The dilemma of parathyroidectomy in chronic renal failure

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Abstract
Our understanding of the pathogenesis of the secondary hyperparathyroidism of uremia is steadily evolving. New findings have been made and new interpretations provided as to the interaction between calcium, phosphorus, and calcitriol with the parathyroid gland cell, including the discovery of a calcium-sensing receptor in the parathyroid gland, the description of heterogenous distribution of the vitamin D receptor across the parathyroid gland, and the observation of a high prevalence of monoclonal, tumorlike growth of parathyroid tissue. These findings must be integrated into our current way of thinking with respect to the mechanisms involved in parathyroid hyperplasia, and to the potential practical consequences in terms of treatment and prevention. The development of new nonhypercalcemic vitamin D derivatives and specific calcium receptor agonists may help to elaborate more efficient treatment schedules. On the other hand, the occurrence of monoclonal parathyroid growth probably explains, at least in part, the frequently observed resistance to medical treatment. In such patients with severe secondary hyperparathyroidism, surgical parathyroidectomy often remains the only therapeutic alternative.

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