Acute Kidney Injury Workup: Prerenal vs Intrinsic vs Postrenal
Clinical Reasoning · 9 min read · 2026-08-28
Introduction
A creatinine that doubles overnight triggers the same reflex in every student: order everything. But the boards - and real medicine - reward the opposite move. AKI is a localization problem, and nearly all of the information you need sits in four data points: the BUN-to-creatinine ratio, the urine sodium, the sediment, and the clinical story.
Step 1: Frame the Three Compartments
Before touching a lab value, sort the patient into one of three buckets:
- Prerenal - the kidney is healthy but underperfused (hypovolemia, heart failure, sepsis early, NSAIDs/ACEi on the renal artery side)
- Intrinsic - the kidney tissue itself is injured (ATN, glomerulonephritis, interstitial nephritis, vascular)
- Postrenal - the plumbing is obstructed (BPH, stones, malignancy, neurogenic bladder)
This framing matters because each compartment has a signature lab pattern, and the exam questions are built around those signatures.
Step 2: The BUN:Creatinine Ratio
- > 20:1 suggests prerenal. Urea is reabsorbed with sodium and water in the proximal tubule; hypoperfusion amplifies this, so BUN climbs out of proportion to creatinine.
- ~10-15:1 is typical of intrinsic injury, where both rise in parallel.
Caveat the boards love: an upper GI bleed also produces a high BUN:Cr ratio (digested blood is a urea load) - volume status will usually disambiguate.
Step 3: Fractional Excretion of Sodium (FENa)
FENa = (Urine Na × Plasma Cr) / (Plasma Na × Urine Cr) × 100
- FENa < 1% - the tubules work and are avidly reabsorbing sodium: prerenal
- FENa > 2% - the tubules are injured and cannot reclaim sodium: ATN
- 1-2% is indeterminate
The classic trap: FENa is invalid in patients on diuretics. Furosemide forces sodium excretion even in a prerenal kidney. Use FEUrea (< 35% = prerenal) instead.
Other exceptions where FENa is low despite intrinsic disease: contrast nephropathy, rhabdomyolysis, early obstruction, and glomerulonephritis. Context beats the number.
Step 4: Read the Urine Sediment
Sediment is the single highest-yield image-based data point in AKI questions - a "muddy brown" cast in a vignette is essentially the diagnosis handed to you.
Step 5: Never Skip the Bladder Scan
Postrenal AKI is the most reversible cause and the easiest to miss. An elderly man with a rising creatinine and a distended bladder needs a catheter, not a nephrology consult. A renal ultrasound showing hydronephrosis confirms obstruction; its absence makes postrenal disease unlikely.
Putting It Together: A Reasoning Sequence
- Confirm AKI (creatinine rise ≥ 0.3 mg/dL in 48h or 1.5× baseline in 7 days).
- Volume status + BUN:Cr → prerenal suspicion.
- FENa (or FEUrea if on diuretics) to test tubular function.
- Sediment to identify intrinsic pathology.
- Bladder scan / ultrasound to exclude obstruction.
Common Pitfalls
- Trusting FENa in a patient who received furosemide in the ED.
- Calling it ATN when the sediment shows RBC casts - that's a nephritic picture until proven otherwise.
- Forgetting that NSAIDs and ACE inhibitors cause a *hemodynamic* prerenal state even in a euvolemic patient.
- Missing obstruction in patients with a single kidney or a pelvic malignancy, where hydronephrosis can be subtle early.
Conclusion
AKI questions are won in the sequence, not in any single number. Ratio first, FENa second, sediment third, ultrasound always. Practice this chain until it's automatic - it's one of the most reliably tested reasoning patterns on Step 2 CK.