The mechanism and significance of creatinuria in the various forms of muscular dystrophy are still not clearly understood. Nevertheless, creatinuria persists as a striking indicator of biochemical disturbance. Creatine is known to figure in the energetics of muscular contraction in the transfer of high-energy phosphate bonds in the system ATP + Creatine→ADP + Creatine PO4,1 and the demonstration of appreciable amounts of creatine in the urine of people with muscular weakness, when they are eating a creatine-free diet, is widely used to support the diagnosis of primary myopathy.2,3 A tolerance test after oral administration of creatine is considered to be of additional value.4 By now it is well-established that most forms of muscular dystrophy are associated with diminished creatinine excretion and pathological creatinuria of a degree, more or less proportional to the stage and severity of the disease.5 Moreover, it has been shown that the bulk of
BOURDAKOS N, WOLF S. Creatine and Muscular Dystrophy: Relationship of Creatine-Creatinine Metabolism to Diet and Drugs. Arch Neurol. 1962;6(6):439–450. doi:10.1001/archneur.1962.00450240017003
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