Maleic acid induced aminoaciduria, studied by free flow micropuncture and continuous microperfusion.

The injection of 200 mg/kg BW maleic acid was found to be a suitable dose for exploring the experimental Fanconi syndrome by micropuncture techniques in rats. In clearance experiments, the fractional excretion of glycine, L-alanine, L-aspartate and taurine was measured. After intraperitoneal administration of maleic acid the excretion of these amino acids was increased in the range between the 20-fold and the 230-fold. Free flow micropuncture experiments showed that the reabsorption of these amino acids is reduced drastically along the whole proximal tubule. Continuous microperfusion experiments lead to the result that, in maleic acid pretreated rats, the reabsorption of 14C-glycine from the proximal convolution was strongly inhibited. It was found, furthermore, that after blocking the saturable glycine transport by L-phenylalanine, the remaining reabsorption of glycine (corresponding to passive diffusion) was exactly the same with and without maleic acid. Microinfusion experiments with 8 mumol.1(-1) L-3H-alanine into the early distal tubule showed a fractional recovery of 103 +/- 4.2% (S.D.) in the control and of 101 +/- 6.5% in presence of maleic acid. It is concluded that maleic acid inhibits the saturable reabsorption mechanism of amino acids along the proximal tubule. Passive permeability of the tubular membrane does not seem to be altered by maleic acid.