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rhabdomyolysis acute kidney injury trauma
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The answer is C. Rhabdomyolysis.
Explanation
Clinical scenario:
- 30-year-old male after road traffic accident (RTA) with femur fracture
- Develops hematuria post-admission
- Serum creatinine = 3 (elevated - AKI)
- Urine RBC = 30 (positive dipstick for blood)
- No pus cells, no cast cells
Why Rhabdomyolysis?
The key diagnostic clue here is the dissociation between dipstick-positive hematuria and the absence of RBC casts/pus cells. This pattern is classic for myoglobinuria masquerading as hematuria.
In rhabdomyolysis from crush injury or femur fracture:
- Muscle damage releases myoglobin into the bloodstream
- Myoglobin is freely filtered by the glomerulus and excreted in urine
- The urine dipstick tests positive for "blood" because myoglobin has peroxidase-like heme activity - it cross-reacts with the dipstick reagent exactly as hemoglobin does
- However, there are relatively few actual RBCs on microscopy, and no casts - because this is tubular pigment deposition, not glomerulonephritis
As Henry's Clinical Diagnosis and Management by Laboratory Methods explains: "The reagent strip urine test for hemoglobin is markedly positive, and protein and a few red blood cells are present... The distinction between hematuria, hemoglobinuria, and myoglobinuria may be difficult - in all three cases, the urine can be dark red to brown, and some erythrocytes are seen in the sediment."
The elevated creatinine (= 3) reflects acute kidney injury from myoglobin-induced tubular toxicity - myoglobin is directly nephrotoxic and causes renal tubular obstruction.
Why NOT the other options?
| Option | Why excluded |
|---|---|
| A. Fat embolism | Causes respiratory failure, petechiae, neurological changes - not hematuria/AKI pattern |
| B. Retention | Would cause obstructive uropathy, not elevated creatinine with hematuria |
| D. Sepsis | No mention of fever, leukocytosis, or hemodynamic instability |
| E. Hypovolemia | Would cause pre-renal AKI with concentrated urine but NOT hematuria; no RBCs |
The Pathophysiology of Rhabdomyolysis-induced AKI
Femur fracture + trauma -> massive muscle destruction -> myoglobin released -> filtered at glomerulus -> precipitates in renal tubules (especially in acidic, concentrated urine) -> direct tubular toxicity + tubular obstruction -> AKI with elevated creatinine.
The urine shows:
- Dipstick positive for heme (myoglobin reacts like hemoglobin)
- Some RBCs (but fewer than true hematuria)
- No RBC casts (casts = glomerular pathology; not present here)
- No pus cells (no infection/interstitial nephritis)
This combination - trauma, hematuria-like picture, AKI, no casts, no pus cells - is the textbook presentation of rhabdomyolysis. A confirmatory test would be markedly elevated serum CK (creatine kinase) and direct urine myoglobin immunoassay.
A 2026 narrative review in Chest (PMID: 41619932) confirms that trauma remains a leading cause of rhabdomyolysis, and AKI is the most feared complication, driven by myoglobin-mediated tubular injury.
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