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Fellype Carvalho Barreto
Departamento de Medicina Interna, Divisao de Nefrologia, Universidade Federal do Parana, Curitiba, PR, BR

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Journal article
Published: 22 February 2021
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This study aimed to evaluate the potential anti-inflammatory effects of vitamin D supplementation under uremic conditions, both in vivo and in vitro, and its effects on the parameters of mineral metabolism. Thirty-two hemodialysis patients were randomly assigned to receive placebo (N=14) or cholecalciferol (N=18) for six months. Serum levels of calcium, phosphate, total alkaline phosphatase, intact parathyroid hormone (iPTH), and vitamin D were measured at baseline and after three and six months. The levels of fibroblast growth factor-23 (FGF-23), interleukin-1β (IL-1β), and high-sensitivity C-reactive protein (hs-CRP) were also measured at baseline and at six months. Human monocytes were used for in vitro experiments and treated with cholecalciferol (150 nM) and uremic serum. Cell viability, reactive oxygen species (ROS) production, and cathelicidin (CAMP) expression were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, dichloro-dihydro-fluorescein diacetate assay, and real time-quantitative polymerase chain reaction, respectively. Both patient groups were clinically and biochemically similar at baseline. After six months, the levels of vitamin D and iPTH were higher and lower, respectively, in the cholecalciferol group than in the placebo group (p<0.05). There was no significant difference between the parameters of mineral metabolism, such as IL-1β and hs-CRP levels, in both groups. Treatment with uremic serum lowered the monocyte viability (p<0.0001) and increased ROS production (p<0.01) and CAMP expression (p<0.05); these effects were counterbalanced by cholecalciferol treatment (p<0.05). Thus, cholecalciferol supplementation is an efficient strategy to ameliorate hypovitaminosis D in hemodialysis patients, but its beneficial effects on the control of secondary hyperparathyroidism are relatively unclear. Even though cholecalciferol exhibited anti-inflammatory effects in vitro, its short-term supplementation was not effective in improving the inflammatory profile of patients on hemodialysis, as indicated by the IL-1β and hs-CRP levels.

ACS Style

Paulo C Gregório; Sergio Bucharles; Regiane S da Cunha; Tárcio Braga; Ana Clara Almeida; Railson Henneberg; Andréa E M Stinghen; Fellype C Barreto. In vitro anti-inflammatory effects of vitamin D supplementation may be blurred in hemodialysis patients. 2021, 76, e1821 .

AMA Style

Paulo C Gregório, Sergio Bucharles, Regiane S da Cunha, Tárcio Braga, Ana Clara Almeida, Railson Henneberg, Andréa E M Stinghen, Fellype C Barreto. In vitro anti-inflammatory effects of vitamin D supplementation may be blurred in hemodialysis patients. . 2021; 76 ():e1821.

Chicago/Turabian Style

Paulo C Gregório; Sergio Bucharles; Regiane S da Cunha; Tárcio Braga; Ana Clara Almeida; Railson Henneberg; Andréa E M Stinghen; Fellype C Barreto. 2021. "In vitro anti-inflammatory effects of vitamin D supplementation may be blurred in hemodialysis patients." 76, no. : e1821.

Articles
Published: 01 December 2020 in Brazilian Journal of Nephrology
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In the study published in this issue of the BJN, Matsumoto et al. investigated the association between deficiency of 25-hydroxyvitamin D and inflammatory and oxidative stress in a cohort of pre-dialysis CKD patients5. The study included 206 pre-dialysis CKD patients who were not using vitamin D supplementation. A large number of inflammatory and oxidative stress biomarkers, such as interleukin (IL)-6, adiponectin, F2-isoprostane, advanced oxidation protein products (AOPP), hs-C reactive protein (hs-CRP), were measured. The prevalence of vitamin D deficiency, defined as serum levels of 25(OH)-vitamin D below 20 ng/mL, in the study population was 27% (55/204) and it was inversely correlated with renal function. The multivariate analyses could not demonstrate any significant effect of vitamin D on the levels of inflammatory and oxidative stress biomarkers5. Contrarily, CKD stages were correlated with oxidative stress. The authors concluded that vitamin D deficiency might not play a role in the increased oxidative stress state commonly seen in pre-dialysis CKD patients5.

