Increased reabsorptive capacity after ureteral obstruction reduces the ability of glucose to inhibit phosphate reabsorption in rat kidney

Background. Proximal tubular reabsorption of glucose (G), phosphate (P-i) and amino acids is energized by the transmembrane Naf 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 P-i 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 P-i (T-P/GFR) and glucose (TG/GFR) were significantly increased: T-P/GFR, 2.0+/-0.2 vs 1.36+/-0.1; T(m)G/GFR, 23.4+/-1.7 vs 18.9+/-1.1 mmol/l. Glucose loading inhibited T-P/GFR only in the CK. Initial Na+ gradient-dependent uptakes of D-glucose and P-i were similar in BBMVs from POK and CK. Conclusions. The increases in T-P/GFR and TG/GFR seen in the POK do not result from decreased glucose delivery or from alterations in BBM P-i and glucose transporters. The reduced ability of glucose to inhibit P-i reabsorption in the POK results primarily from a generalized increase in proximal tubular reabsorption of Na+ and cotransported P-i and glucose. A specific rise in distal P-i transport capacity may be an additional adaptive response to the low filtered load of P-i in the POK. In addition, absent distal glucose reabsorption may further facilitate P-i reclamation at these sites.