Acute Renal Failure - AKI

Question 1

AKI definition

Answer 1

1) Abrupt (w/in 48 hrs) absolute increase in serum creatinine of >0.3 mg/dl from baseline.
2) a percentage in crease in serum concentration of >50%
3) oliguria of

Question 2

Azotemia definition

Answer 2

High level of nitrogenous waste products in the blood due to failure of kidney’s excretory ability

Question 3

Pre-renal azotemia hallmarks

Answer 3

Renal vasoconstriction and increased Na absorption

- volume depletion, heart failure, sepsis/peripheral vasodilation

Question 4

Etiologies of pre-renal azotemia (4 main ones)

Answer 4

1) Loss of intravascular body fluids:
- hemorrhage, GI losses, sweating, renal losses
2) Sequestration of fluids outside of vasculature
- burns, ascites, pancreatitis, crush injuries
3) Decreased renal perfusion from vasodilation (sepsis, antihypertensives)
4) heart failure

Question 5

Clinical signs of volume depletion

Answer 5

postural hypotension
decreased skin turgor
dry mucous membranes
decreased axillary sweat

Question 6

Clinical signs of pre-renal azotemia

Answer 6

• very low urine sodium (increased filtration fraction) due to increased aldosterone (true or effective volume depletion)
• elevated BUN/Cr ratio (normal is 10-15:1)
• Increased urine osmolality (>400 mOsm/L) and specific gravity.

Question 7

Hepatorenal syndrome

Answer 7

Form of pre-renal azotemia in patients with severe liver disease, caused by marked vasoconstriction of renal arteries (unknown etiology)

Question 8

Meds NOT to give in pre-renal azotemia

Answer 8

NSAIDs/aspirin and ARB’s/ACE I’s.

• NSAIDs decrease prostaglandin –> vasoconstriction
• ACE I’s inhibit constrictive action on eferrent arterioles which is necessary to maintain glomerular capillary ultrafiltration pressure in the presence of markedly reduced perfusion.

Question 9

What is retrograde pyelography?

Answer 9

Injecting contrast into the bladder and back up ureters to show blockage

Question 10

Clinical signs of post-renal azotemia

Answer 10

Note: exclude blockage in EVERY case!

• high sodium excretion (decreased sodium reabsorption)
• anuria (if complete blockage. If partial blockage may get a range)
• NOTE: Unilateral obstruction does not cause progressive severe AKI. Must be BILATERAL
• hydropnephrotic kidney (dilation on ultrasound)

Question 11

5 causes of hospital acquired AKI

Answer 11

Decreased renal perfusion (44%)
Meds
Contrast
Post-op
sepsis

Question 12

AKI Stage I

Answer 12

Increase of serum creatinine by 0.3 mg/dL or 150-200% from baseline; urine output 6 hours

Question 13

AKI Stage II

Answer 13

• Cr increase 200-300% Baseline

- Urine output 12 hrs

Question 14

AKI Stage III

Answer 14

Over 300% increase in Cr from baseline or >4.0

urine output 24 hrs or anuria for 12 hrs

Question 15

Urinary findings in ATN

Answer 15

• high urinary Na and FeNa (>1%)
• Unchanged BUN/cr ratio
• fixed urine osmolarity (300) and specific gravity (1.010)

Question 16

Nephrotoxins in ATN

Answer 16

HgCl2, uranyl nitrate, gentamicin, cisplatinum, cyclosporin, certain antibiotics (aminoglycosides, vancomycin, cephalosporins), non-traumatic rhabdo, ethylyne glycol.

Question 17

Why is GFR reduced in ATN?

Answer 17

• Vasoconstriction
• back leak of tubular fluid
• intratubular obstruction
• altered glomerular permeability