Acute Renal Failure Acute Renal Success




What is “prerenal syndrome”?

The renal tubules remain intact and avidly conserve salt and water in the face of sensed renal hypoperfusion. When normal renal hemodynamics are restored, urine flow returns to normal. Because this is undoubtedly a good response (a means of organ protection), prerenal syndrome is often called “acute renal success”.

Acute Renal Success

What is meant by the term: “acute tubular necrosis”?

A variety of injuries will cause the renal tubules become necrotic and lose their ability to conserve salt and water. When normal renal hemodynamics are restored, urine flow remains low. The persistent reduction of GFR to less than 10% of baseline is ascribed to tubular obstruction by necrotic cells at pars recta, where the proximal tubule narrows into the descending loop of Henle. Proximal intraluminal pressure increases and lessens the glomerular-tubular gradient; GFR declines. Injury to the tubular basement membrane results in back leak of tubular fluid into the interstitial tissue

Causes of Renal Failure

What is the connection between pre-renal syndrome  and acute tubular necrosis (ATN)?

 The difference between acute renal success and acute renal failure.

It is apparent that the physiologic, reversible prerenal syndrome may deteriorate into frank ATN if the ischemic insult persists long enough. A prerenal state also sensitizes the kidney to nephrotoxic insults. Nephrotoxic agents such as nonsteroidal anti-inflammatory drugs (NSAIDs), aminoglycoside antibiotics, intravenous radiocontrast dye, and cyclosporin A are much more likely to induce ATN in a dehydrated patient.

How am I supposed to differentiate the two if the patient is putting out very little urine?

As we have said, a normally functioning kidney is able to conserve salt and water. A sensitive indicator of tubular function is sodium handling because the ability of an injured tubule to reabsorb sodium is impaired, whereas an intact tubule can maintain this reabsorbtive capacity in the face of a hemodynamic stress. With a prerenal insult, the urine sodium should be less than 20, and the calculated fractional excretion of sodium should be less than 1%. If the patient has tubular damage for any reason (i.e. ATN) the urinary sodium will be greater than expected (>80 mEq). Likewise, urinary osmolality is high in pre-renal syndrome and low in ATN (see table below). The use of diuretics, however, can complicate the interpretation of these results.

Table 1: Evaluation Of Oliguria

  Pre-Renal ATN

  U:P Osmolality



  U:P Creatinine



  Urine Na (mEq/L)



  FENa (%)



  RFI %



  CCR (mL/min)






ATN = acute tubular necrosis; CCR = creatinine clearance; FENa = fractional excretion of sodium; Na = sodium; U:P = urine:plasma. RFI = Renal Failue Index, calculated as Urinary Sodium / (Urinary Creatinine / Serum Creatinine)




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