AKI

Question 1

What is the hallmark of AKI?

Answer 1

azotemia (incr. BUN and creatinine), often with oliguria.

divided into prerenal, post-renal, and intrarenal.

Question 2

prerenal azotemia

Answer 2

due to decr. blood flow to the kidneys. decr. blood flow causes decr. GFR, azotemia, and oliguria.
BUN:creatinine ration >15-20 and both are high. Ratio changes because BUN resorption increases (low BP causes aldo release, which increases both Na AND BUN resorption). H2O is also resorbed in the kidney.
tubular function remains intact. Fractional excretion of sodium is less than 1% and urine osmolarity is > 500.

Question 3

fractional excretion of sodium

Answer 3

(urine sodium X serum creatinine)/ (serum sodium X urine creatine).
or, sodium clearance/GFR.

Question 4

post-renal azotemia

Answer 4

d/t obstruction of the urinary tract downstream from the kidney (ie. ureters).
decr. outflow causes decr. GFR, azotemia, and oliguria.
during early stage of obstruction, incr. tubular pressure “forces” BUN into the blood (serum BUN:Cr >15. tubular function remains intact (FENa < 1%; osm > 500).
with long-standing obstruction, tubular damage ensues. this causes decreased reabsorption of BUN (serum BUN:Cr 2%), and inability to concentrate urine (osm < 500).

Question 5

acute tubular necrosis: findings, defiinition

Answer 5

injury and necrosis of tubular epithelial cells. most common cause of AKI.
necrotic cells plug tubules and obstruction decreases GFR. brown, granular casts are seen in the urine.
dysfunctional tubular epithelium results in decreased resorption of BUN (serum BUN:Cr < 15; FENa > 2%) and inability to concentrate the urine (osm <500).

Question 6

etiology of acute tubular necrosis. What areas are most susceptible?

Answer 6

1. ischemia: decr. blood supply results in necrosis of tubules. often preceded by prerenal azotemia. porximal tubule and the medullary segment of the thick ascending limb are especially susceptible to ischemic damage.
2. nephrotoxic: toxic agents result in necrosis of tubules. proximal tubule is especially susceptible. causes include aminoglycosides (most common), heavy metals (lead), myoglobinuria (muscle breakdown), cisplatin, ehtyelene glycol (associated with oxalate crystals in urine), radiocontrast dye, and urate (tumor lysis syndrome). hydration and allopurinol are used prior to initiation of chemo to reduce the risk of urate-induced ATN.
   (My CYSter’s Ugly LEAD tube = myoglobuinuria, cysplatin, lead, ethylene glycol, aminoglycosides, dye; tubular necrosis)

Question 7

clinical features of acute tubular necrosis

Answer 7

oliguria with brown granular casts, elevated BUN and Creatinine, hyperkalemia (d/t dec.r renal excretion) with metabolic acidosis.
reversible but often requires supportive dialysis since electolyte imbalances may be fatal.
oliguria can persist for 2-3 wks before recovery, tubular cells take time to reenter the cycle and regenerate.

Question 8

acute interstitial nephritis

Answer 8

drug induced hypersensitivity involving the interstitium and tubules. results in acute renal failure. causes include NSAIDs, penicillin, and diuretics. presents as oliguria, fever, rash, days to weeks after starting a drug. eosinophils may be seen in urine. resolves with cessation of drug but may progress to renal papillary necrosis.

Question 9

renal papillary necrosis

Answer 9

necrosis of the renal papillae. presents wit hgross hematuria and flank pain. causes include chronic analgesic abuse (phenacetin or ASA), DM, sickle cell trait or disease, severe acute pyelonephritis