Acute Renal Failure (ARF) Flashcards

1
Q

What is Acute Renal Failure (ARF)?

A

Acute, severe decrease in renal function

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2
Q

How fast does Acute Renal Failure (ARF) develop?

A

Within days

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3
Q

What are the hallmark findings of Acute Renal Failure (ARF)?

A
  • Azotemia (Inc. nitrogenous waste products in the blood)
  • Increased BUN and Creatinine (Cr)
  • Oliguria (low urine production)
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4
Q

What three categories is ARF divided into based on etiology?

A
  • Prerenal azotemia
  • Postrenal azotemia
  • Intrarenal azotemia
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5
Q

What causes PreRenal Azotemia?

A

Due to decreased blood flow to the kidneys (e.g., cardiac failure)

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6
Q

What is a common cause of ARF?

A

PreRenal Azotemia

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7
Q

What does decreased blood flow in PreRenal Azotemia result in?

A
  • Dec. GFR
  • Azotemia
  • Oliguria
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8
Q

What happens to fluid and BUN in PreRenal Azotemia?

A

Resorption of fluid and BUN ensues (serum BUN:Cr ratio >15)

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9
Q

What happens to tubular function and urine osmolality in PreRenal Azotemia?

A

Tubular function remains intact

-Fractional excretion of sodium [FENa] 500 mOsm/kg

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10
Q

What process in PreRenal Azotemia leads to serum BUN:Cr >15?

A
  1. Dec. blood flow to the kidney
  2. RAAS activated
  3. Aldosterone released
  4. Reabsorb Na+ and H2O
  5. Additional BUN flows into blood
  6. BUN:Cr >15
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11
Q

What is the normal BUN:Cr ratio?

A

15

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12
Q

What causes PostRenal Azotemia?

A

Due to obstruction of urinary tract downstream from the kidney (e.g. ureters)

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13
Q

What does decreased outflow in PostRenal Azotemia result in?

A
  • Dec. GFR
  • Azotemia
  • Oliguria
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14
Q

What happens to BUN and tubular function during the early stage of obstruction/PostRenal Azotemia?

A
  1. Increased tubular pressure
  2. Forces BUN into the blood (serum BUN:Cr >15)
  3. Tubular function remains intact (FENa 500 mOsm/kg.)
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15
Q

What happens to BUN and tubular function during long-standing obstruction/PostRenal Azotemia?

A
  1. Tubular damage ensues.

2. Decreased reabsorption of BUN (serum BUN:Cr ratio2%), and inability to concentrate urine (urine osm

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16
Q

What is the most common cause of acute renal failure?

A

Acute Tubular Necrosis (ATN)

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17
Q

What is another name for Acute Tubular Necrosis (ATN)?

A

Intrarenal Azotemia

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18
Q

What is ATN?

A

Injury and necrosis of tubular epithelial cells

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19
Q

What plugs the tubules in ATN?

A

Necrotic cells

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20
Q

What does obstruction of the tubules in ATN cause?

A

Decrease in GFR

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21
Q

What is seen in the urine with ATN?

A

Brown, granular casts

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22
Q

What does the dysfunction tubular epithelium in ATN do to BUN, Na and urine concentration?

A

Results in decreased reabsorption of BUN (serum BUN:Cr ratio 2%), decreased resorption of sodium and inability to concentrate urine (urine osm

23
Q

What two things might the etiology be for ATN?

A
  1. Ischemia

2. Nephrotoxic

24
Q

What is Ischemic ATN?

A

Decreased blood supply results in necrosis of tubules

25
Q

What often precedes ischemic ATN?

A

PreRenal Azotemia

26
Q

What is azotemia?

A

Increased nitrogenous waste products in the blood

27
Q

What molecule cannot be reabsorbed in the kidney tubules?

A

Creatinine

28
Q

What forms the brown, granular casts seen in the urine with ATN?

A

Epithelial cells die and form the cast (plugged tubule)

29
Q

What area is the most susceptible to ischemic damage from Acute Tubular Necrosis (ATN)?

A
  1. Proximal tubule
    AND
  2. Medullary segment of thick ascending limb
30
Q

What is Nephrotoxic ATN?

A

Toxic agents result in necrosis of tubules.

31
Q

What area is particularly susceptible to Nephrotoxic ATN?

A

Proximal tubule

32
Q

What is the most common cause of Nephrotoxic ATN?

A

Aminoglycosides

33
Q

What are other causes of Nephrotoxic ATN?

A
  • Heavy metals (e.g. lead)
  • Myoglobinuria (e.g. from crush injury to muscle)
  • Ethylene glycol (Antifreeze)
  • Radiocontrast dye
  • Urate (eg tumor lysis syndrome)
34
Q

What can consuming Ethylene glycol cause other than nephrotoxic ATN?

A

Oxalate crystals in the urine (kids can accidentally consume this –> antifreeze)

35
Q

What treatment is used to decrease the risk of urate-induced ATN?

A

Hydration and Allopurinol

36
Q

What is given after Hydration and Allopurinol for ATN?

A

Chemotherapy is initiated

37
Q

What leads to tumor necrosis syndrome?

A

Uric acid damage

38
Q

What are the three clinical features associated with ATN?

A
  1. Oliguria with brown, granular casts
  2. Elevated BUN and creatinine
  3. Hyperkalemia (due to decreased renal excretion) with metabolic acidosis
39
Q

Is ATN reversible?

A

Yes

40
Q

What does ATN often require for treatment? Why?

A

Supportive dialysis because electrolyte imbalances can be fatal

41
Q

What can persist for 2-3 weeks before recovery in ATN?

A

Oliguria

42
Q

Why does Oliguria persist for so long in ATN?

A

Tubular cells (stable cells) take time to reenter the cell cycle and regenerate

43
Q

What is Acute Interstitial Nephritis (AIN)?

A

Drug-induced hypersensitivity involving the interstitium and tubules

44
Q

What does Acute Interstitial Nephritis result in?

A

Acute Renal Failure (ARF) = Intrarenal Azotemia

45
Q

What are causes of Acute Interstitial Nephritis?

A
  • NSAIDs
  • Penicillin
  • Diuretics
46
Q

What does Acute Interstitial Nephritis present with?

A
  • Oliguria
  • Fever
  • Rash
47
Q

When do patients with Acute Intersitial Nephritis present?

A

Days to weeks after starting a drug

48
Q

What may be seen in the urine with Acute Interstitial Nephritis?

A

Eosinophils

49
Q

When does Acute Interstitial Nephritis resolve?

A

With cessation of drug

50
Q

What may Acute Interstitial Nephritis progress to?

A

Renal Papillary Necrosis

51
Q

What is Renal Papillary Necrosis?

A

Necrosis of renal papillae

52
Q

What does Renal Papillary Necrosis present with (two things)?

A
  1. Gross hematuria

2. Flank pain

53
Q

What are the four main causes of Renal Papillary Necrosis?

A
  1. Chronic analgesic abuse (e.g. long-term phenacetin or aspirin use)
  2. Diabetes Mellitus (DM)
  3. Sickle cell trait or disease
  4. Severe acute pyelonephritis