X Wang1, B Sun, F Zhou, J Hu, X Yu, T Peng. 1. Department of Nephrology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
Abstract
OBJECTIVE: To clarify the role of vitamin D receptor (VDR) expression in parathyroid proliferation and resistance of parathyroid glands to 1,25(OH)2D3 with secondary hyperparathyroidism (SHPT). METHODS: This study used archive parathyroid with 7 uremic patients. The expression of proliferation cell nuclear antigen (PCNA) and VDR was evaluated in nineteen-surgically excised parathyroid tissues, including 11 diffuse hyperplasia (DH-type) and 8 nodular hyperplasia (NH-type) of parathyroid glands, by immunohistochemistry (avidin-biotin complex method). RESULTS: The weight of parathyroid in SHPT was remarkably increased by 16.1 times. The numbers of parathyroid cells were increased by 1.86 times. The rate of PCNA was remarkably increased in parathyroid hyperplasia with SHPT compared with that in control group [(6.35 +/- 3.36)@1000 vs (1.73 +/- 1.31)@1000, P < 0.001]. The number of PCNA in DH-type was lower than that in NH-type (P < 0.001). The density of VDR in the parathyroid with SHPT was significantly decreased [(40.28 +/- 13.13)% vs (83.79 +/- 3.77)%, P < 0.001], VDR immunoreactivity expression in NH-type was lower than that in DH-type [(27.14 +/- 4.12)% vs (49.84 +/- 7.33)%, P < 0.001]. A significantly negative correlation was found between VDR density and the weight of the parathyroid (r = -0.46, P < 0.05), the same as VDR and PCNA (r = -0.75, P < 0.001). CONCLUSION: VDR density was significantly decreased in parathyroid tissue of uremic patients showing nodular hyperplasia compared with that in diffuse hyperplasia and there was significantly negative correlation between VDR density and the weight of the parathyroid, and this may contribute to the progression of SHPT. Furthermore, VDR deficiency may cause the resistance of parathyroid cells to 1,25(OH)2D3, in part.
OBJECTIVE: To clarify the role of vitamin D receptor (VDR) expression in parathyroid proliferation and resistance of parathyroid glands to 1,25(OH)2D3 with secondary hyperparathyroidism (SHPT). METHODS: This study used archive parathyroid with 7 uremic patients. The expression of proliferation cell nuclear antigen (PCNA) and VDR was evaluated in nineteen-surgically excised parathyroid tissues, including 11 diffuse hyperplasia (DH-type) and 8 nodular hyperplasia (NH-type) of parathyroid glands, by immunohistochemistry (avidin-biotin complex method). RESULTS: The weight of parathyroid in SHPT was remarkably increased by 16.1 times. The numbers of parathyroid cells were increased by 1.86 times. The rate of PCNA was remarkably increased in parathyroid hyperplasia with SHPT compared with that in control group [(6.35 +/- 3.36)@1000 vs (1.73 +/- 1.31)@1000, P < 0.001]. The number of PCNA in DH-type was lower than that in NH-type (P < 0.001). The density of VDR in the parathyroid with SHPT was significantly decreased [(40.28 +/- 13.13)% vs (83.79 +/- 3.77)%, P < 0.001], VDR immunoreactivity expression in NH-type was lower than that in DH-type [(27.14 +/- 4.12)% vs (49.84 +/- 7.33)%, P < 0.001]. A significantly negative correlation was found between VDR density and the weight of the parathyroid (r = -0.46, P < 0.05), the same as VDR and PCNA (r = -0.75, P < 0.001). CONCLUSION:VDR density was significantly decreased in parathyroid tissue of uremic patients showing nodular hyperplasia compared with that in diffuse hyperplasia and there was significantly negative correlation between VDR density and the weight of the parathyroid, and this may contribute to the progression of SHPT. Furthermore, VDR deficiency may cause the resistance of parathyroid cells to 1,25(OH)2D3, in part.