RODRIGO BUENO DE OLIVEIRA
Projetos de Pesquisa
Unidades Organizacionais
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina
3 resultados
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- Pharmacotherapy of chronic kidney disease and mineral bone disorder(2011) BARRETO, Fellype Carvalho; OLIVEIRA, Rodrigo Azevedo de; OLIVEIRA, Rodrigo Bueno; JORGETTI, VandaIntroduction: Disturbances of the bone and mineral metabolism are a common complication of chronic kidney disease (CKD); these disturbances are known as CKD-mineral bone disorder (CKD-MBD). A better understanding of the pathophysiological mechanisms of CKD-MBD, along with its negative impact on other organs and systems, as well as on survival, has led to a shift in the treatment paradigm of this disorder. The use of phosphate binders changed dramatically over the last decade when noncalcium-containing phosphate binders, such as sevelamer and lanthanum carbonate, became possible alternative treatments to avoid calcium overload. Vitamin D receptor activators, such as paricalcitol and doxercalciferol, with fewer calcemic and phosphatemic effects, have also been introduced to control parathormone production and the interest in native vitamin D supplementation has grown. Furthermore, a new drug class, the calcimimetics, has recently been introduced into the therapeutic arsenal for treating secondary hyperparathyroidism. Areas covered: This review discusses the advantages and disadvantages of the above pharmacological options to treat CKD-MBD. Expert opinion: The individual-based use of phosphate binders, vitamin D and calcimimetics, separately or in combination, constitute a reasonable approach to treat CKD-MBD. These treatments aim to achieve a rigorous control of phosphorus and parathormone levels, while avoiding calcium overload.
- The quest for a better understanding of chronic kidney disease complications: an update on uremic toxins(2014) BARRETO, Fellype Carvalho; STINGHEN, Andréa Emilia Marques; OLIVEIRA, Rodrigo Bueno de; FRANCO, Ana Tereza Barufi; MORENO, Andréa Novais; BARRETO, Daniela Veit; PECOITS-FILHO, Roberto; DRüEKE, Tilman B.; MASSY, Ziad A.Chronic kidney disease is characterized by a progressive reduction of glomerular filtration rate and/or the appearance of proteinuria, and subsequently the progressive retention of organic waste compounds called uremic toxins (UT). Over the last decades, a large number of such compounds have been identified and their effects on organs and tissues, especially the cardiovascular system, has been demonstrated. In this review, we present the current classification of UT, as proposed by the EUTox Group, and the effects of some of the probably most important UTs, such as phosphate, FGF-23, PTH, AGEs, indoxyl sulfate and para-cresyl sulfate. We provide an overview on therapeutic approaches aimed to increase their extracorporeal removal via convective and/or adsorptive strategies and to lower their intestinal production/ absorption via dietetic and pharmacological interventions. The recognition that multiple toxins contribute to the uremia supports the need for new therapeutic targets, with a potentially positive impact on CKD progression and survival.
- 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.