Clearance and
micropuncture studies were performed in 23 dogs without
glucose loading to examine the tubule mechanism of
renal glycosuria. Studies were carried out in three groups of animals before and after 10% extracellular volume expansion, and administration of
maleic acid in low dose at 150 mumol/kg and in high dose at 300 mumol/kg. Specific
hexokinase methods were used for the determination of
glucose in tubule fluid and urine. Under control conditios,
glucose reabsorption occurred predominantly in the proximal tubule. In all three groups, proximal tubule reabsorption of both
sodium and
glucose was inhibited in the second phase, showing a good correlation between the two. In contrast, fractional urinary
glucose excretion remained unchanged after volume expansion and low-dose
maleic acid, indicating reabsorption of virtually all the increased
glucose load at a further "distal" site. On the other hand, significant
glycosuria developed after high-dose
maleic acid that was a result of reduced
glucose reabsorption in the distal nephron, in addition to the proximal effect. It was concluded that distal
glucose transport plays a significant role in regulating urinary
glucose excretion and maintains renal thershold for
glucose,