Bone morphometric analysis of bone lesions in primary hyperparathyroidism that has progressed to end-stage renal failure

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Bone morphometric analysis of bone lesions in primary hyperparathyroidism that has progressed to end-stage renal failure

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Co-author 1

Shoya Taniguchi shoya0815@outlook.jp Toranomon hospital,Kajigaya Nephrology Center Kanagawa Japan *

Co-author 2

Yuki Oba pugpug.yuki008@gmail.com Toranomon hospital,Kajigaya Nephrology Center Kanagawa Japan -

Co-author 3

Hiroki Mizuno hilomiz@yahoo.co.jp Toranomon hospital,Kajigaya Nephrology Center Kanagawa Japan -

Co-author 4

Akinari Sekine akinari-s@toranomon.gr.jp Toranomon hospital Nephrology Center Tokyo Japan -

Co-author 5

Masahiko Yamanouchi yamanouchi.masayuki@gmail.com Toranomon hospital,Kajigaya Nephrology Center Kanagawa Japan -

Co-author 6

Eiko Hasegawa eiko-hase@hotmail.co.jp Toranomon hospital Nephrology Center Tokyo Japan -

Co-author 7

Tatsuya Suwabe suwabetat@yahoo.co.jp Toranomon hospital,Kajigaya Nephrology Center Kanagawa Japan -

Co-author 8

Takehiko Wada takewada@gmail.com Toranomon hospital Nephrology Center Kanagawa Japan -

Co-author 9

Yoshihumi Ubara yoshifumiubara@gmail.com Toranomon hospital,Kajigaya Nephrology Center Kanagawa Japan -

Co-author 10

Naoki Sawa naokis@toranomon.gr.jp Toranomon hospital,Kajigaya Nephrology Center Kanagawa Japan -

Co-author 11

Kei Kono k.kono0317@gmail.com Toranomon hospital Department of Pathology Tokyo Japan -

Co-author 12

Yutaka Takazawa yutakazawa@toranomon.gr.jp Toranomon hospital Department of Pathology Tokyo Japan -

Co-author 13

Co-author 14

Co-author 15

Introduction

原発性副甲状腺機能亢進症は、副甲状腺ホルモン（PTH）の過剰産生を特徴とし、血清カルシウム値の上昇につながります。高カルシウム血症の長期化は腎結石を引き起こすことがよく知られており、腎機能障害の原因となることが報告されています。

Methods

59歳の男性が、高カルシウム血症を伴う末期腎不全の精密検査のために来院しました。過去10年間、血清カルシウム値は10 mg/dLを超えており、腰痛、胸痛、胸椎後弯症を経験していました。入院時の血清クレアチニンは6.4 mg/dLでしたが、血清カルシウムは上昇しており（10.3 mg/dL）、完全型副甲状腺ホルモンは有意に上昇していました（2837 pg/mL）。頭蓋骨X線検査では塩コショウ徴候、腰椎X線検査ではラガージャージー徴候が認められました。骨痛の精密検査のため、右腸骨の生検を行ないました。

Results

Cortical bone showed thinning associated with porosity, cancellous bone showed islanding due to bone loss, and the bone marrow had a high fat content. Some vigorous bone formation by osteoblasts was observed, but osteoclast-mediated bone resorption was predominant, suggesting osteoporosis with severe bone loss. Primary hyperparathyroidism was suspected as the underlying condition, so parathyroidectomy was performed. The largest gland weighed 6618 mg, corresponding to an adenoma, but the other three glands were smaller and showed multiple nodular hyperplastic lesions.

Conclusion

This case is a rare example of late diagnosis of primary hyperparathyroidism in a patient with end-stage renal failure and severe bone lesions.

Kewords