Acute kidney injury: prerenal, intrinsic and postrenal

What it is

Acute kidney injury, formerly known as acute renal failure, is an abrupt decline in renal function as measured by a rise in creatinine and BUN, or by oliguria or anuria. It is divided by mechanism into prerenal azotemia, intrinsic renal failure and postrenal azotemia, and the whole approach at the bedside is the determination of which of the three is present.

Prerenal azotemia is due to decreased renal perfusion, for example hypotension, with a fall in GFR. Sodium, water and urea are retained by the kidney in an attempt to conserve volume. That raises the BUN to creatinine ratio, because urea is reabsorbed and creatinine is not, and the fractional excretion of sodium falls.

Intrinsic renal failure is most commonly due to acute tubular necrosis, from ischemia or toxins, and less commonly to acute glomerulonephritis such as RPGN or hemolytic uremic syndrome, or to acute interstitial nephritis. In ATN there is patchy necrosis with debris obstructing the tubule and fluid backflow across the necrotic tubule, so GFR falls. Urea reabsorption is impaired, so the BUN to creatinine ratio falls while the fractional excretion of sodium rises.

Postrenal azotemia is due to outflow obstruction from stones, BPH, neoplasia or congenital anomalies, and develops only with bilateral obstruction or in a solitary kidney.