ACS Style

Fellype Carvalho Barreto; Andréa Emilia Marques Stinghen. Vitamin D and chronic kidney disease: an uneasy relationship. Brazilian Journal of Nephrology 2020, 42, 386 -387.

AMA Style

Fellype Carvalho Barreto, Andréa Emilia Marques Stinghen. Vitamin D and chronic kidney disease: an uneasy relationship. Brazilian Journal of Nephrology. 2020; 42 (4):386-387.

Chicago/Turabian Style

Fellype Carvalho Barreto; Andréa Emilia Marques Stinghen. 2020. "Vitamin D and chronic kidney disease: an uneasy relationship." Brazilian Journal of Nephrology 42, no. 4: 386-387.

Review
Published: 20 June 2020 in Toxins
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Uremic toxins can induce endothelial dysfunction in patients with chronic kidney disease (CKD). Indeed, the structure of the endothelial monolayer is damaged in CKD, and studies have shown that the uremic toxins contribute to the loss of cell–cell junctions, increasing permeability. Membrane proteins, such as transporters and receptors, can mediate the interaction between uremic toxins and endothelial cells. In these cells, uremic toxins induce oxidative stress and activation of signaling pathways, including the aryl hydrocarbon receptor (AhR), nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) pathways. The activation of these pathways leads to overexpression of proinflammatory (e.g., monocyte chemoattractant protein-1, E-selectin) and prothrombotic (e.g., tissue factor) proteins. Uremic toxins also induce the formation of endothelial microparticles (EMPs), which can lead to the activation and dysfunction of other cells, and modulate the expression of microRNAs that have an important role in the regulation of cellular processes. The resulting endothelial dysfunction contributes to the pathogenesis of cardiovascular diseases, such as atherosclerosis and thrombotic events. Therefore, uremic toxins as well as the pathways they modulated may be potential targets for therapies in order to improve treatment for patients with CKD.

ACS Style

Regiane Stafim Da Cunha; Andressa Flores Santos; Fellype Carvalho Barreto; Andréa Emilia Marques Stinghen. How do Uremic Toxins Affect the Endothelium? Toxins 2020, 12, 412 .

AMA Style

Regiane Stafim Da Cunha, Andressa Flores Santos, Fellype Carvalho Barreto, Andréa Emilia Marques Stinghen. How do Uremic Toxins Affect the Endothelium? Toxins. 2020; 12 (6):412.

Chicago/Turabian Style

Regiane Stafim Da Cunha; Andressa Flores Santos; Fellype Carvalho Barreto; Andréa Emilia Marques Stinghen. 2020. "How do Uremic Toxins Affect the Endothelium?" Toxins 12, no. 6: 412.

Articles
Published: 01 June 2020 in Brazilian Journal of Nephrology
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There are more than 150 different rare genetic kidney diseases. They can be classified according to diagnostic findings as (i) disorders of growth and structure, (ii) glomerular diseases, (iii) tubular, and (iv) metabolic diseases. In recent years, there has been a shift of paradigm in this field. Molecular testing has become more accessible, our understanding of the underlying pathophysiologic mechanisms of these diseases has evolved, and new therapeutic strategies have become more available. Therefore, the role of nephrologists has progressively shifted from a mere spectator to an active player, part of a multidisciplinary team in the diagnosis and treatment of these disorders. This article provides an overview of the recent advances in rare hereditary kidney disorders by discussing the genetic aspects, clinical manifestations, diagnostic, and therapeutic approaches of some of these disorders, named familial focal and segmental glomerulosclerosis, tuberous sclerosis complex, Fabry nephropathy, and MYH-9 related disorder.

ACS Style

Mariana Faucz Munhoz Da Cunha; Gabriela Sevignani; Giovana Memari Pavanelli; Mauricio De Carvalho; Fellype Carvalho Barreto. Rare inherited kidney diseases: an evolving field in Nephrology. Brazilian Journal of Nephrology 2020, 42, 219 -230.

