On the prevention of secondary hyperparathyroidism in experimental chronic renal disease using “proportional reduction” of dietary phosphorus intake

On the prevention of secondary hyperparathyroidism in experimental chronic renal disease. Secondary hyperparathyroidism in chronic renal disease appears to begin with the first phase of nephron destruction and to progress in severity with advancing nephron loss. If phosphorus (P) intake remains constant during the evolution of chronic renal disease, each time that glomerular filtration rate (GFR) decreases, a transient period of P retention will follow. The ionized calcium concentration presumably will fall under these circumstances and the latter will stimulate the parathyroid glands. To prevent the development of secondary hyperparathyroidism, studies were performed in a group of seven dogs in which P intake was decreased in the diet proportionally to the decrease in GFR. P intake initially was 1200 mg/ 24 hrs and gradually was decreased to a mean of 234±15.7 mg/ 24 hrs. In control studies mean GFR was 56 ml/min and tubular reabsorption of phosphorus (TRP), 95 %. As GFR was decreased progressively to a mean of 12 ml/min, TRP remained at 92%. Parathyroid hormone (PTH) levels averaged 43 ± 4.6 µl equivalents per ml in the control phase and 45 ± 4.6 µl Eq/ml in the final phase of the study. These data provide support for the view that the adaptation in P excretion imposed by a constant P intake and a decreasing nephron population plays an important role in the pathogenesis of secondary hyperparathyroidism. Moreover, they suggest that if the necessity for the adaptation is obviated, hyperparathyroidism may be prevented, at least until the onset of vitamin D resistance