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Pathoma - Kidney and Urinary Tract Pathology > Acute Renal Failure (ARF) > Flashcards

Acute Renal Failure (ARF) Flashcards

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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?

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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?

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A
  1. Ischemia

2. Nephrotoxic

24
Q

What is Ischemic ATN?

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A

Decreased blood supply results in necrosis of tubules

25
What often precedes ischemic ATN?
PreRenal Azotemia
26
What is azotemia?
Increased nitrogenous waste products in the blood
27
What molecule cannot be reabsorbed in the kidney tubules?
Creatinine
28
What forms the brown, granular casts seen in the urine with ATN?
Epithelial cells die and form the cast (plugged tubule)
29
What area is the most susceptible to ischemic damage from Acute Tubular Necrosis (ATN)?
1. Proximal tubule AND 2. Medullary segment of thick ascending limb
30
What is Nephrotoxic ATN?
Toxic agents result in necrosis of tubules.
31
What area is particularly susceptible to Nephrotoxic ATN?
Proximal tubule
32
What is the most common cause of Nephrotoxic ATN?
Aminoglycosides
33
What are other causes of Nephrotoxic ATN?
- Heavy metals (e.g. lead) - Myoglobinuria (e.g. from crush injury to muscle) - Ethylene glycol (Antifreeze) - Radiocontrast dye - Urate (eg tumor lysis syndrome)
34
What can consuming Ethylene glycol cause other than nephrotoxic ATN?
Oxalate crystals in the urine (kids can accidentally consume this --> antifreeze)
35
What treatment is used to decrease the risk of urate-induced ATN?
Hydration and Allopurinol
36
What is given after Hydration and Allopurinol for ATN?
Chemotherapy is initiated
37
What leads to tumor necrosis syndrome?
Uric acid damage
38
What are the three clinical features associated with ATN?
1. Oliguria with brown, granular casts 2. Elevated BUN and creatinine 3. Hyperkalemia (due to decreased renal excretion) with metabolic acidosis
39
Is ATN reversible?
Yes
40
What does ATN often require for treatment? Why?
Supportive dialysis because electrolyte imbalances can be fatal
41
What can persist for 2-3 weeks before recovery in ATN?
Oliguria
42
Why does Oliguria persist for so long in ATN?
Tubular cells (stable cells) take time to reenter the cell cycle and regenerate
43
What is Acute Interstitial Nephritis (AIN)?
Drug-induced hypersensitivity involving the interstitium and tubules
44
What does Acute Interstitial Nephritis result in?
Acute Renal Failure (ARF) = Intrarenal Azotemia
45
What are causes of Acute Interstitial Nephritis?
- NSAIDs - Penicillin - Diuretics
46
What does Acute Interstitial Nephritis present with?
- Oliguria - Fever - Rash
47
When do patients with Acute Intersitial Nephritis present?
Days to weeks after starting a drug
48
What may be seen in the urine with Acute Interstitial Nephritis?
Eosinophils
49
When does Acute Interstitial Nephritis resolve?
With cessation of drug
50
What may Acute Interstitial Nephritis progress to?
Renal Papillary Necrosis
51
What is Renal Papillary Necrosis?
Necrosis of renal papillae
52
What does Renal Papillary Necrosis present with (two things)?
1. Gross hematuria | 2. Flank pain
53
What are the four main causes of Renal Papillary Necrosis?
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

Pathoma - Kidney and Urinary Tract Pathology (9 decks)

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