AMA Style

Mariana Faucz Munhoz Da Cunha, Gabriela Sevignani, Giovana Memari Pavanelli, Mauricio De Carvalho, Fellype Carvalho Barreto. Rare inherited kidney diseases: an evolving field in Nephrology. Brazilian Journal of Nephrology. 2020; 42 (2):219-230.

Chicago/Turabian Style

Mariana Faucz Munhoz Da Cunha; Gabriela Sevignani; Giovana Memari Pavanelli; Mauricio De Carvalho; Fellype Carvalho Barreto. 2020. "Rare inherited kidney diseases: an evolving field in Nephrology." Brazilian Journal of Nephrology 42, no. 2: 219-230.

Scholarlyarticle
Published: 01 April 2020 in Journal of the Endocrine Society
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We read with interest the article by Colares Neto GP et al [1] recently published in the Journal of the Endocrine Society about the risk factors that can influence the appearance of nephrocalcinosis in patients with X-Linked Hypophosphatemia (XLH). However, we have some concerns about the information provided.

ACS Style

Maria Helena Vaisbich; Juliana Caires De Oliveira Achili Ferreira; Fellype De Carvalho Barreto. Letter to the Editor: "Nephrocalcinosis and Nephrolithiasis in X-Linked Hypophosphatemic Rickets: Diagnostic Imaging and Risk Factors". Journal of the Endocrine Society 2020, 4, bvaa013 .

AMA Style

Maria Helena Vaisbich, Juliana Caires De Oliveira Achili Ferreira, Fellype De Carvalho Barreto. Letter to the Editor: "Nephrocalcinosis and Nephrolithiasis in X-Linked Hypophosphatemic Rickets: Diagnostic Imaging and Risk Factors". Journal of the Endocrine Society. 2020; 4 (4):bvaa013.

Chicago/Turabian Style

Maria Helena Vaisbich; Juliana Caires De Oliveira Achili Ferreira; Fellype De Carvalho Barreto. 2020. "Letter to the Editor: "Nephrocalcinosis and Nephrolithiasis in X-Linked Hypophosphatemic Rickets: Diagnostic Imaging and Risk Factors"." Journal of the Endocrine Society 4, no. 4: bvaa013.

Journal article
Published: 01 September 2019 in Brazilian Journal of Nephrology
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Introduction: Treating secondary hyperparathyroidism (SHPT), a common condition associated with death in patients with chronic kidney disease, is a challenge for nephrologists. Calcimimetics have allowed the introduction of drug therapies no longer based on phosphate binders and active vitamin D. This study aimed to assess the safety and effectiveness of cinacalcet in managing chronic dialysis patients with severe SHPT. Methods: This retrospective study included 26 patients [age: 52 ± 12 years; 55% females; time on dialysis: 54 (4-236) months] on hemodialysis (N = 18) or peritoneal dialysis (N = 8) with severe SHPT (intact parathyroid hormone (iPTH) level > 600 pg/mL) and hyperphosphatemia and/or persistent hypercalcemia treated with cinacalcet. The patients were followed for 12 months. Their serum calcium (Ca), phosphorus (P), alkaline phosphatase (ALP), and iPTH levels were measured at baseline and on days 30, 60, 90, 180, and 365. Results: Patients with hyperphosphatemia (57.7%), hypercalcemia (23%), or both (19.3%) with iPTH > 600 pg/mL were prescribed cinacalcet. At the end of the study, decreases were observed in iPTH (1348 ± 422 vs. 440 ± 210 pg/mL; p < 0.001), Ca (9.5 ± 1.0 vs. 9.1 ± 0.6 mg/dl; p = 0.004), P (6.0 ± 1.3 vs. 4.9 ± 1.1 mg/dl; p < 0.001), and ALP (202 ± 135 vs. 155 ± 109 IU/L; p = 0.006) levels. Adverse events included hypocalcemia (26%) and digestive problems (23%). At the end of the study, 73% of the patients were on active vitamin D and cinacalcet. Three (11.5%) patients on peritoneal dialysis did not respond to therapy with cinacalcet, and their iPTH levels were never below 800 pg/mL. Conclusion: Cinacalcet combined with traditional therapy proved safe and effective and helped manage the mineral metabolism of patients with severe SHPT.

