Renal handling of phosphate following release of ureteral obstruction.

The handling of phosphate by the kidney following release of unilateral ureteral obstruction (UUO) was investigated in intact and thyroparathyroidectomized (TPTX) dogs, and compared to that in the kidney following unilateral release of bilateral ureteral obstruction (BUO). By contrast to the kidney after release of BUO, the kidney following release of UUO showed a much lower fractional excretion (FE) of phosphate in TPTX animals (BUO 21.5 +/- 6.8%; UUO 1.3 +/- 0.5%) and a blunted phosphaturic response to PTH (BUO delta + 25.8%; UUO delta + 2.6%). Administration of cyclic AMP, prostaglandin synthetase inhibitors and ammonium chloride failed to correct the hypophosphaturia or the blunted response to PTH. Raising the filtered load of phosphate, however, raised the FE of phosphate in TPTX dogs in the kidney after release of UUO to levels comparable to those in BUO (BUO 21.5 +/- 6.8%; UUO 21.8 +/- 5.1%) and restored the responsiveness to PTH (BUO 49.0 +/- 8.2%; UUO 39.7 +/- 10%). When reabsorptive capacity (RC) was calculated during stepwise increments of serum phosphate, an additional difference was identified between the kidney after release of UUO on the one hand, and the control kidney and the kidney after release of BUO on the other: RC for phosphate was 294 +/- 66 micrograms/min . kg in UUO, 130 +/- 16 micrograms/min . kg in control, and 62 +/- 19 micrograms/min . kg in BUO. It is concluded that, in addition to the role of reduced filtered load of phosphate, an increased capacity to reabsorb phosphate is responsible in part for the hypophosphaturia observed in the kidney following release of UUO.