[Role of phosphorus in hyperparathyroidism secondary to non-dialysed adult chronic renal insufficiency]

Abstract

Secondary hyperparathyroidism (HPT II) occurs early in the course of chronic renal failure (CRF), mainly because of decreased calcitriol levels, low levels of serum calcium, retention of phosphorus, abnormal parathyroid gland function and hyperplasia, and peripheral resistance to the action of parathormone (PTH). Amongst these factors, phosphorus retention plays a crucial role in moderate and advanced CRF, by inhibiting renal calcitriol synthesis, lowering serum calcium levels and stimulating PTH secretion. In patients with mild CRF, phosphorus restriction prevents the development of HPT II by increasing renal calcitriol secretion. In patients with advanced CRF, the suppressive effect of phosphorus restriction may be obtained independent of any changes in plasma calcitriol levels, suggesting a direct effect of phosphorus on parathyroid function. Phosphorus restriction should be used in the early stages of CRF, together with a sufficient intake of calcium in the form of phosphorus chelating salts. When phosphorus and calcium serum concentrations are normalised but PTH levels are not in the target range, 1 alpha hydroxy vitamin D3 derivatives may be used, with a careful monitoring to avoid high serum levels of phosphorus or calcium.