ACS Style

Sérgio Gardano Elias Bucharles; Fellype Carvalho Barreto; Miguel Carlos Riella. The impact of cinacalcet in the mineral metabolism markers of patients on dialysis with severe secondary hyperparathyroidism. Brazilian Journal of Nephrology 2019, 41, 336 -344.

AMA Style

Sérgio Gardano Elias Bucharles, Fellype Carvalho Barreto, Miguel Carlos Riella. The impact of cinacalcet in the mineral metabolism markers of patients on dialysis with severe secondary hyperparathyroidism. Brazilian Journal of Nephrology. 2019; 41 (3):336-344.

Chicago/Turabian Style

Sérgio Gardano Elias Bucharles; Fellype Carvalho Barreto; Miguel Carlos Riella. 2019. "The impact of cinacalcet in the mineral metabolism markers of patients on dialysis with severe secondary hyperparathyroidism." Brazilian Journal of Nephrology 41, no. 3: 336-344.

Review
Published: 13 May 2019 in Toxins
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Endothelial microparticles (EMPs) are vesicles derived from cell membranes, which contain outsourced phosphatidylserine and express adhesion molecules, such as cadherin, intercellular cell adhesion molecule-1 (ICAM-1), E-selectin, and integrins. EMPs are expressed under physiological conditions and continue circulating in the plasma. However, in pathologic conditions their levels increase, and they assume a pro-inflammatory and pro-coagulant role via interactions with monocytes; these effects are related to the development of atherosclerosis. Chronic kidney dysfunction (CKD) characterizes this dysfunctional scenario through the accumulation of uremic solutes in the circulating plasma, whose toxicity is related to the development of cardiovascular diseases. Therefore, this review aims to discuss the formation of EMPs and their biological effects in the uremic environment. Data from previous research demonstrate that uremic toxins are closely associated with the activation of inflammatory biomarkers, cardiovascular dysfunction processes, and the release of EMPs. The impact of a decrease in circulating EMPs in clinical studies has not yet been evaluated. Thus, whether MPs are biochemical markers and/or therapeutic targets has yet to be established.

ACS Style

Giane Favretto; Regiane Stafim Da Cunha; Maria Aparecida Dalboni; Rodrigo Bueno De Oliveira; Fellype De Carvalho Barreto; Ziad A. Massy; Andréa Emilia Marques Stinghen. Endothelial Microparticles in Uremia: Biomarkers and Potential Therapeutic Targets. Toxins 2019, 11, 267 .

AMA Style

Giane Favretto, Regiane Stafim Da Cunha, Maria Aparecida Dalboni, Rodrigo Bueno De Oliveira, Fellype De Carvalho Barreto, Ziad A. Massy, Andréa Emilia Marques Stinghen. Endothelial Microparticles in Uremia: Biomarkers and Potential Therapeutic Targets. Toxins. 2019; 11 (5):267.

Chicago/Turabian Style

Giane Favretto; Regiane Stafim Da Cunha; Maria Aparecida Dalboni; Rodrigo Bueno De Oliveira; Fellype De Carvalho Barreto; Ziad A. Massy; Andréa Emilia Marques Stinghen. 2019. "Endothelial Microparticles in Uremia: Biomarkers and Potential Therapeutic Targets." Toxins 11, no. 5: 267.

