Acute Renal Failure/ AKI

Question 1

definition of AKI?

Answer 1

Acute renal failure

= absolute increase in serum creatnine of .3 mg/dL

= 50% increase in serum creatinine

= reduction in urine output consisting of oliguria of less than 0.5 mL/kg/hr for longer than 6 hours

Question 2

signs of chronic renal failure

Answer 2

anemia, hyperparathyroidism (osteodystrophy), A/V fistula, Hyperphosphatemia

Question 3

sediment on U/A

Answer 3

see casts, RBCs and WBCs = think acute renal failure

Question 4

hyaline casts

Answer 4

seen in pre-renal AKI

• secreted from tubular epithelial cells, due to low urine flow, concentrated urine, acidic encironment, dehydration, etc.

Question 5

muddy brown, granular, epithelial casts

Answer 5

intrarenal AKI, tubular cell injury

granular casts: second most common type of casts - result from breakdwon of cellular casts or inclusion of aggregates of plasma proteins

Question 6

pyuria, hematuria, mild proteinuria, granular and epithelial casts, eosinophilia

Answer 6

intrarenal AKI: acute interstitial nephritis

Question 7

hematuria, marked proteinuria, RBC casts, granular casts

Answer 7

intrarenal AKI: glomulonephritis

Question 8

normal/hematuria, mild proteinuria

Answer 8

intrarenal AKI: vascular disorder

Question 9

see normal or hematuria, granular casts and pyuria

Answer 9

postrenal AKI

Question 10

waxy casts

Answer 10

represent end product of cast evolution, suggest very low urine flow associated w/ severe, longstanding kidney disease and renal failure

Question 11

pre-renal

Answer 11

FeNa = 20:1

Question 12

ATN

Answer 12

FeNa = >1%
urine sodium >20 (kidney is damaged, so urine sodium is high)

BUN:Cr : <20:1

Question 13

toxic injury

Answer 13

> 1% FeNa
urine sodium >20 (kidney is damaged, so urine sodium is high)

BUN:Cr <20:1

Question 14

glomerulonephritis

Answer 14

<20:1

Question 15

vascular disorders

Answer 15

<20:1

Question 16

damage of prerenal azothemia?

Answer 16

this is normal physio. response to dehydration, the kidney tries to keep the fluid, they will recover

Question 17

causes of pre-renal azothemia?

Answer 17

Intravascular volume depletion and or hypotension

• Hemorrhage
• GI loss: vomiting/diarrhea
• Renal loss: diuretics, diabetes (mellitus and incipidus)
• Dermal losses (sweating)

Decreased effective intravascular volume

• Congestive heart failure
• Cirrhosis
• Hepatorenal syndrome,
• Peritonitis

Systemic vasodilation/renal vasoconstriction

• Sepsis
• Hepatorenal syndrome

Large-vessel renal vascular disease

• Renal artery thrombosis or embolism
• Renal artery stenosis

Question 18

what meds make prerenal azothemia worse and may even push pt. into acute tubular necrosis?

Answer 18

NSAIDs: inhibit the production of prostaglandins which are natural dilators in response to hypoperfusion (they don’t constrict affarent arterioles, but NSAIDs keep prostaglandins from dilating them)

ACEIs and ARBs: dilate the efferent arterioles and drop perfusion pressure

cyclosproine, radiocontrast, tacrolimus

Question 19

upper GI bleeds result in what?

Answer 19

super elevated BUN levels due to increased RBCs being broken down

Question 20

acute interstitial nephritis

Answer 20

= hypersensitivity reaction

• has damaged kidneys, has extension after initiation phase, the kidneys must regenerate, so might see an increase in creatinine levels, even after tx.
• will go into maintenance phase and will stay the same b/c they are regenerating
• will see recovery and drop in creatinine levels in a week

difference: in pre-renal you give fluids and they are immediately better creatinine levels

Question 21

nephrotoxic medications resulting in ARF?

Answer 21

Aminoglycosides
Radiocontrast agents
Acyclovir
Cisplatin
Sulfonamides
Methotrexate
Cyclosporine
Tacrolimus
Amphotericin B
Foscarnet
Pentamidine
Ethylene glycol
Toluene
Cocaine
HMG-CoA reductase inhibitors

Question 22

Wegner’s granulomatosis vs. Goodpasture sx

Answer 22

Wegners: see ANCA
goodpastures: see anti-GBM