Parathyroid growth and regression in experimental uremia

Taniguchi, Masatomo; Tokumoto, Masanori; Matsuo, Dai; Tsuruya, Kazuhiko; Hirakata, Hideki; Iida, Mitsuo

doi:10.1038/sj.ki.5000090

Cited by 23 publications

(22 citation statements)

References 33 publications

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“…The present ultrastructural examination clarified these cellular changes morphologically. A similar effect of calcitriol has been reported [20], but was not evident in the present study.…”

Section: Discussionsupporting

confidence: 73%

Development and Prevention of Morphologic and Ultrastructural Changes in Uremia-induced Hyperplastic Parathyroid Gland

Shiizaki

Hatamura

Mato

et al. 2011

Ultrastructural Pathology

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The detailed ultrastructural changes of uremia-induced hyperplastic parathyroid gland and the effects of current medical treatments for secondary hyperparathyroidism were investigated. Marked enlargement of parathyroid cell with accumulation of mitochondria and lipids and a significant increase in the thickness of the pericapillary area with increased fibrosis and appearance of fibroblast like cells were noted in the hyperplastic gland caused by uremia and phosphate retention. These ultrastructural changes and biochemical findings indicating hyperparathyroidism were significantly suppressed by all of the treatment using phosphate restriction, calcitriol, and cinacalcet. The characteristic ultrastructural changes, including the morphologic evidence of nodule formation, were indicated.

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“…The present ultrastructural examination clarified these cellular changes morphologically. A similar effect of calcitriol has been reported [20], but was not evident in the present study.…”

Section: Discussionsupporting

confidence: 73%

Development and Prevention of Morphologic and Ultrastructural Changes in Uremia-induced Hyperplastic Parathyroid Gland

Shiizaki

Hatamura

Mato

et al. 2011

Ultrastructural Pathology

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“…The induction of apoptosis in parathyroid cells, as well as the upregulation of VDR and calcium-sensing receptor, by vitamin D therapy, has also been demonstrated in model animals. 39,40 Calcimimetic agents suppress parathyroid function through calcium-sensing receptors. 41 As the development of parathyroid hyperplasia was prevented by dietary calcium supplement in VDR-ablated mice, 42 it is possible that calcium signals may stimulate an independent pathway to control parathyroid function, including cell proliferation.…”

Section: Development Of Parathyroid Hyperplasia In Ckdmentioning

confidence: 99%

Regulation of parathyroid function in chronic kidney disease (CKD)

et al. 2006

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In chronic kidney disease (CKD), several abnormalities in bone and mineral metabolism develop in the majority of patients. The parathyroid plays a very important role in regulating bone and mineral metabolism; thus, control of parathyroid function is one of the main targets of the management of CKD-mineral and bone disorder (CKD-MBD). In the development of secondary hyperparathyroidism, it has recently been suggested that fibroblast growth factor 23 (FGF23) plays a crucial role, both as a phosphaturic factor and as a suppressor of active vitamin D (1,25D) production in the kidney. FGF23 is originally secreted to prevent hyperphosphatemia in CKD, but this occurs at the expense of low 1,25D and hyperparathyroidism ("trade-off" hypothesis revisited). Furthermore, recent data suggest that FGF23 could be another useful marker for the prognosis of hyperparathyroidism, because a high serum level may reflect the cumulative dose of vitamin D analogues previously administered. We have also demonstrated that severe hyperparathyroidism was associated with the production and secretion of a new form of parathyroid hormone (PTH) molecule, which can be detected by third-generation assays for PTH, but not by the second-generation assays. For the regression of already established nodular hyperplasia, the more advanced type of parathyroid hyperplasia, it is certainly necessary, in the near future, to develop new agents that specifically induce apoptosis in parathyroid cells. Until such agents are developed, prevention and early recognition of nodular hyperplasia is mandatory for the effective and safe management of hyperparathyroidism in CKD.

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“…Calcitriol has shown to decrease cell proliferation and increase apoptosis restoring the levels of CaSR and VDR, leading to a regression of the parathyroid hyperplasia in uremic rats [78]. The direct injection of calcitriol or other vitamin D analogues into hyperplasic glands has also been able to induce cell apoptosis, suggesting this could be a valid, alternative method to reduce the size of the parathyroid gland [79].…”

Section: Contribution Of the In Vivo Animal Modelsmentioning

confidence: 98%