@article{oai:niigata-u.repo.nii.ac.jp:00024552,
 author = {渡辺, 繁子},
 issue = {10},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Oct},
 note = {Children with nephrotic syndrome are frequently at risk for osteodystrophy due to secondary hyperparathyroidism. Severe proteinuria is accompanied by loss of 25－OH－Vit. D3, which causes hyperparathyroidism following hypocalcemia. On the other hand, administred glucocorticoid suppresses protein synthesis in osteoblasts to cause osteoporosis, and disturbs absorption of calcium in the intestine, which also leads to hyperparathyroidism. In this study 66 children with nephrotic syndrome were examined to elucidate bone metabolism associated with proteinuria and glucocorticoid therapy. Children with nephrotic syndrome showed high free hydroxyproline in urine（a parameter of turnover of the bone）and high NcAMP（which correlates with PTH）, suggesting that administration of glucocorticoid for 1.5 to 2 months might cause secondary hyperparathyroidism. In children with nephrotic syndrome, the more glucocorticoid was given, the less bone mineral content was. These findings suggest that measurement of free Hyp and NcAMP, and analysis of bone construction with bone mineral analyzer or microdensitometer may be useful to estimate bone metabolism in children with nephrotic syndrome.},
 pages = {602--613},
 title = {特発性ネフローゼ症候群における骨代謝},
 volume = {100},
 year = {1986}
}