title: Uremic toxin and bone metabolism.
abstract: Patients with end-stage renal disease (ESRD) develop various kinds of abnormalities in bone and mineral metabolism, widely known as renal osteodystrophy (ROD). Although the pathogenesis of ESRD may be similar in many patients, the response of the bone varies widely, ranging from high to low turnover. ROD is classified into several types, depending on the status of bone turnover, by histomorphometric analysis using bone biopsy samples [1,2]. In the mild type, bone metabolism is closest to that of persons with normal renal function. In osteitis fibrosa, bone turnover is abnormally activated. This is a condition of high-turnover bone. A portion of the calcified bone loses its lamellar structure and appears as woven bone. In the cortical bone also, bone resorption by osteoclasts is active, and a general picture of bone marrow tissue infiltration and the formation of cancellous bone can be observed. In osteomalacia, the bone surface is covered with uncalcified osteoid. This condition is induced by aluminum accumulation or vitamin D deficiency. The mixed type possesses characteristics of both osteitis fibrosa and osteomalacia. The bone turnover is so markedly accelerated that calcification of the osteoid cannot keep pace. In the adynamic bone type, bone resorption and bone formation are both lowered. While bone turnover is decreased, there is little osteoid. The existence of these various types probably accounts for the diversity in degree of renal impairment, serum parathyroid hormone (PTH) level, and serum vitamin D level in patients with ROD. However, all patients share a common factor, i.e., the presence of a uremic condition.
authors.affiliation: Department of Health Sciences, Oita University of Nursing and Health Sciences, 2944-9 Megusuno, Oita, 870-1201, Japan.
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Iwasaki
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Yamato
authors.forename: Tomoko
authors.initials: T
authors.lastname: Nii-Kono
authors.forename: Ayako
authors.initials: A
authors.lastname: Fujieda
authors.forename: Motoyuki
authors.initials: M
authors.lastname: Uchida
authors.forename: Atsuko
authors.initials: A
authors.lastname: Hosokawa
authors.forename: Masaru
authors.initials: M
authors.lastname: Motojima
authors.forename: Masafumi
authors.initials: M
authors.lastname: Fukagawa
mesh_terms: D000535:Aluminum / Q000378:metabolism; D001847:Bone Diseases / Q000378:metabolism; D001862:Bone Resorption; D001842:Bone and Bones / Q000378:metabolism*; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000473:pathology*; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D007200:Indican / Q000378:metabolism; D010002:Osteitis Fibrosa Cystica / Q000473:pathology; D053244:Osteoprotegerin; D010281:Parathyroid Hormone / Q000097:blood; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D014118:Toxins, Biological; D014511:Uremia / Q000378:metabolism / Q000473:pathology*; D014807:Vitamin D / Q000378:metabolism
chemical_list: D006023:Glycoproteins; D053244:Osteoprotegerin; D010281:Parathyroid Hormone; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C506030:TNFRSF11B protein, human; D014118:Toxins, Biological; D014807:Vitamin D; D000535:Aluminum; D007200:Indican