Renal reabsorption of Vitamin C

General principles
The kidney actively reabsorbs ascorbate present in the
glomerular fi ltrate, thereby maximizing vitamin C
conservation in the body and helping the intestine to
maintain the circulating vitamin in its useful, reduced
state. The kidneys of all mammals handle vitamin C in
a similar manner. Renal reabsorption of vitamin C is
an essential process for humans as, without it, urinary
loss would far exceed the average daily intake of the
vitamin. Although species that have the ability to synthesize
ascorbic acid might be able to replace that lost
in the urine, the metabolic costs would be high.
Transport mechanisms
Ascorbic acid
Renal uptake of the L-ascorbate anion at the brushborder
membrane of the absorptive cell of the proximal
convoluted tubule is, like intestinal uptake in the
human or guinea pig, a sodium-coupled, secondary
active transport system (Rose, 1986; Bowers-Komro
& McCormick, 1991). Unlike the corresponding intestinal
transport system, however, the renal system
is electrogenic, indicating a Na+/ascorbate– coupling
ratio of 2:1 (Toggenburger et al., 1981). As the loaded
carrier bears a net positive charge, its transport is accelerated
by the negative membrane potential. Rapid
renal reabsorption of ascorbate is essential considering
that the transit time in the proximal tubule is only
about 10 s. Ascorbate is transported across the basolateral
membrane by sodium-independent facilitated
diffusion (Bianchi & Rose, 1985a).
Dehydroascorbic acid
The mechanism of dehydroascorbic acid transport in
renal brush-border (Bianchi & Rose, 1985b) and basolateral
(Bianchi & Rose, 1985a) membrane vesicles
appears to be facilitated diffusion. A favourable gradient
for continued renal reabsorption is maintained
dehydroascorbic acid (Rose, 1989). Dehydroascorbic
acid is taken up also from the blood across the basolateral
cell membrane and subsequently reduced to
ascorbate, which is then returned to the circulation
(Rose, 1989). The kidney participates with the intestine
and blood components in promoting reduction
of dehydroascorbic acid derived from the blood.