Small Group 3 AKI

Question 1

1. Differentiate causes of oliguric AKI (including the major categories of AKI) based on history.

Answer 1

pre-renal: hypo perfusion due to volume depletion, sepsis, CHF, meds (radio contrast, antibiotic), near syncope, reduced fluid intake

intra-renal: GN, AIN or ATN (ischemic or toxic) due to intrinsic injury (radio contrast, hepatorenal syndrome, myoglobinuria, AIN or RPGN)

post-renal: obstruction (BPH, malignancy, stricture, stones, radiation),

Question 2

1. Differentiate causes of oliguric AKI (including the major categories of AKI) based on PE.

Answer 2

pre-renal: hypo perfusion: orthopnea, edema, fever (signs of infection), trauma

intra-renal: looks similar to pre renal, note pre-renal can progress to intra renal

post-renal: supra-pubic tenderness and resonance up to belly button, mass of pelvic exam

Question 3

1. Differentiate causes of oliguric AKI (including the major categories of AKI) based on lab findings.

Answer 3

pre-renal: “bland UA,” volume depleted (dark colored urine), FEna< 3.5

intrarenal FEna>3.5

post-renal: supra-pubic tenderness and resonance up to belly button, mass of pelvic exam, typically benign UA

Question 4

2. Describe the long-term outcomes of AKI. What is the time frame of recovery?

Answer 4

(short term mortality is high 50% die in ICU due to infection)

of those who survive long term: 45% will recover fully, 50% will have CKD and 5% will require dialysis

recovery takes 2-12 weeks, most who recover, show improvement at 5 weeks

Question 5

4. What diagnostic tests and therapeutic maneuvers are indicated in the setting of influenza like sickness.

Answer 5

normal saline to replete the volume loss (in cases of CHF use albumin and pressors) and give a large bolus at start

later check the blood pressure and monitor for expansion acidosis, start a saline drip

note normal values like pre renal azotemia should reverse typically within 24 hours

Question 6

4. What therapeutic maneuvers are indicated in the setting of trauma, both immediate and short term therapies.

Answer 6

therapy to address the hyperkalemia is important to prevent systole (signs include peaked T waves)

strategy includes: 1. protect heart (calcium gluconate or calcium chloride) 2. Shift K+ intracellularly: B agonist, insulin and glucose, sodium bicarb 3. get rid of K in the urine or gut: give K+ binding resins (kayexelate ion exchange resin, sorbitol can cause diarrhea (much more loss)) (and loop diuretic if fluid overloaded)
4. hemodialysis

long term management: provide high protein nutrition, support blood pressure with RBC and pressers, restrict Na, K, and fluids to prevent extracellular expansion

Question 7

Describe how a crush injury can cause kidney damage if kidney is initially not involved.

Answer 7

crush injuries can cause rhabdomyalysis and myoglobin is cytotoxic

IV contrast to access injuries can be vasoconstrictive

Question 8

3. Explain the reasons for hyperkalemia in our patient with crush injuries, why is his K+ so high?

Answer 8

lysing of cells causes hyperkalemia in conjunction with metabolic acidosis (lactic acids, citrate in blood products, AKI/ AKF leads to decreased acid excretion) leading to H+ sequestered in cells in exchange for K+ (these processes are synergistic in producing hyperkalemia)

not hypovolemia leading to aldosterone system initiation

Question 9

How do we clinically differentiate AKI from chronic kidney disease.

Answer 9

difficult to know; clues include past creatinines, CKD often also has phosphorus, anemia

ultrasound to size kidney: small (chronic), normal/big (acute)