Topics (6)

Skills (13)

Research experience

  • Jan 2008–
    present
    Research: Research projects on renal physiology, Renin Anagiotensin System, pediatric kidney diseases and experimental models of human diseases
    Federal University of Minas Gerais · Departamento de Pediatria · Pediatric Nephrology, INCT-Molecular Medicine
    Brazil · Belo Horizonte
    Research projects on molecular genetics of pediatric kidney diseases and inflammatory mediators in renal diseases
  • Jan 1997–
    Dec 2012
    Research: Federal University of Minas Gerais
    Federal University of Minas Gerais · Faculdade de Medicina
    Brazil · Belo Horizonte

Education

  • Jan 2003–
    Oct 2003
    Medical College of Wisconsin
    Molecular Biology · Post-PhD
    USA · Milwaukee
  • Mar 1996–
    Dec 2000
    Federal University of Minas Gerais
    Healthy Sciences · PhD
    Brazil · Belo Horizonte
  • Mar 1993–
    Oct 1994
    Federal University of Minas Gerais
    Renal Physiology · Master
    Brazil · Belo Horizonte
  • Jan 1991–
    Jan 1993
    Federal University of Minas Gerais
    Pediatrics · Medical Residence
    Brazil · Belo Horizonte
  • Jan 1985–
    Dec 1990
    Federal University of Minas Gerais
    Medicine · MD
    Brazil · Belo Horizonte