Case reports
Published: 17 May 2018 in Brazilian Journal of Nephrology
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MYH9-related disease is an autosomal dominant disorder caused by mutations of the MYH9 gene, which encodes the non-muscle myosin heavy chain IIA on chromosome 22q12. It is characterized by congenital macrothrombocytopenia, bleeding tendency, hearing loss, and cataracts. Nephropathy occurs in approximately 30% of MYH9-related disease in a male patient carrier of a de novo missense mutation in exon 1 of the MYH9 gene [c.287C > T; p.Ser(TCG)96(TTG)Leu]. He presented all phenotypic manifestations of the disease, but cataracts. Renal alterations were microhematuria, nephrotic-range proteinuria (up to 7.5 g/24h), and rapid loss of renal function. The decline per year of the glomerular filtration rate was 20 mL/min/1.73m2 for five years. Blockade of the renin-angiotensin system, the only recommended therapy for slowing the progression of this nephropathy, was prescribed. Although MYH9-related disease is a rare cause of glomerulopathy and end-stage renal disease, awareness of rare genetic kidney disorders is essential to ensure accurate diagnosis and proper management of orphan disease patients.

ACS Style

Gabriela Sevignani; Giovana Memari Pavanelli; Sibele Sauzem Milano; Bianca Ramos Ferronato; Maria Aparecida Pachaly; Hae Ii Cheong; Maurício De Carvalho; Fellype Carvalho Barreto. Macrothrombocytopenia, renal dysfunction and nephrotic syndrome in a young male patient: a case report of MYH9-related disease. Brazilian Journal of Nephrology 2018, 40, 198 -200.

AMA Style

Gabriela Sevignani, Giovana Memari Pavanelli, Sibele Sauzem Milano, Bianca Ramos Ferronato, Maria Aparecida Pachaly, Hae Ii Cheong, Maurício De Carvalho, Fellype Carvalho Barreto. Macrothrombocytopenia, renal dysfunction and nephrotic syndrome in a young male patient: a case report of MYH9-related disease. Brazilian Journal of Nephrology. 2018; 40 (2):198-200.

Chicago/Turabian Style

Gabriela Sevignani; Giovana Memari Pavanelli; Sibele Sauzem Milano; Bianca Ramos Ferronato; Maria Aparecida Pachaly; Hae Ii Cheong; Maurício De Carvalho; Fellype Carvalho Barreto. 2018. "Macrothrombocytopenia, renal dysfunction and nephrotic syndrome in a young male patient: a case report of MYH9-related disease." Brazilian Journal of Nephrology 40, no. 2: 198-200.

Review
Published: 19 October 2017 in Diabetology & Metabolic Syndrome
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Diabetes complications and osteoporotic fractures are two of the most important causes of morbidity and mortality in older patients and share many features including genetic susceptibility, molecular mechanisms, and environmental factors. Type 2 diabetes mellitus (T2DM) compromises bone microarchitecture by inducing abnormal bone cell function and matrix structure, with increased osteoblast apoptosis, diminished osteoblast differentiation, and enhanced osteoclast-mediated bone resorption. The linkage between these two chronic diseases creates a possibility that certain antidiabetic therapies may affect bone quality. Both glycemic and bone homeostasis are under control of common regulatory factors. These factors include insulin, accumulation of advanced glycation end products, peroxisome proliferator-activated receptor gamma, gastrointestinal hormones (such as the glucose-dependent insulinotropic peptide and the glucagon-like peptides 1 and 2), and bone-derived hormone osteocalcin. This background allows individual pharmacological targets for antidiabetic therapies to affect the bone quality due to their indirect effects on bone cell differentiation and bone remodeling process. Moreover, it's important to consider the fragility fractures as another diabetes complication and discuss more deeply about the requirement for adequate screening and preventive measures. This review aims to briefly explore the impact of T2DM on bone metabolic and mechanical proprieties and fracture risk.

ACS Style

Claudia Pinheiro Sanches; Andre Gustavo Daher Vianna; Fellype De Carvalho Barreto. The impact of type 2 diabetes on bone metabolism. Diabetology & Metabolic Syndrome 2017, 9, 85 .

AMA Style

Claudia Pinheiro Sanches, Andre Gustavo Daher Vianna, Fellype De Carvalho Barreto. The impact of type 2 diabetes on bone metabolism. Diabetology & Metabolic Syndrome. 2017; 9 (1):85.

