Question:medium
Pre-renal azotemia is characterized by all of the following except:
Pre-renal azotemia is characterized by all of the following except:
Show Hint
A salt-starved pre-renal kidney hoards sodium, so a high urine sodium is the exception.
Updated On: Jun 24, 2026
- Fractional excretion of Na < 1%
- Urinary osmolality > 500 mosm/kg
- Urinary sodium concentration > 40 meq/l
- Reversible with replacement fluids
Show Solution
The Correct Option is C
Solution and Explanation
The task is to find the single index that does not belong to pre-renal azotemia. The whole physiology turns on one idea: in pre-renal failure the kidney is starved of blood but its tubules still work, so it clamps down and hoards salt and water.
Start from that principle and each true option falls out. A working, salt-hungry tubule excretes almost no sodium, so the fractional excretion of sodium drops under 1 percent. The same avidity means the raw urinary sodium stays low, usually under 20 meq/l. Strong ADH activity lets the intact tubules concentrate the urine, pushing urine osmolality past 500 mosm/kg. And because nothing is structurally damaged yet, simply refilling the tank with fluids reverses the azotemia.
Now test the suspect option. A urine sodium of more than 40 meq/l means the kidney is leaking salt, which is the signature of intrinsic damage in acute tubular necrosis, where the injured tubules can no longer reabsorb sodium. This directly contradicts the salt-conserving pre-renal state.
So three options describe a sodium-retaining, concentrating, fluid-responsive kidney, and only the high urine sodium of $>40$ meq/l betrays tubular injury instead.
\[\boxed{\text{Urinary sodium concentration} > 40 \text{ meq/l}}\]
Start from that principle and each true option falls out. A working, salt-hungry tubule excretes almost no sodium, so the fractional excretion of sodium drops under 1 percent. The same avidity means the raw urinary sodium stays low, usually under 20 meq/l. Strong ADH activity lets the intact tubules concentrate the urine, pushing urine osmolality past 500 mosm/kg. And because nothing is structurally damaged yet, simply refilling the tank with fluids reverses the azotemia.
Now test the suspect option. A urine sodium of more than 40 meq/l means the kidney is leaking salt, which is the signature of intrinsic damage in acute tubular necrosis, where the injured tubules can no longer reabsorb sodium. This directly contradicts the salt-conserving pre-renal state.
So three options describe a sodium-retaining, concentrating, fluid-responsive kidney, and only the high urine sodium of $>40$ meq/l betrays tubular injury instead.
\[\boxed{\text{Urinary sodium concentration} > 40 \text{ meq/l}}\]
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