Decreased reabsorption of sodium
    • FeNa >2%
  • Inability to concentrate urine
    • urine osm <500 mOsm/kg
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11
Q

What are the two possible etiologies of Acute Tubular Necrosis?

A
  1. Ischemia
  2. Nephrotoxic
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12
Q

What etiologic theory of Acute Tubular necrosis states that decreased blood supply results in necrosis of tubules?

A

Ischemic

(often preceded by prerenal azotemia)

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13
Q

What tubular segments are particularly susceptible to ischemic damage?

A
  • Proximal tubule
  • Medullary segment of Thick Ascending Limb
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14
Q

What etiologic theory of Acute Tubular Necrosis states that toxic agents cause necrosis of tubules?

A

Nephrotoxic

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15
Q

What tubular segment is particularly susceptible to Acute Nephrotoxic Tubular Necrosis?

A

proximal tubule

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16
Q

What are toxic agents that cause Acute Nephrotoxic Tubular Necrosis?

A
  • Aminoglycosides
    • most common
  • Heavy metals
    • lead
  • Myoglobinuria
    • from crush injury to muscle
  • Ethylene glycol
    • associated with oxalate crystals in urine
  • Radiocontrast dye
  • Urate
    • tumor lysis syndrome
17
Q

What two things are used prior to the initiation of chemotherapy to decrease the risk of urate-induced Acute Tubular Necrosis?

A
  • Hydration
  • Allopurinol
18
Q

What are the three main clinical features of Acute Tubular Necrosis due to nephrotoxic etiology?

A
  1. Oliguria with brown, granular casts
  2. Elevated BUN and creatinine
  3. Hyperkalemia with Metabolic Acidosis
    1. due to decreased renal excretion
19
Q

Is Acute Tubular Necrosis irreversible or reversible?

A
  • Reversible
    • but often requires supportive dialysis since electrolyte imbalances can be fatal
20
Q

How long can the oliguria persist before recovery from Acute Tubular Necrosis? Why?

A
  • 2-3 weeks
    • tubular cells (stable cells) take time to reenter the cell cycle and regenerate
21
Q

What cause of Intra-renal Azotemia is a drug-induced hypersensitivity involving the interstitium and tubules?

A

Acute Interstitial Nephritis

22
Q

What drugs can cause Acute Interstitial Nephritis?

A
  • NSAIDs
  • Penicillin
  • Diuretics
23
Q

How does Acute Interstitial Nephritis present?

A
  • Oliguria
  • Fever
  • Rash
  • Eosinophils in urine

***Sx start days to weeks after beginning drug

***Resolves with cessation of drug

24
Q

What could Acute Interstitial Nephritis potentially progress to?

A

Renal Papillary Necrosis

25
Q

How does Renal Papillary Necrosis typically present?

A
  • Gross hematuria
  • Flank pain
26
Q

What are the possible causes of Renal Papillary Necrosis?

A
  • Chronic analgesis abuse
    • long-term phenacetin or aspirin use
  • Diabetes mellitus
  • Sickle cell trait or disease
  • Severe acute pyelonephritis

CRRAB II Week 5 - WLB (10 decks)

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