Abstract
1) An introduction was made of a theoretical model in consideration of several factors involved in the structural specificity of nephron. A stoichiometric analysis of aminoacid transfer mechanism in tubular cells was tried by a mathematical treatment. Urinary amino-acid excretion was formulated as follows : ln <CAA>/<GFR>=A- B/V 2) appropriateness of an equation induced by a theoretical model was tested by observing changes of urinary aminoacid excretion due to changes of a minute urine volume and proven to be valid. The normal kidneys of dogs and human beings were put on mannitol and water diuresis and urinary aminoacid excretion rate was measured. Changes of urinary aminoacid may be expressed as In <CAA>/<GFR>-=ln a - B/V with a high statistical reliance. 3) A deformed histidine titration curve suggesting a decrease of equilibrium constant k of transfer reaction in the diseased kidney proved to be the same as that of the normal kidney following correction of some factors on the basis of the theoretical formula. Reduction in reabsorption ratio and reaction constant resulted from an increased urine volume per nephron. 4) In the aminoaciduria in a narrow sense e. g. Fanconi syndrome, evaluation of changes only in the active transfer system becomes possible by correcting other factors by inducing such a theoretical formula. It is believed that this formula can be used as the basis of in-vivo stoichiometric treatment of the transfer mechanism.