Other

Publications (93) View all

  • Article: Clinical outcome of children with chronic kidney disease in a pre-dialysis interdisciplinary program
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    ABSTRACT: The purpose of this retrospective cohort study was to describe the outcome of 107 patients with chronic kidney disease (CKD) admitted to a pre-dialysis interdisciplinary management program from 1990 to 2006. The events of interest were progression to CKD stage 5 (renal survival), patient survival, hypertension, and somatic growth. Survival was studied by the Kaplan–Meier method. Patients were classified into four groups according to their primary renal disease: congenital nephro-uropathies; glomerular diseases; cystic disease, and miscellaneous. Median follow-up time was 94months [Interquartile (IQ) range 38–145]. The probability of reaching CKD stage 5 was estimated to be 36% by 5years after admission. As a whole, the mean estimated glomerular filtration rate (GFR) decrease per year was 5.8ml/min per 1.73m2 body surface area [standard deviation (SD) 12.4]. The glomerular diseases group showed a median rate of GFR deterioration of 10ml/min per 1.73m2 per year (IQ range −24 to −5.7), whereas the median rate of GFR deterioration for the groups with cystic diseases, congenital nephro-uropathies, and miscellanea were 2.5ml/min (IQ range −10 to +0.34), 2.2ml/min (IQ range −5.0 to −0.52), and 0.36ml/min (IQ range −2.5 to +2.6), respectively (P < 0.001). The results of this study support the view that children and adolescents with glomerular diseases present a faster deterioration of renal function. Therefore, patients with glomerular diseases need to be referred early to a pediatric nephrology center so that suboptimal pre-dialysis care might possibly be avoided.
    Pediatric Nephrology 04/2012; 23(11):2039-2046. · 2.52 Impact Factor
  • Article: [Inflamação na doença renal crônica: papel de citocinas] article in portugueseInflammation in chronic kidney disease: the role of cytokines
    [show abstract] [hide abstract]
    ABSTRACT: Chronic kidney disease (CKD) is a serious public health problem whose prevalence has increased in the last few years. Its progression is associated with high morbidity and mortality. Several factors are associated with the onset and progression of CKD, such as obesity, hypertension and diabetes mellitus. Beyond these factors, there is evidence of a pathophysiological role for inflammation in CKD. Several cytokines and chemokines have been detected in the plasma and urine of patients at early stages of CKD, and have also been related to CKD complications. The expression of these mediators and renal injury may be influenced by drugs such as angiotensin-converting enzyme inhibitors, statins and antagonists of cytokine receptors. Modulation of the immune-inflammatory response can become a target for CKD treatment. The aim of this study was to review the scientific evidence on the role of inflammation in CKD, especially the effects of cytokines and chemokines.
    Jornal Brasileiro de Nefrologia. 01/2011; 33(3):351-364.
  • Article: [Inflammation in chronic kidney disease: the role of cytokines] Text in Portuguese
    [show abstract] [hide abstract]
    ABSTRACT: Chronic kidney disease (CKD) is a serious public health problem whose prevalence has increased in the last few years. Its progression is associated with high morbidity and mortality. Several factors are associated with the onset and progression of CKD, such as obesity, hypertension and diabetes mellitus. Beyond these factors, there is evidence of a pathophysiological role for inflammation in CKD. Several cytokines and chemokines have been detected in the plasma and urine of patients at early stages of CKD, and have also been related to CKD complications. The expression of these mediators and renal injury may be influenced by drugs such as angiotensin-converting enzyme inhibitors, statins and antagonists of cytokine receptors. Modulation of the immune-inflammatory response can become a target for CKD treatment. The aim of this study was to review the scientific evidence on the role of inflammation in CKD, especially the effects of cytokines and chemokines.
    Orgão oficial de Sociedades Brasileira e Latino-Americana de Nefrologia 01/2011; 33(3):351-364.
  • Article: Effect of propranolol on the splanchnic and peripheral renin angiotensin system in cirrhotic patients.
    [show abstract] [hide abstract]
    ABSTRACT: To evaluate the effect of beta-blockade on angiotensins in the splanchnic and peripheral circulation of cirrhotic patients and also to compare hemodynamic parameters during liver transplantation according to propranolol pre-treatment or not. Patients were allocated into two groups: outpatients with advanced liver disease(LD) and during liver transplantation(LT). Both groups were subdivided according to treatment with propranolol or not. Plasma was collected through peripheral venipuncture to determine plasma renin activity(PRA), Angiotensin(Ang) I, Ang II, and Ang-(1-7) levels by radioimmunoassay in LD group. During liver transplantation, hemodynamic parameters were determined and blood samples were obtained from the portal vein to measure renin angiotensin system(RAS) components. PRA, Ang I, Ang II and Ang-(1-7) were significantly lower in the portal vein and periphery in all subgroups treated with propranolol as compared to non-treated. The relationships between Ang-(1-7) and Ang I levels and between Ang II and Ang I were significantly increased in LD group receiving propranolol. The ratio between Ang-(1-7) and Ang II remained unchanged in splanchnic and peripheral circulation in patients under beta-blockade, whereas the relationship between Ang II and Ang I was significantly increased in splanchnic circulation of LT patients treated with propranolol. During liver transplantation, cardiac output and index as well systemic vascular resistance and index were reduced in propranolol-treated subgroup. In LD group, propranolol treatment reduced RAS mediators, but did not change the ratio between Ang-(1-7) and Ang II in splanchnic and peripheral circulation. Furthermore, the modification of hemodynamic parameters in propranolol treated patients was not associated with changes in the angiotensin ratio.
    World Journal of Gastroenterology 12/2008; 14(44):6824-30. · 2.47 Impact Factor
  • Article: Angiotensin converting enzyme 2, Angiotensin-(1-7) and Mas receptor axis in inflammation and fibrosis.
    A C Simões E Silva, K D Silveira, A J Ferreira, M M Teixeira
    [show abstract] [hide abstract]
    ABSTRACT: Recent advances have improved our understanding of the Renin-Angiotensin System (RAS). These have included the recognition that Angiotensin (Ang)-(1-7) is a biologically active product of the RAS cascade. The identification of the angiotensin-converting enzyme (ACE) homolog ACE2, which forms Ang-(1-7) from Ang II, and the G-protein-coupled receptor Mas as an Ang-(1-7) receptor have provided the necessary biochemical and molecular background and tools to study the biological significance of Ang-(1-7). Most available evidence supports a counter-regulatory role for Ang-(1-7) by opposing many actions of Ang II on AT1 receptors, especially vasoconstriction and proliferation. Many studies have now shown that Ang-(1-7) by acting via Mas receptor exerts inhibitory effects on inflammation and on vascular and cellular growth mechanisms. Ang-(1-7) has also been shown to reduce key signaling pathways and molecules thought to be relevant for fibrogenesis. Here, we review recent findings related to the function of the ACE2/Ang-(1-7)/Mas axis and focus on the role of this axis in modifying processes associated with acute and chronic inflammation, including leukocyte influx, fibrogenesis and proliferation of certain cell types. More attention will be given to the involvement of the ACE2/Ang-(1-7)/Mas axis in the context of renal disease, because of the known relevance of the RAS for the function of this organ and for the regulation of kidney inflammation and fibrosis. Taken together, this knowledge may help in paving the way for the development of novel treatments for chronic inflammatory and renal diseases.
    British Journal of Pharmacology 03/2013; · 4.41 Impact Factor

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