Cause:Often multiple
Pathophys:GFR decreases before tubular function decreases; fortunate, otherwise would dehydrate quickly. Tubular necrosis interstitial edema more oliguria due to increased extratubular pressure
Recovery in 10-30 d if maintain with dialysis; 30-40% will be left with a diminished GFR or concentrating ability
(Chronic Kidney Disease); CHF
r/o other causes of acute oliguria (Nejm 1998;338:671) like: obstructive disease; other intrinsic renal diseases like acute GN and interstitial nephritis, esp drug (NSAID)-induced type; and prerenal causes including hypovolemia and low cardiac output syndromes
Lab:
Path:Gross shows swollen kidney; congested medullary pyramids with pale cortex; microscopic shows tubular necrosis, esp proximally with poisons; interstitial edema; regenerating tubules by day 3
Urine:Smell absent, unlike prerenal azotemia (Nejm 1980;303:1125).
Urine osmoles <350-400 in contrast to prerenal azotemia where >500; osmole/plasma osmole ratio <1.7; Na >40 mEq/L unlike <20 in prerenal azotemia; urea nitrogen <3× plasma unlike >8 in prerenal azotemia; creatinine <20× plasma unlike >40 in prerenal azotemia; volume <400 cc/24 h, 50% false neg but thats more benign type anyway
UA sediment shows tubular casts
Rx:
Avoid diuretics, which can worsen prognosis and dont help (Jama 2002;288:2547)
Supportive with protein limitation to <30 gm/day; water to 400 cc plus urine output + insensibles; watch K+ by avoiding old blood if transfuse, and treat elevations with Na polystyrene (Kayexalate); peritoneal or hemodialysis, esp if muscle breakdown, peritoneal less good than hemo, at least if ATN caused by infection (Nejm 2002;347:895, 933)
Radiocontrast nephropathy-type (Nejm 2006;354:379; Jama 2006;295:2765):