Acute Kidney Injury

Question 1

When a disproportionate increase in BUN is seen vs. creatine, where is the location of kidney inujury?

Answer 1

Pre-renal AKI

Question 2

When a disproportionate increase in creatnine vs. BUN is seen where is the location of kidney injury?

Answer 2

Intra-renal

Question 3

When urine sodium is decreased, what does this reflect?

Answer 3

Decreased renal perfusion as the RAAS is activated which causes aldosterone to be released and leads to Na reabsorption.

Question 4

What describes a pre-renal AKI? What is the process that occurs during this type of RF? What can occur to pre-renal AKI if not treated soon enough?

Answer 4

Decreased perfusion to the kidneys. RAAS is stimulated resulting in aldosterone, angiotensin II and ADH secretion. Angiotensin II causes vasoconstriction of renal BV (leaving kidney to preserve blood flow), ADH causes water reabsorption, and aldosterone causes Na reabsorption. Intra-renal AKI as if CO is not corrected, the continuing decreased O2 supply will cause renal cells to die.

Question 5

What are two different causes of intra-renal AKI?

Answer 5

Ischemia (from pre-renal) and nephrotoxins

Question 6

What is the process during ischemic intra-renal AKI? Is the ischemia localized or wide-spread?

Answer 6

Dec renal perfusion persists, tubular cells experience ischemia and cells switch from aerobic to anaerobic metabolism and cell death occurs. Wide-spread

Question 7

What is the process during nephrotoxic intra-renal AKI? Are necrotic cells generalized or localized?

Answer 7

Concentration of toxins cause cellular necrosis. Basement membrane stays intact, necrotic cells slough off into tubule lumen and clog, necrotic areas are localized.

Question 8

What are ways to prevent AKI?

Answer 8

Avoid nephrotoxic drugs, IV isotonic hydration, adequate MAP (>60-70)

Question 9

What are nephrotoxic drugs?

Answer 9

Amnioglycosides (gentamycin, tobramycin, streptomycin), amphotericin, penicillin abx (Pip Tazo), cyclosporin, corticosteroids, lasix, contrast dye

Question 10

How do NSAIDS and ACE I interrupt BF to kidneys?

Answer 10

ACE I prevents efferent arteriole from constricting (comp. mechanism can not play out) NSAIDS stop afferent arteriole from dilating (due to lack of prostaglandins.- comp mech not affective)

Question 11

What are two conditions that would lead to intra-renal AKI?’

Answer 11

Rhabdo and intra-abdominal compression