What is the role of isosthenuria in the pathophysiology of acute kidney injury (AKI)?

Updated: Dec 24, 2020
  • Author: Biruh T Workeneh, MD, PhD, FASN; Chief Editor: Vecihi Batuman, MD, FASN  more...
  • Print

A physiologic hallmark of ATN is a failure to maximally dilute or concentrate urine (isosthenuria). This defect is not responsive to pharmacologic doses of vasopressin. The injured kidney fails to generate and maintain a high medullary solute gradient, because the accumulation of solute in the medulla depends on normal distal nephron function.

Failure to excrete concentrated urine even in the presence of oliguria is a helpful diagnostic clue in distinguishing prerenal from intrinsic renal disease. In prerenal azotemia, urine osmolality is typically more than 500 mOsm/kg, whereas in intrinsic renal disease, urine osmolality is less than 300 mOsm/kg.

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!