Prerenal azotemia vs Intrinsic AKI
How to tell Prerenal azotemia and Intrinsic AKI apart when a board question makes them look alike.
Prerenal: FeNa under 1 percent, BUN to creatinine above 20:1, bland sediment; intrinsic AKI: FeNa above 2 percent with active sediment.
Side by side
Volume loss or low effective arterial volume with concentrated urine and sodium retention.
Kidney tissue injury with impaired concentrating ability and sodium wasting.
Renal perfusion is low, but tubules are still able to conserve salt and water.
Tubules, glomeruli, interstitium, or vessels are directly injured.
BUN:Cr above 20, FeNa below 1%, and high urine osmolality favor prerenal physiology.
FeNa above 2%, granular casts, RBC casts, or WBC casts favor intrinsic injury.
The trap
A rising creatinine does not localize where AKI is happening. The same number can be prerenal, intrinsic, or postrenal. Force three checks before naming the cause: (1) BUN to creatinine ratio (above 20:1 favors prerenal), (2) FeNa (under 1 percent prerenal, above 2 percent intrinsic) but FeNa is unreliable in patients on loop diuretics, where FeUrea under 35 percent is the better substitute, (3) urine sediment (bland in prerenal, active in intrinsic). Postrenal obstruction must be excluded with renal ultrasound when no clear etiology emerges.
Watch it explained
The repair move
Ask whether the tubule is responding appropriately. If yes, think prerenal; if not, think intrinsic.
Try a free question
CoreA patient with vomiting and poor intake develops AKI. Urine osmolality is high, FeNa is below 1%, and BUN:Cr is above 20. Which diagnosis is most likely?
Show answer and explanation
Answer: A. Prerenal azotemia. Low perfusion with intact tubular sodium and water conservation indicates prerenal azotemia.
Why the other choices are tempting
- B. Intrinsic AKI usually has tubular dysfunction with sodium wasting or active sediment.
- C. Postrenal AKI needs obstruction clues.
- D. AIN causes WBC casts and allergy-pattern findings.
- E. Nephrotic syndrome causes heavy proteinuria and edema.
Flashcards
Tap a card to flip it.
What FeNa pattern favors prerenal azotemia?
FeNa below 1% means tubules are still conserving sodium in response to low perfusion.
Why is BUN:Cr high in prerenal azotemia?
Low flow increases proximal urea reabsorption, so BUN rises disproportionately compared with creatinine.
Quick answers
What is the fastest way to tell Prerenal azotemia from Intrinsic AKI?
Prerenal: FeNa under 1 percent, BUN to creatinine above 20:1, bland sediment; intrinsic AKI: FeNa above 2 percent with active sediment.
What is the key clue for Prerenal azotemia?
Volume loss or low effective arterial volume with concentrated urine and sodium retention.
What is the key clue for Intrinsic AKI?
Kidney tissue injury with impaired concentrating ability and sodium wasting.
What is the common trap with Prerenal azotemia vs Intrinsic AKI?
A rising creatinine does not localize where AKI is happening. The same number can be prerenal, intrinsic, or postrenal. Force three checks before naming the cause: (1) BUN to creatinine ratio (above 20:1 favors prerenal), (2) FeNa (under 1 percent prerenal, above 2 percent intrinsic) but FeNa is unreliable in patients on loop diuretics, where FeUrea under 35 percent is the better substitute, (3) urine sediment (bland in prerenal, active in intrinsic). Postrenal obstruction must be excluded with renal ultrasound when no clear etiology emerges.