title: [Hypertension, CKD and bone metabolism].
abstract: The patients with "Hypertension" and "Chronic Kidney Disease (CKD) " are accompanied with an osteoporosis. In hypertension patients, excess urinary calcium secretion induces secondary parathyroidsim to increase serum calcium (Ca) level, which may lead to Ca release from bone. In this aspect, there are several reports that anti-hypertensive drugs, especially thiazides, increase bone mineral density and decrease the incidence of bone fracture. In addition, we demonstrated that renin-angiotensin system can be involved in the process of osteoporosis. Angiotensin II significantly induced the expression of RANKL (receptor activator of NF-κB ligand) in osteoblasts, leading to the activation of osteoclasts, while these effects were completely blocked by an Ang II type 1 receptor blockade. As for CKD, excess phosphorus (P) due to renal dysfunction induces secondary parathyroidism to decrease serum P level, which similarly leads to osteoporosis. Moreover, excess P can increase FGF23 expression and decrease activated vitamin D, which also resulted in progression of osteoporosis. Both "Hypertension" and "Chronic Kidney Disease (CKD) " are inducible factor to osteoporosis.
authors.affiliation: Division of Vascular Medicine and Epigenetics, Osaka University, United Graduate School of Child Development.
authors.forename: Hironori
authors.initials: H
authors.lastname: Nakagami
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Morishita
mesh_terms: D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D015519:Bone Density / Q000187:drug effects; D001842:Bone and Bones / Q000378:metabolism*; D002118:Calcium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D002908:Chronic Disease; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000378:metabolism; D050723:Fractures, Bone / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy / Q000378:metabolism*; D007674:Kidney Diseases / Q000150:complications* / Q000378:metabolism*; D010010:Osteoclasts; D010024:Osteoporosis / Q000209:etiology / Q000517:prevention & control*; D010758:Phosphorus / Q000378:metabolism; D053246:Receptor Activator of Nuclear Factor-kappa B / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology; D049971:Thiazides / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; C000717427:FGF23 protein, human; D053246:Receptor Activator of Nuclear Factor-kappa B; D049971:Thiazides; D010758:Phosphorus; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23; D002118:Calcium