Skeletal resistance to pth as a basic abnormality underlying uremic bone diseases.
Skeletal resistance to parathyroid hormone (PTH) was suggested initially as a mechanism of PTH hypersecretion in uremia. Because of the effective suppression of PTH by recently developed therapeutic modalities, this background abnormality has been uncovered and currently recognized as relative hypoparathyroidism in terms of its relation to bone turnover. Thus, PTH levels two to three times greater than normal are usually required to keep bone turnover normal in uremia. Recent studies suggested that PTH activity may be overestimated using the conventional intact PTH assay. In addition, several steps to osteoclastogenesis are suspected to be disturbed in uremia. Additional studies at cellular and molecular levels are needed to establish preventive and therapeutic modalities for this abnormality.
Fukagawa
M
M
Division of Nephrology and Dialysis Center, Kobe University School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. fukagawa@med.kobe-u.ac.jp
Kazama
J J
JJ
Shigematsu
T
T
D001862:Bone Resorption / Q000209:etiology / Q000378:metabolism*; D001842:Bone and Bones / Q000378:metabolism*; D018450:Disease Progression; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D006965:Hyperplasia; D053244:Osteoprotegerin; D010280:Parathyroid Glands / Q000378:metabolism / Q000473:pathology; D010281:Parathyroid Hormone / Q000378:metabolism*; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor; D014511:Uremia / Q000150:complications / Q000378:metabolism*
D006023:Glycoproteins; D053244:Osteoprotegerin; D010281:Parathyroid Hormone; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human