Acute renal failure due to rhabdomyolysis in McArdle's disease following binge drinking with seizures

Citation
B. Haslinger et al., Acute renal failure due to rhabdomyolysis in McArdle's disease following binge drinking with seizures, DEUT MED WO, 126(45), 2001, pp. 1265-1268
Citations number
15
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Volume
126
Issue
45
Year of publication
2001
Pages
1265 - 1268
Database
ISI
SICI code
Abstract
History and admission findings: A 36-year-old gardener was admitted for ton ic-clonic seizures after binge drinking. The next days he developed massive rhabdomyolysis with acute renal failure. Past medical history was unremark able except for a similar episode of acute renal failure 14 years ago. At t hat time he had consumed alcohol as well. Furthermore, the patient complain ed of exercise-related painful muscle cramping and swelling. Investigations: The serum creatinine peaked at 8.5 mg/dl, blood urea at 126 mg/dl and the maximal level of serum creatinin kinase was 108300 U/I. Beca use of the massive rhabdomyolysis and the patient's past medical history a metabolic myopathy was suspected and a muscle biopsy was performed. Histoch emical staining of muscle frozen sections for phosphorylase revealed no act ivity which is typical for myophosphorylase deficiency (McArdle's disease). Additional biochemical analysis of the muscle biopsy specimen confirmed th e diagnosis. Treatment and course: By vigorous intravenous hydration and forced alkaline diuresis, the patient had a sufficient urinary output and lacked uremic si gns. The serum creatinine and urea fell continuously and reached normal lev els after 6 weeks. At that time serum creatinine kinase was still elevated (867 U/I), which is typical for McArdle's disease. Avoiding alcohol, a new episode of rhabdomyolysis and acute renal failure did not occur. Conclusions: Besides exercise alcohol is likely to be a further possible tr igger of rhabdomyolysis and acute renal failure in McArdle's disease. Postu lated mechanisms by which alcohol induces muscle injury include direct musc le toxicity and inhibition of gluconeogenesis, as these patients are probab ly more dependent on the gluconeogenetic pathway for muscle cell metabolism .