We measured nephrogenous cyclic adenosine monophosphate (NcAMP) excretion, an in vivo bioassay for endogenous parathyroid hormone (PTH) secretion, and renal phosphate threshold (TmP/GFR) in 33 renal allograft recipients with stable renal function (creatinine clearance greater than or equal to 60 ml/min/1.73 m2 body surface area, 6 months or more post-transplant) and in 9 kidney donors. Sixteen patients had normal parathyroid function, 8 had hypercalcemic hyperparathyroidism and 9 had normocalcemic hyperparathyroidism; the latter were apparently resistant to the hypercalcemic actions of endogenous PTH, but the cause for this was not apparent. In all four subject groups, TmP/GFR was significantly and similarly lower (by 0.8-1.0 mg/dl) than predicted by multiple regression on age, sex, corrected plasma calcium and NcAMP (determined in 306 subjects spanning a wide range of parathyroid function) indicating a major PTH-independent mechanism for reducing phosphate reabsorption in the presence of a single kidney. In all four groups the contribution of this mechanism to the observed depression of TmP/GFR was substantially greater than the contribution of increased PTH secretion. In all groups, but more so in the recipients than in the donors, fasting urinary phosphate excretion/GFR was increased, so that fasting plasma phosphate, although reduced, did not accurately reflect the severity of the defect in phosphate reabsorption. We conclude that the dominant mechanism for the adaptive decrease in renal tubular phosphate transport in response to nephron reduction does not require the participation of PTH and is manifest in the presence of fasting hypophosphatemia.