Bit · Renal

Acute Kidney Injury — Prerenal vs Intrinsic vs Postrenal

AKI splits at the start: is the kidney getting blood, working properly, or able to drain? Three categories, three different labs.

Mechanism

AKI is a rapid (< 7 days) rise in creatinine and/or fall in urine output. Three causes:

Differentiator Table

PrerenalIntrinsic (ATN)Postrenal
MechanismUnderperfusionTubular cell deathOutflow obstruction
BUN:Cr ratio> 20:1< 15:1Variable (high early, low late)
Urine Na< 20 mEq/L> 40 mEq/LVariable
FENa< 1%> 2%Variable
Urine osmolality> 500 mOsm/kg≈ 300 (isosthenuria)Variable
CastsHyalineMuddy brown granularNone specific
ImagingNormalNormal initiallyHydronephrosis
ReversibilityQuick with fluidDays to weeksQuick if obstruction relieved

The Pivot

Three labs do most of the work:

  1. BUN:Cr ratio. > 20:1 → prerenal. < 15:1 → intrinsic.
  2. FENa (fractional excretion of sodium). < 1% → prerenal. > 2% → intrinsic.
  3. Urine sediment. Muddy brown casts → ATN. RBC casts → GN. WBC casts + eosinophils → AIN. Hyaline only → prerenal.

Postrenal needs a renal ultrasound — hydronephrosis confirms it.

NBME-Style Stem

A 78-year-old man with metastatic prostate cancer presents with anuria for 24 hours. Serum creatinine has risen from 1.0 to 4.6 mg/dL over 3 days. Bladder is non-distended. Renal ultrasound shows bilateral hydronephrosis. Which of the following is the most likely cause of his acute kidney injury?
Concept Anchor
Three places blood and urine can fail in the kidney pipeline: not enough blood in (prerenal), the kidney itself is broken (intrinsic), or no urine out (postrenal). BUN:Cr and FENa split prerenal from intrinsic; ultrasound finds postrenal.

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