02 - AKI

Question 1

Why can’t CrCl be used to renal status in AKI?

Answer 1

renal status not stable

Question 2

What factors are involved in the clinical presentation of AKI?

Answer 2

wt (edema)
BP

UOP

UA: spec grav inc (pre of fxn); hemat or proteinuria, + RBC and casts

FEna: <1% then prerenal or fxn; >= then injury

Question 3

Describe the different categories of UOP.

Answer 3

acute anuria <50 mL in 24 h

oliguria <400 mL in 24 h

non-oliguira >400 mL in 24 hr

Question 4

Define prerenal RF

Answer 4

hypoperfusion of kidney

Question 5

Define functional ARF

Answer 5

decr in glomerular hydrostatic pressure leads to decr GR (NSAIDs, ACEI)

Question 6

Define actue intrinsic RF

Answer 6

damage to kidney itself

Question 7

Define post renal obstruction

Answer 7

exactly what it sounds like

Question 8

How can AKI be prevented

Answer 8

use less nephrotoxic agent

hydration

sodium loadng

ID at-risk pts (DM!)

Question 9

Describe supportive theray for AKI.

Answer 9

critical may need insulin

nutrition: 20-30 kcal/kg/d
protein: up to 1.7 g/kg/d if CRRT in hypercatabolic state

avoid aminoglycosides, dopamine, fondolopam, ANP

Question 10

How can volume be controlled to treat AKI?

Answer 10

CRRT

diuretics, esp loop

Question 11

Describe the moa, prev, and Tx of NSAID/Cox II Inhibitor nephrotoxicity.

Answer 11

moa: ischemic damage d/t decr vasodilator prostaglandins and aff vasoconstriction
prev: avoid use if at risk: CHF, liver disease, vol depletion

Tx: d/c

Question 12

Describe the moa, prev, and Tx of APAP nephrotoxicity.

Answer 12

acute tub necr

d/c

Question 13

Describe the moa, prev, and Tx of aminoglycoside nephrotoxicity.

Answer 13

PCT inj –> necr; rise in SCr occurs 5-10 d after initiation

prev once daily dose

Tx dc

Question 14

Describe the moa, prev, and Tx of ACEI/Ang II blockers nephrotoxicity.

Answer 14

moa: vasodilation of eff arteriol, decr filtration pressure
prev: lose dose and titrate up. mon SCr (if incr >30% , dc)

dc

Question 15

Describe the moa, prev, and Tx of Amphotericine B nephrotoxicity.

Answer 15

moa: direct tub damage; aff vasoconstriction
prev: use liposomal amphotericin B; vol replacment w 1L NS p/t drug amin

dc

Question 16

Describe the moa, prev, and Tx of contrast media nephrotoxicity.

Answer 16

moa: direct tub tox and ischemia
prev: alternate imaging methods, low dose, avoid high osmolar iodinated contrast media

Question 17

Describe the moa, prev, and Tx of cisplatin/carboplatin nephrotoxicity.

Answer 17

moa: PCT dam
prev: decr dose and freq; saline hydration

tx: supportive, may D

Question 18

Describe the moa, prev, and Tx of cyclosporine/tacrolimus nephrotoxicity.

Answer 18

moa: vasoconstriction of aff and eff; interstitial fibrosis
prev: PK mon, decr dose

Tx: cyc: decr dose until SCr is <30% above baseline

Tac–lower dose possible

Question 19

Describe the moa, prev, and Tx of lithium nephrotoxicity.

Answer 19

moa: acute tub necr and nephrogenic DI –> conc urine
prev: avoid dehydration, low dose
tx: dc, may req D

Question 20

Describe the moa, prev, and Tx of PPI nephrotoxicity.

Answer 20

moa: acute interstitial nephritis
prev: diff to determine if at risk

Tx: dc drug; prenisone