Secondary hyperparathyroidism, a common consequence of chronickidney disease, results from abnormal regulation of calciumand phosphate homeostasis. Three factors are central to itsdevelopment. The first, reduced renal synthesis of 1,25-dihydroxyvitaminD (calcitriol), emerges in the early stages of chronic kidneydisease. As the disease progresses, the second and the thirdfactors come into play: renal phosphate clearance and net calciumbalance become inadequate to maintain serum phosphorus and ionizedcalcium levels within an optimal range. The synthesis and releaseof parathyroid hormone are stimulated by a low serum calciumlevel, reduced inhibitory activity of calcitriol, and an elevated. . . [Full Text of this Article]
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From INSERM Unité 507 and the Service de Néphrologie, Hôpital Necker, Paris (T.B.D.); and the Department of Nutrition, University of California, Davis (D.A.M.).
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