Reversal of hyperparathyroidism in response to dietary phosphorus restriction in the uremic dog

Reversal of hyperparathyroidism in response to dietary phosphorus restriction in the uremic dog. The role of phosphorus in the genesis of uremic hyperparathyroidism is well established. Prophylactic reduction of dietary phosphorus intake (PRS-P) in exact proportion to GFR reduction prevents renal hyperparathyroidism, but its effects on established hyperparathyroidism, serum calcium and phosphate concentration, and phosphorus balance are not known. Seven chronically uremic dogs (2 to 5 months) were housed in metabolic cages and maintained on a controlled phosphorus intake of 1,200 mg/day. After a control period of 10 days, the dogs were subjected to PRS-P. Control GFR averaged 16 ± 4 ml/min; serum phosphate concentration (SP), 4.3 ± 0.2 mg/dl; serum ionized calcium concentration (SICa), 4.67 ± 0.29 mg/dl; parathyroid hormone level (PTH), 610 ± 91 µl · Eq/ml; and 24-hr urine phosphate excretion (UPO4V), 845 ± 84 mg. During PRS-P, no change in GFR or SP occurred (17 ml/min and 4.3 mg/dl, respectively). SICa increased significantly by day 2 and plateaued by day 4 at 5.13 ± 0.20 mg/dl. PTH fell progressively over the 16 days of PRS-P to 170 ± 49 µl · Eq/ml. UPO4V fell on day 1 of PRS-P and plateaued by day 2. Stool phosphorus excretion averaged 43% of intake. Total phosphorus excretion (urine plus stool) did not differ significantly from measured intake. Tubular maximum phosphate reabsorption/GFR averaged 2.7 ± 0.4 mg/100 ml before PRS-P and increased significantly to 4.9 ± 0.2 mg/100 ml after 18 days of PRS-P. In summary, dietary therapy with PRS-P appears to be an effective method, not only for preventing uremic hyperparathyroidism, but for reversing established uremic hyperparathyroidism. In view of the growing evidence that PTH may be a major “uremic toxin”, PRS-P could represent an important element in the future therapy of chronic renal failure. Réversion de l'hyperparathyroicarondisme en réponse à la restriction alimentaire de phosphate chez le chien urémique. Le rôle du phosphore dans la génèse de l'hyperparathyroicarondisme est bien établi. La réduction prophylactique de l'apport alimentaire de phosphore (PRS-P) dans la même proportion que celle du débit de filtration glomérulaire empêche l'hyperparathyroicaron;disme mais son effet sur l'hyperparathyroicaron;disme installé, sur les concentrations plasmatiques de calcium et de phosphore et sur le bilan de phosphore, ne sont pas connus. Sept chiens urémiques chroniques (2 à 5 mois) ont été installés dans