Purpose of reviewThe aim of this article is to review the most recent development on the reversibility of secondary hyperparathyroidism after kidney transplantation. A successful kidney transplantation is expected to correct the abnormalities of mineral metabolism that during uremia lead to secondary hyperparathyroidism. Kidney transplanted patients might, however, still present persistent hyperparathyroidism and hypercalcemia. In order to improve the understanding of the fate of secondary hyperparathyroidism after kidney transplantation an experimental model on reversal of uremia by an experimental isogenic kidney transplantation was established.Recent findingsIn recent years clinical and experimental studies have suggested an important role of the calcium sensing receptor and vitamin D receptor in the parathyroid glands for the abnormal regulation of parathyroid hormone secretion and parathyroid cell proliferation in uremia. The expression of these receptors is diminished in the parathyroid glands of uremic patients with severe secondary hyperparathyroidism and in experimental models of uremic rats on a high phosphorus diet. Secondary hyperparathyroidism is reversed rapidly by reversal of uremia by an experimental kidney transplantation in the rat. Despite normalization of the circulating parathyroid hormone levels, diminished expression of parathyroid calcium sensing and vitamin D receptor messenger RNA persist. Implantation of several isogenic parathyroid glands into a single rat results in a transient, short lasting period of hypercalcemia followed by normalization of parathyroid hormone and plasma calcium levels, despite persistent increased parathyroid mass.SummaryAdvances are clearly being made in the understanding of the molecular mechanisms of disturbed parathyroid function in uremia. How the hyperplastic uremic parathyroid glands are regulated after reversal of uremia by kidney transplantation remains, however, to be elucidated.