12.2 Acute Renal Failure

Question 1

Acute tubular necrosis

• etiology (2 main mechs)
• what parts of tubules are most susceptible to each?

Answer 1

1. ischemia
   - PCT, medullary part of thick ascending limb
2. nephrotoxicity
   - PCT

Question 2

Postrenal azotemia

• cause
• early vs late stage, lab values

(BUN/Cr, FENa, urine osm)

Answer 2

-blockage distal to kidney, causes deceased GFR, oliguria, azotemia

early:

1. BUN/Cr >15 (increased pressure actually forces BUN through tubules)
2. FENa
3. urine osm >500 mOsm/kg
   late: opposite b/c of tubular damage

(2%,

Question 2

Acute interstitial nephritis

• how presents?
• timeframe

Answer 2

• oliguira, fever, rash days to week after starting a drug
• eosinophils may be seen in urine!

Question 3

renal papillary necrosis

-causes (4 most common)

Answer 3

1. chronic analgesic abuse (eg long term phenacetin or aspirin use, which caused acute interstitial nephritis)
2. DM2
3. sickle cell trait/disease
4. severe acute pyelonephritis

Question 4

• eosinophils in urine
• what to suspect?

Answer 4

• Acute Interstitial Nephritis (drug induced hypersensitivity rxn)
• almost pathognomonic for this

Question 5

Hallmark clinical findings with ARF

Answer 5

• azotemia (increased BUN, creatinine)
• oliguria
• occurs within days

Question 5

acute tubular necrosis

• treatment?
• timeframe

Answer 5

• Reversible b/c cells can regenerate. Symptoms can last 2-3 weeks before recovery b/c tubular cells (stable) take time to reenter cell cycle and regenerate
• often requires supportive dialysis (electrolyte imbalances can be fatal)

Question 6

acute tubular necrosis

• clinical findings (4)
• lab values?

Answer 6

• brown, granular casts in urine (dead tubular cells)
• oliguria
• hyperkalemia (decreased renal excretion)
• metabolic acidosis (decreased acid excretion)
  1. BUN/Cr
  2. FENa >2%
  3. urine osm

Question 7

• gross hematuria, flank pain
• Suspect what kidney disorder?

Answer 7

renal papillary necrosis

Question 8

acute tubular necrosis:

• causes of nephrotoxicity (6)
• which is most common

Answer 8

1. aminoglycosides (most common)
2. heavy metals (eg lead)
3. myoglobinuria (muscle crush injury)
4. ethylene glycol (antifreeze, associated with oxalate crystals in urine)
5. radiocontrast dye
6. urate (eg tumor lysis syndrome)

Question 9

what is the most common cause of nephrotoxic acute tubular necrosis?

Answer 9

-aminoglycosides

Question 10

Prerenal azotemia

• cause
  1. BUN:Cr ratio?
  2. FENa?
  3. urine osmolality?

Answer 10

• decreased blood flow to kidneys (eg cardiac failure)
  1. ratio >15 (because tubules can still reabsorb urea)

2.

3. >500 mOsm/kg (because tubules can still concentrate urine)

Question 11

Acute interstitial nephritis

• what is it
• what can it progress to?

Answer 11

• Acute renal failure caused by:
• drug induced hypersensitivity involving intersitium and tubules

(inflammation of connective tissue btwn tubules)

-renal papillary necrosis

Question 13

Acute interstitial nephritis

-causes (3 common ones)

Answer 13

• drug-induced
• NSAIDs, penicillin, diuretics (+ others)

Question 14

FENa

Answer 14

fractional excretion of Na

If

If >2%, tubules have problems

Question 15

Acute interstitial nephritis

-tx?

Answer 15

-cessation of culprit drug (it’s a hypersensitivity rxn)

Question 16

what problem is oxalate crystals in the urine associated with?

Answer 16

antifreeze toxicity, causing acute tubular necrosis

(ethylene glycol)

Question 18

tumor lysis syndrome:

• what is it, what effect on kidneys?
• how to prevent?

Answer 18

(urate-induced ATN)

• Lysing a tumor (eg chemo on leukemia pt) will induce rapid breakdown of nuclear material and release it into the blood. This will raise urate levels and can cause acute tubular necrosis.
• prevent with hydration and allopurinol prior to chemo

Question 19

renal papillary necrosis

-how presents?

Answer 19

• gross hematuria
• flank pain