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Background: Persistent hyperparathyroidism in kidney transplant recipients may be prolonged for a few years, and in these cases, parathyroidectomy is indicated even if graft function is satisfactory. The aim of this study was to characterize the parathyroid glands in long-term dialysis recipients and determine the pathogenesis of persistent hyperparathyroidism., Methods: We analyzed 44 parathyroid glands resected from 11 patients who underwent parathyroidectomy after kidney transplantation. The histopathologic types and weights of all the parathyroid glands were evaluated., Results: The mean dialysis period was 15.8 years, and the time from kidney transplantation to parathyroidectomy ranged from 3.5 to 89 months. Nodular hyperplasia was present in parathyroid glands in all cases. The mean glandular weight was 396.0 ± 299.0 mg, and the maximum glandular weight was 3200 mg. Seven patients who underwent parathyroidectomy >1 year after kidney transplantation (late PT) were compared with 4 patients who underwent parathyroidectomy within 10 months after transplantation (early PT). The maximum (442.9 vs 1503 mg; P = .018) and mean (312.5 ± 177.4 mg vs 1135.6 ± 977.7 mg; P = .001) glandular weights were significantly lower in patients who underwent late PT compared with those who received early PT. Based on the histopathologic type and glandular weight of each parathyroid gland, nodular hyperplasia in glands ≤150 mg was common in patients who underwent late PT., Conclusions: The presence of nodular hyperplasia in parathyroid glands with a low weight may be involved in long-lasting persistent hyperparathyroidism in patients undergoing long-term dialysis., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Deceased donor kidney transplantation in long-term dialysis patients in Japan has been increasing because of a severe lack of donors. Parathyroid glands of long-term dialysis patients often show qualitative morphological changes from diffuse to nodular hyperplasia. Only a few studies have reported the clinicopathological analysis of persistent hyperparathyroidism after kidney transplantation in long-term (>10 years) dialysis patients. This study on consecutive deceased donor kidney transplantation performed from 2002 to 2010 measured biochemical parameters related to bone and mineral disorders and examined parathyroid tissues in parathyroidectomy cases. Thirty-four subjects (22 males; mean age, 53.8 ± 7.9 years; mean dialysis period, 14.4 ± 4.3 years) were enrolled. Multivariate analysis of potential predictors for the hypercalcemia group at 12 months after transplantation showed that pre-transplantation and early post-transplantation calcium and parathyroid hormone levels were significant determinants. Pathological examination showed that a number of glands showed nodular hyperplasia, even in small glands weighing < 100 mg. In long-term dialysis patients, hyperparathyroidism and hypercalcemia developed at an early stage after transplantation and persisted for a long period (>4 years), with nodular hyperplasia being found even in low-weight parathyroid glands. Pre-transplant high calcium and parathyroid hormone levels were the predictors for the prolonged hypercalcemia. Persistent hyperparathyroidism was considered to be caused by remaining nodular hyperplasia, even if the glands were small. Although the best treatment option is to perform a parathyroidectomy in the waiting period before transplantation, we suggest that it be performed in cases with prolonged hypercalcemia of >6 months after transplantation., (© 2013 The Authors. Therapeutic Apheresis and Dialysis © 2013 International Society for Apheresis.)

