The Correct Answer is C
Statement C is NOT true: In acute glomerulonephritis, the urine sediment is NOT inactive—it is characteristically active with red blood cells, red blood cell casts, dysmorphic RBCs, and often proteinuria. 1
Analysis of Each Statement
A) Prerenal AKI and FENa <1% - TRUE
In prerenal acute kidney injury, the fractional excretion of sodium is typically <1%, reflecting intact tubular function and appropriate sodium reabsorption in response to decreased renal perfusion 2, 3. However, important caveats exist:
- Diuretic use can elevate FENa even in prerenal states 3, 4
- FENa <1% can also occur in acute glomerulonephritis, contrast nephropathy, pigment nephropathy, and occasionally non-oliguric ATN 3, 4
- Recent evidence shows that 38% of patients with muddy brown casts (diagnostic of ATN) had FENa <1%, demonstrating poor concordance 5
Clinical pitfall: Do not rely solely on FENa to exclude intrinsic renal injury—always correlate with urine sediment examination 5.
B) BUN/Creatinine Ratio in ATN <40 - TRUE
In acute tubular necrosis, the serum urea-to-creatinine ratio is typically <40 (or <20:1 when using conventional units). This occurs because:
- Both BUN and creatinine rise proportionally in intrinsic renal injury
- There is no preferential urea reabsorption as seen in prerenal states
- Prerenal azotemia typically shows BUN/Cr ratio >40 due to enhanced urea reabsorption 6
C) Inactive Sediment in Glomerulonephritis - FALSE
This statement is definitively incorrect. Acute glomerulonephritis presents with highly active urine sediment characterized by:
- Red blood cells and red blood cell casts (pathognomonic)
- Dysmorphic RBCs
- Proteinuria (often nephritic range)
- Sometimes white blood cells
The presence of RBC casts is virtually diagnostic of glomerular disease and represents one of the most important findings on urinalysis 1, 7. Urinary sediment analysis with evaluation of casts and cellular elements remains a well-established diagnostic tool in nephrology 1.
D) Leukocytes and Casts in Interstitial Nephritis - TRUE
Acute interstitial nephritis characteristically shows:
- White blood cells (leukocytes) in urine
- White blood cell casts
- Eosinophiluria (though not always present and not specific)
- Sterile pyuria
This finding helps distinguish AIN from other causes of AKI 6.
E) Normal Sediment in Postrenal AKI - TRUE
Postrenal (obstructive) acute kidney injury typically presents with:
- Bland or normal urine sediment initially
- Absence of casts, significant proteinuria, or hematuria
- May develop pyuria if infection supervenes
The diagnosis is confirmed by renal ultrasonography showing hydronephrosis 8, 7.
Diagnostic Algorithm for AKI Etiology
Step 1: Obtain urinalysis with microscopy
- Active sediment (RBC casts) → glomerulonephritis
- WBC casts → interstitial nephritis
- Muddy brown/granular casts → ATN
- Bland sediment → consider prerenal or postrenal
Step 2: Calculate urinary indices (FENa, BUN/Cr ratio)
- Use as adjuncts, NOT sole determinants
- FENa <1% suggests but does not confirm prerenal etiology
Step 3: Imaging (renal ultrasound) if obstruction suspected
Step 4: Consider clinical context, medication history, and volume status
The key message: Urine sediment examination is essential and should not be replaced by biochemical indices alone 1, 7, 5.