Chicago/Turabian Style

Claudia Pinheiro Sanches; Andre Gustavo Daher Vianna; Fellype De Carvalho Barreto. 2017. "The impact of type 2 diabetes on bone metabolism." Diabetology & Metabolic Syndrome 9, no. 1: 85.

Review
Published: 25 September 2017 in Diabetology & Metabolic Syndrome
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Diabetes complications and osteoporotic fractures are two of the most important causes of morbidity and mortality in older patients, and they share many features, including genetic susceptibility, molecular mechanisms, and environmental factors. Type 2 diabetes mellitus (T2DM) compromises bone microarchitecture by inducing abnormal bone cell function and matrix structure with increased osteoblast apoptosis, diminished osteoblast differentiation, and enhanced osteoclast-mediated bone resorption. The linkage between these two chronic diseases creates a possibility that certain antidiabetic therapies may affect bone function. The treatment of T2DM has been improved in the past two decades with the development of new therapeutic drugs. Each class has a pathophysiologic target related to the regulation of the energy metabolism and insulin secretion. However, both glycemic homeostasis and bone homeostasis are under the control of common regulatory factors. This background allows the individual pharmacological targets of antidiabetic therapies to affect bone quality due to their indirect effects on bone cell differentiation and the bone remodeling process. With a greater number of diabetic patients and antidiabetic agents being launched, it is critical to highlight the consequences of this disease and its pharmacological agents on bone health and fracture risk. Currently, there is little scientific knowledge approaching the impact of most anti-diabetic treatments on bone quality and fracture risk. Thus, this review aims to explore the pros and cons of the available pharmacologic treatments for T2DM on bone mineral density and risk fractures in humans.

ACS Style

A. G. D. Vianna; C. P. Sanches; F. C. Barreto. Review article: effects of type 2 diabetes therapies on bone metabolism. Diabetology & Metabolic Syndrome 2017, 9, 75 .

AMA Style

A. G. D. Vianna, C. P. Sanches, F. C. Barreto. Review article: effects of type 2 diabetes therapies on bone metabolism. Diabetology & Metabolic Syndrome. 2017; 9 (1):75.

Chicago/Turabian Style

A. G. D. Vianna; C. P. Sanches; F. C. Barreto. 2017. "Review article: effects of type 2 diabetes therapies on bone metabolism." Diabetology & Metabolic Syndrome 9, no. 1: 75.

Review
Published: 17 April 2017 in Toxins
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Recently, the clinical and experimental evidences that support the toxic effects of indoxyl sulfate, a protein-bound uremic toxin in chronic kidney disease (CKD) patients, has been discussed. In this panorama, the authors described several in vitro and in vivo studies, suggesting that indoxyl sulfate may play a part in the pathogenesis of low turnover bone disease. However, the discussion claims the need for relevant clinical studies in CKD patients whose bone turnover biomarkers and bone histomorphometry were assessed in order to demonstrate the association between serum levels of indoxyl sulfate and bone turnover. We would like to underline the availability of this clinical data to support the concept that indoxyl sulfate may play a part in the pathogenesis of low turnover bone disease in CKD patients.

ACS Style

Fellype C. Barreto; Daniela V. Barreto; Andrea E. M. Stinghen; Ziad A. Massy. Comment on Indoxyl Sulfate-Review of Toxicity and Therapeutic Strategies. Toxins 2016, 8, 358. Toxins 2017, 9, 142 .

AMA Style

Fellype C. Barreto, Daniela V. Barreto, Andrea E. M. Stinghen, Ziad A. Massy. Comment on Indoxyl Sulfate-Review of Toxicity and Therapeutic Strategies. Toxins 2016, 8, 358. Toxins. 2017; 9 (4):142.

Chicago/Turabian Style

Fellype C. Barreto; Daniela V. Barreto; Andrea E. M. Stinghen; Ziad A. Massy. 2017. "Comment on Indoxyl Sulfate-Review of Toxicity and Therapeutic Strategies. Toxins 2016, 8, 358." Toxins 9, no. 4: 142.