Vitamin D receptor and PCNA expression in severe parathyroid hyperplasia of uremic patients

Objective To clarify the role of vitamin D receptor (VDR) expression in par athyroid proliferation and resistance of parathyroid glands to 1,25(OH)(2)D -3 with secondary hyperparathyroidism (SHPT). Methods This study used archive parathyroid with 7 uremic patients. The exp ression of proliferation cell nuclear antigen (PCNA) and VDR was evaluated in nineteen-surgically excised parathyroid tissues, including 11 diffuse hy perplasia (DH-type) and 8 nodular hyperplasia (NH-type) of parathyroid glan ds, 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 r ate of PCNA was remarkably increased in parathyroid hyperplasia with SHPT c ompared with that in control group [(6.35 +/- 3.36)parts per thousand vs (1 .73 +/- 1.31)parts per thousand, 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 parat hyroid 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 w eight 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 de nsity and the weight of the parathyroid, and this may contribute to the pro gression of SHPT. Furthermore, VDR deficiency may cause the resistance of p arathyroid cells to 1, 25(OH)(2)D-3, in part.