Rhabdomyolysis usually presents with high creatine phosphokinase (CPK) levels, a beacon of muscle breakdown culminating in myoglobin-driven acute kidney injury (AKI). Yet, in a 22-year-old male with no comorbidities, this expected signal was eerily absent. Following intense exertion, he presented with oliguria and fatigue, progressing to dialysis-dependent AKI within 48 hours. Laboratory findings revealed a serum creatinine of 8.2 mg/dL and urinalysis showing 3+ blood but no red blood cells—hallmarks of pigmenturia—yet CPK lingered at a normal 142 U/L. A renal biopsy unveiled pigment nephropathy suggestive of rhabdomyolysis, with granular casts staining the tubules, despite no evidence of hemolysis (normal haptoglobin, LDH). Five explanations emerge: the timing of CPK measurement (potentially post-peak at 48 hours), a mild or atypical rhabdomyolysis sparing CPK surge, rapid CPK clearance, alternative pigments like hemoglobin (less likely), or co-contributors such as dehydration amplifying subtle muscle injury. After five days of dialysis, renal function recovered, with creatinine normalizing to 0.9 mg/dL by one month. This case, mirroring just one prior report, defies the CPK-centric diagnostic norm, spotlighting renal biopsy as a pivotal tool. It challenges clinicians to rethink rhabdomyolysis in exertional AKI when CPK whispers rather than roars, urging reliance on histological and urinary clues to unmask this silent culprit.
Sagar et al. (Wed,) studied this question.
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