Nephrology Dialysis Transplantation, Vol 13, Issue 7 1675-1681, Copyright © 1998 by Oxford University Press
C Westenfelder, M Loghman-Adham, R Baranowski, R Brownley and C Kablitz
Background: Proximal tubular reabsorption of glucose
(G), phosphate (Pi) and amino acids is energized by the transmembrane
Na+ gradient, which explains why decreased
concentration of one solute can enhance the transport of another.
Accordingly, we postulated that the consistent increase in Pi reabsorption
seen in the post-obstructed kidney (POK) could be caused, in part, by the
low filtered load of glucose and reversed by glucose loading.
Methods: Renal function was examined before and after
i.v. glucose loading in POKs (after release of 24 h of unilateral ureteral
obstruction) and control kidneys (CK) of 10 adult rats. Brush-border
membrane vesicle (BBMV) transports of Pi and glucose were assessed in POKs
and CKs. Results: In POKs GFR, urine flow and
Na+ excretion were significantly reduced and tubular
reabsorption of both Pi (TP/GFR) and glucose (TF/GFR) were significantly
increased: TP/GFR, 2.0±0.2 vs
1.36±0.1; TmG/GFR, 23.4±1.7 vs
18.9±1.1 mmol/l. Glucose loading inhibited TP/GFR only in the
CK. Initial Na+ gradient-dependent uptakes of
D-glucose and Pi were similar in BBMVs from POK and
CK. Conclusions: The increases in TP/GFR and TG/GFR
seen in the POK do not result from decreased glucose delivery or from
alterations in BBM Pi and glucose transporters. The reduced ability of
glucose to inhibit Pi reabsorption in the POK results primarily from a
generalized increase in proximal tubular reabsorption of
Na+ and cotransported Pi and glucose. A specific
rise in distal Pi transport capacity may be an additional adaptive response
to the low filtered load of Pi in the POK. In addition, absent distal
glucose reabsorption may further facilitate Pi reclamation at these sites.
Key words: brush border membrane vesicle transport;
proline; thromboxane synthase
ORIGINAL ARTICLES
Increased reabsorptive capacity after ureteral obstruction reduces the ability of glucose to inhibit phosphate reabsorption in rat kidney
Divisions of Adult and Pediatric Nephrology, University of Utah and Veterans Affairs Medial Centers, Salt Lake City, UT, USA; Corresponding author at: Division of Nephrology and Hypertension, University of Utah Health Science Center, and Section of Nephrology (11H), Veterans Affairs Medical Center, 500 Foothill Boulevard, Salt Lake City, UT 84148, USA
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