RODRIGO BUENO DE OLIVEIRA
Projetos de Pesquisa
Unidades Organizacionais
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina
5 resultados
Resultados de Busca
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bookPart Litíase renal(2013) OLIVEIRA, Rodrigo Bueno- Disturbances of Wnt/beta-catenin pathway and energy metabolism in early CKD: effect of phosphate binders(2013) OLIVEIRA, Rodrigo B. de; GRACIOLLI, Fabiana G.; REIS, Luciene M. dos; CANCELA, Ana L. E.; CUPPARI, Lilian; CANZIANI, Maria E.; CARVALHO, Aluizio B.; JORGETTI, Vanda; MOYSES, Rosa M. A.Mineral bone disorder (MBD) is an early complication of chronic kidney disease (CKD), with complex interactions in the bonekidneyenergy axis. These events lead to impaired bone remodelling, which in turn is associated with cardiovascular disease. Recently, we reported on a positive effect of phosphate binder treatment on bone remodelling markers and a reduction in serum FGF-23 levels in predialysis-CKD patients. The goal of the present study of this trial was to examine the effects of phosphate binders on energy-regulating hormones and Wnt pathway. In this present post hoc analysis of the above randomized, open-label, 8-week trial, which compared the effects of increasing doses of sevelamer-HCl or calcium acetate on various CKD-MBD parameters in 40 normophosphatemic CKD Stage 34 patients, we measured serum sclerostin, Dickkopf-1, leptin, adiponectin and serotonin concentrations. Serum sclerostin, Dickkopf-1 and leptin were elevated at baseline despite normal calcium, phosphorus levels and daily urinary phosphorus excretion. There were significant and positive correlations between sclerostin and FGF-23, as well between leptin and Dickkopf-1. Treatment with both phosphate binders led to a significant decrease in phosphate overload. However, sevelamer-HCl, but not with calcium acetate, led to a significant decrease in serum FGF-23, sclerostin and leptin, and to a significant increase in bone alkaline phosphatase levels. Early stages of CKD are associated with an impairment of the Wnt pathway, as reflected by elevated sclerostin, and a dysregulation of energy-regulating hormones. Many of these disturbances can be ameliorated by phosphate binder treatment, more with sevelamer-HCl than with calcium acetate.
bookPart Doença renal crônica(2013) OLIVEIRA, Rodrigo Bueno- Protocolo clínico e diretrizes terapêuticas para o tratamento do hiperparatireoidismo secundário em pacientes com doença renal crônica(2013) CUSTÓDIO, Melani Ribeiro; CANZIANI, Maria Eugênia Fernandes; MOYSÉS, Rosa Maria Affonso; BARRETO, Fellype Carvalho; NEVES, Carolina Lara; OLIVEIRA, Rodrigo Bueno de; KAROHL, Cristina; SAMPAIO, Elisa de Albuquerque; GUEIROS, José Edevanilson de Barros; JORGETTI, Vanda; CARVALHO, Aluízio Barbosa de
- Calcificação vascular em doença renal crônica: uma revisão(2013) OLIVEIRA, Rodrigo Bueno de; OKAZAKI, Hirokazu; STINGHEN, Andrea E. Marques; DRüEKE, Tilman B.; MASSY, Ziad A.; JORGETTI, VandaVascular calcification (VC), an independent and strong predictor of cardiovascular risk, is often found in CKD patients. The degree of VC is providing incremental prognostic value over traditional risk markers. There is interest in improving our understanding of mechanisms, establishing diagnostic methods and effective prevention and treatment modalities. The abnormal mineral metabolism of CKD is known to facilitate the progression of VC, in concert with altered activities of VC inhibitors. Possible measures to prevent VC include the control of serum calcium and phosphate as well as other factors involved in its progression, including vitamin D sterols, parathyroid hormone, fibroblast growth factor-23, klotho, and VC inhibitors. In addition, we discuss new possible therapeutic approaches to halt VC or reverse its progression. The principal aim of this review is to provide an updated overview of VC in patients with CKD, with particular focus on pathophysiology, diagnosis, prevention and treatment.