Changes in renal phosphate reabsorption in the aged rat

Depletion of inorganic phosphate (P-i) reserves occurs frequently in aged animals and can result in diminished hone mineralization and osteoporosis. This altered P-i balance results from a reduction in intestinal P-i absorption and an elevation in renal P-i excretion, Since the kidney plays a central role in maintaining P, homeostasis, we tested whether the increased phosphaturia seen with aging is a consequence of changes in the intrinsic tubular capacity to reabsorb P-i (TmPi). Male Wistar rats (12-, 18-, and 24-months-old) were acutely thyroparathyroidectomized (TPTX) and prepared for renal clearance studies in the presence and absence at fixed levels of parathyroid hormone (synthetic PTH-(1-34), 1U/kg/min). The maximum capacity for P-i transport (TmPi) was assessed by infusion of P-i at progressively higher rates (0-6 mu mol/min) to increase the filtered load of P-i and facilitate the determination of the TmPi. TmPi declined significantly with age (3.51 +/- 0.12 vs 3.04 +/- 0.19 vs 2.30 +/- 0.18 mu mol/ml, for 12- 18-, and 24-month-old rats, respectively, P < 0.05) in TPTX rats. Administration of PTH markedly reduced the TmPi in all age groups. Although the TmPi attained was similar among the age groups (1.15 +/- 0.13 vs 1.15 +/- 0.06 vs 1.03 +/- 0.09 mu mol/ml, for 12-, 18-, and 24-month-old rats, respectively), the magnitude of the reduction in the presence of PTH declined from 67% in 12-month-old rats to 62% and 55% in 18- and 24-month-old rats, respectively. These results demonstrate that aging is associated with a PTH-Independent decrease in the intrinsic capacity of the kidney to reabsorb phosphate. Further, the kidney of the aged rat can respond to a pharmacological dose of PTH with appropriate reductions in the TmPi although the magnitude of the response declines with age.