Background: Whether bone mineral density (BMD) is improved at 5 years after parathyroidectomy (PTx) for secondary hyperparathyroidism (SHPT) remains unknown., Objective: To investigate BMD after PTx by dual energy X-ray absorptiometry (DXA)., Methods: BMD was measured at the distal 1/3 of the radius (non-shunt side) and at the lumbar supine (L2-L4, lateral view) before and 5 years after PTx in 35 hemodialysis patients who had undergone surgery from April 1994 to May 2004. The data were analyzed retrospectively., Results: Intact PTH decreased significantly from 1,100 ± 530 (range: 446 - 2,300) pg/ ml before PTx to 75 ± 68 (2 - 251) pg/ml at 5 years after PTx (p < 0.01). Before PTx, the radial BMD and lumbar BMD were both decreased -3.3 ± 1.9 SD and -1.3 ± 2.4 SD compared with the corresponding normal mean T-score, respectively. Radial BMD increased significantly from 0.522 ± 0.113 g/cm2 before PTx to 0.545 ± 0.114 g/cm2 (p = 0.01) at 5 years after PTx, while the T-score improved to -2.8 ± 2.0 SD. In contrast, lumbar BMD showed no significant change between before (0.734 ± 0.202 g/cm2) and 5 years after PTx (0.746 ± 0.199 g/cm2), and neither did the T-score (-1.1 ± 2.3 SD). None of the patients suffered any fractures during follow up., Conclusion: These findings indicate that maintaining iPTH at < 300 pg/ml for 5 years after PTx results in an increase of radial BMD in SHPT patients with preoperative BMD levels in the osteoporosis range (below -2.5 SD) according to the WHO, as well as stabilizing lumbar BMD.

We trace the 34-year history of a member of the first Japanese family in which lecithin-cholesterol acyltransferase (LCAT) deficiency was diagnosed. Marriage between cousins with low LCAT activity was responsible for familial LCAT deficiency (FLD). In 1976, a 27-year-old Japanese man was noted to have FLD based on proteinuria, hematuria, grayish corneal opacity and low LCAT activity (9.83%). Genetic analysis showed insertion of G-G-C coding glycine at codon 141. Total cholesterol (C) was low at 108 mg/dl and the ratio of C-ester to total C was very low (12%), while the lecithin (phosphatidylcholine) level was very high (97.3%). When his serum creatinine reached 2.6 mg/dl at the age of 41 years (in 1991), renal biopsy was performed. This showed expansion of the mesangial matrix and irregularly thickened capillary walls with a bubble-like appearance because of lipid deposits consisting of two components (partly lucent vacuolated areas and partly deeply osmiophilic areas). Magnification of the latter deposits showed curvilinear and serpiginous striated membranous structure. Hemodialysis was started in 1990 and has been continued for over 20 years until August 2010. Clinical problems have included AV shunt failure requiring 4 operations and 13 percutaneous transcatheter angioplasty procedures, as well as episodes of hemolytic anemia that subsided after infusion of fresh frozen plasma. Cardiovascular events have not yet occurred, although severe calcification of abdominal aorta has been detected by computed tomography.

Background: Cinacalcet treatment for secondary hyperparathyroidism (SHPT) has demonstrated parathyroid size regression and morphological changes, such as cystic degeneration and hypovascularisation, on ultrasonography. However, there have been very few reports regarding the histopathological alterations of hyperplastic parathyroid glands in patients with SHPT after administration of cinacalcet. The aim of this study was to elucidate the effects of cinacalcet for histopathological alterations on the parathyroid glands., Methods: A total of 92 hyperplastic parathyroid glands were obtained from 24 dialysis patients with severe SHPT who underwent total parathyroidectomy and were enrolled in this study. Patients were divided into those treated with and without cinacalcet (cinacalcet group and conventional group, respectively; both n=12). The areas of oxyphil cells, cystic degeneration, haemorrhagic changes and haemosiderin deposition were assessed semiquantitatively., Results: Total maximal parathyroid gland weight and maximal-to-minimal parathyroid gland weight ratio were significantly higher in the cinacalcet group compared with the conventional group (1798.7±1658.3 mg vs 764.2±471.1 mg, p=0.018, 15.8±13.9 vs p=0.047, 6.6±4.2, respectively). Significant increases were observed in oxyphil cell area (61.7%±17.1% vs 36.7%±15.6%, p=0.001) and haemosiderosis score (1.50±1.24 vs 0.42±0.51, p=0.029) in the former rather than the latter group., Conclusions: These results suggest that cinacalcet may induce specific qualitative alterations of hyperplastic parathyroid glands in patients with severe SHPT.