01-21 AKI

Question 1

AKI used to be called?

Answer 1

ARF - acute renal failure

Question 2

Definition (theoretical and clinical) of AKI

Answer 2

THEORETICAL DEFINITION
—25+% loss of GFR over hours or days

CLINICAL DEFINITION
—acute incr in serum Cr

Question 3

When someone recovers from AKI, regeneration of which cell type makes this possible?

Answer 3

RTE - renal tubular epithelium

Question 4

Creatinine production

Answer 4

Creatinine is produced at a constant rate by muscle cells and is distributed equally in the TBW.

—The average 70kg (155lb) person makes 1000mg/day.

—A 70kg person has ~40L TBW, so this means 2.5mg/dL/day.

—Serum Cr could rise that much per day if there was a GFR of zero.

Question 5

Three major diagnostic categories of AKI?
—Which is commonest in hospitalized patients? In the community setting?
—Give major DDx for each

Answer 5

1. hemodynamic (pre-renal)
   **commonest cause of AKI in hospital
   —shock
   —fluid-overload/low ECV states (cirrhosis, CHF)
2. intrinsic (intra-renal)
   —
   —
3. obstructive (post-renal)
   —
   —

Question 6

What is the pathophys of how ECV causes AKI?

Answer 6

1. ECV (which is defined as the pressure sensed at arterial and venous baroreceptors) falls
2. body responds:
   —Symp: direct kidney ↑ of Na+/H2O + periph constriction ∆ing blood flow to heart and brain
   —R.A.A.S. system activated
   —ADH release
   —∆sing in intrinsic renal modulators (e.g. PGs)
3. this results in:
   —decreased urine volume that is more dilute
   —↑ed energy demand to reclaim all this Na+ which, combined with ‪↓‬ed RBF eventually causes ischemia and nercosis

Question 7

What are the two possible outcomes of AKI?

Answer 7

—reversible AKI if ECV is restored before death

—die and slough off or undergo apoptosis which is “ATN”

Question 8

What does needing dialysis s/p AKI mean prognostically for your patient?

Answer 8

not necessarily a bad sign. mean that AKI progressed to ATN, but often RTE can regrow in a period of days-weeks during which time dialysis may be needed

Question 9

Histo ∆s seen with hemodynamic AKI

Answer 9

—in pre-renal hemodynamic AKI: remarkably benign
—hemodynamic AKI: vacuolated or abnormal brush border/loss of polarity of these specialized cells → apoptosis; or, death w/ sloughing → casts

Question 10

Which patients are at an increased risk of developing hemodynamic AKI?

Answer 10

—already had ‪↓‬ GFR from CKD/DM/etc.
—‪↓‬ RBF: ACEIs, CHF, RAS, cirrhosis
—abnl renal vasc: old, athero, DM, meds like NSAIDs or cyclosporine
—coinciding toxic insult (iondinated contrast)

Question 11

How does one dx hemodynamic pre-renal AKI?

Answer 11

—↑ S_Cr
—in the setting of ‪↓‬ ECV (‪past hours/days; look at chart of S_Cr) which can be inferred from clinical signs like: tachy, hypotense, orthostatic, confusion, etc.
—oliguric/anuric
—Urine microscopy: may be unremarkable in pre-renal AKI just maybe a few cells; RTE cells/casts, “muddy brown” casts in ATN
Biochem (see other card)

Question 12

Urine chemistry ∆s from hemodynamic AKI → ATN

Answer 12

—Osm: AKI=concentrated; ATN=isosthenuric

—Urine [Na+]: AKI20mEq/L

—FENa: AKI2%

Question 13

What is the equation for FENa? When is it useful?

Answer 13

—useful in evaluating the progression of oliguric hemodynamic AKI to ATN
—FENa = (U_Na X P_Cr)/(P_Na X U_Cr)