THE pathogenesis of the nephrotic syndrome is not entirely clear. The alterations in the electrophoretic pattern of the serum and its albumin fractions in nephrotic patients,1 along with changes in the esterase activity of their plasma,2 have focused attention on the liver as the source of these modifications.3 These reports, however, have not been conclusive.
A study of any metabolic process involving the integrity of both renal and hepatic activity for its ultimate consummation would be helpful in the evaluation of the role played by each organ. This observation would be particularly true, if, knowing the specific function of each organ involved, one could measure alterations in the intermediate and end products of the metabolic cycle in nephrotic subjects. It might then be possible to indicate the system at fault.
The metabolism of creatinine lends itself well to such an investigation. The process is initiated in the
FLOOD RG, PINELLI RW. URINARY GLYCOCYAMINE, CREATINE AND CREATININE: Their Excretion in Children with the Nephrotic Syndrome. Am J Dis Child. 1949;78(1):67–71. doi:10.1001/archpedi.1949.02030050076006
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