RANKL Is a Mediator of Bone Resorption in Idiopathic Hypercalciuria

• Grant number: 09/01269-8
• Support Opportunities: Regular Research Grants - Publications - Scientific article
• Start date: April 01, 2009
• End date: September 30, 2009
• Field of knowledge: Health Sciences - Medicine - Medical Clinics
• Principal Investigator: Ita Pfeferman Heilberg
• Grantee: Ita Pfeferman Heilberg
• Host Institution: Departamento de Medicina. Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Background and objectives: This study aimed to determine the expression of osteoprotegerin, receptor activator of nuclearfactor B ligand, interleukin-1, transforming growth factor-, and basic fibroblast growth factor in stone-forming patientswith idiopathic hypercalciuria.Design, setting, participants, & measurements: Immunohistochemical analysis was performed in undecalcified bonesamples previously obtained from 36 transiliac bone biopsies of patients who had idiopathic hypercalciuria and whosehistomorphometry had shown lower bone volume, increased bone resorption, and prolonged mineralization lag time.Results: Bone expression of receptor activator of nuclear factor B ligand and osteoprotegerin was significantly higher inpatients with idiopathic hypercalciuria versus control subjects. Transforming growth factor- immunostaining was lower inpatients with idiopathic hypercalciuria than in control subjects and correlated directly with mineralization surface. Interleukin-1 and basic fibroblast growth factor staining did not differ between groups. Receptor activator of nuclear factor B ligandbone expression was significantly higher in patients who had idiopathic hypercalciuria and exhibited higher versus normalbone resorption.Conclusion: A higher expression of receptor activator of nuclear factor B ligand in bone tissue suggests that increased boneresorption in patients with idiopathic hypercalciuria is mediated by receptor activator of nuclear factor B ligand. Osteoprotegerinbone expression might have been secondarily increased in an attempt to counteract the actions of receptor activator ofnuclear factor B ligand. The low bone expression of transforming growth factor- could contribute to the delayed mineralizationfound in such patients (AU)