腎と骨代謝 Vol.27 No.2(7)


特集名 骨と多臓器連関
題名 骨と腎
発刊年月 2014年 04月
著者 高橋 浩雄 東海大学医学部腎内分泌代謝内科
著者 角田 隆俊 東海大学医学部腎内分泌代謝内科
著者 深川 雅史 東海大学医学部腎内分泌代謝内科
【 要旨 】 腎臓はCaやPを尿中に排泄する一方,活性型ビタミンDの産生臓器として,腸管でのCa吸収や骨代謝の維持にも関与している.このため,慢性腎臓病(CKD)患者では,1,25(OH)2D低下やP蓄積に加え骨病変,ミネラル代謝異常が出現する.この病態はおもに骨病変に着目され,腎性骨異栄養症として認識されてきた.
CKDの血管石灰化はCa,Pの過飽和に伴い石灰沈着が血管壁に析出することがおもな要因と考えられていた.近年,複数の観察研究により,この病態が血管石灰化を介して死亡リスクの増大に関与していることが示された.データの蓄積を背景に「慢性腎臓病に伴う骨ミネラル代謝異常(CKD-MBD)」という全身性疾患としての概念を創出し,管理も生命予後をアウトカムとして行われるようになった.CKD-MBDとは(1) Ca,P,PTHなどの検査値異常,(2) 骨の異常,(3) 血管石灰化の三つの異常で構成される.
Theme The multifaced role of bone for multisystem illness
Title Kidney, bone and CKD-MBD
Author Hiroo Takahashi Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine
Author Takatoshi Kakuta Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine
Author Masafumi Fukagawa Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine
[ Summary ] The kidneys play an important role in mineral metabolism. In addition to being a target organ for various hormones involved in calcium and phosphorus metabolism, the kidneys are the primary organ activating vitamin D.
SHPT is a common complication of CKD, characterized by persistently elevated levels of PTH and parathyroid hyperplasia.
It develops early in the course of CKD as an adaptive response to altered mineral homeostasis due to decreased kidney function, i.e., hyperphosphatemia, hypocalcemia, and 1,25(OH)2D deficiency.
In the last decade, it has become widely accepted that improper mineral metabolism in patients with CKD results not only in association with bone disease, but also a higher risk of cardiovascular disease and reduced survival rates, through the development of vascular calcification. This has led to a proposal for a new concept, termed "CKD-mineral and bone disorder". CKD-MBD is a systemic condition that manifests as abnormalities in PTH, calcium, phosphorus and vitamin D levels, bone abnormalities and extraskeletal calcification. Because this is a systemic disease, management of these abnormalities should ultimately be aimed at reducing the risk of cardiovascular events, bone fractures and extending survival rates.
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