Publications by authors named "Marlene Reis"

131 Publications

Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process.

J Immunol Res 2021 7;2021:6668739. Epub 2021 Apr 7.

Department of Microbiology, Immunology and Parasitology, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil.

The association between inflammatory processes and intestinal neuronal destruction during the progression of Chagasic megacolon is well established. However, many other components play essential roles, both in the long-term progression and control of the clinical status of patients infected with . Components such as neuronal subpopulations, enteric glial cells, mast cells and their proteases, and homeostasis-related proteins from several organic systems (serotonin and galectins) are differentially involved in the progression of Chagasic megacolon. This review is aimed at revealing the characteristics of the intestinal microenvironment found in Chagasic megacolon by using different types of already used biomarkers. Information regarding these components may provide new therapeutic alternatives and improve the understanding of the association between infection and immune, endocrine, and neurological system changes.
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http://dx.doi.org/10.1155/2021/6668739DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8049798PMC
April 2021

Renal Manifestations of Fabry Disease: A Narrative Review.

Can J Kidney Health Dis 2021 19;8:2054358120985627. Epub 2021 Jan 19.

Nephrology Service, Department of Internal Medicine, Federal University of Paraná, Curitiba, Brazil.

Purpose Of Review: In this narrative review, we describe general aspects, histological alterations, treatment, and implications of Fabry disease (FD) nephropathy. This information should be used to guide physicians and patients in a shared decision-making process.

Source Of Information: Original peer-reviewed articles, review articles, and opinion pieces were identified from PubMed and Google Scholar databases. Only sources in English were accessed.

Methods: We performed a focused narrative review assessing the main aspects of FD nephropathy. The literature was critically analyzed from a theoretical and contextual perspective, and thematic analysis was performed.

Key Findings: FD nephropathy is related to the progressive accumulation of GL3, which occurs in all types of renal cells. It is more prominent in podocytes, which seem to play an important role in the pathogenesis of this nephropathy. A precise detection of renal disorders is of fundamental importance because the specific treatment of FD is usually delayed, making reversibility unlikely and leading to a worse prognosis.

Limitations: As no formal tool was applied to assess the quality of the included studies, selection bias may have occurred. Nonetheless, we have attempted to provide a comprehensive review on the topic using current studies from experts in FD and extensive review of the literature.
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http://dx.doi.org/10.1177/2054358120985627DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7960898PMC
January 2021

In situ evaluation of podocytes in patients with focal segmental glomerulosclerosis and minimal change disease.

PLoS One 2020 4;15(11):e0241745. Epub 2020 Nov 4.

Department of Pathology, Genetics and Evolution, Discipline of General Pathology, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil.

Podocyte injury in focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) results from the imbalance between adaptive responses that maintain homeostasis and cellular dysfunction that can culminate in cell death. Therefore, an in situ analysis was performed to detect morphological changes related to cell death and autophagy in renal biopsies from adult patients with podocytopathies. Forty-nine renal biopsies from patients with FSGS (n = 22) and MCD (n = 27) were selected. In situ expression of Wilms Tumor 1 protein (WT1), light chain microtubule 1-associated protein (LC3) and caspase-3 protein were evaluated by immunohistochemistry. The foot process effacement and morphological alterations related to podocyte cell death and autophagy were analyzed with transmission electronic microscopy. Reduction in the density of WT1-labeled podocytes was observed for FSGS and MCD cases as compared to controls. Foot process width (FPW) in control group was lower than in cases of podocytopathies. In FSGS group, FPW was significantly higher than in MCD group and correlated with proteinuria. A density of LC3-labeled podocytes and the number of autophagosomes in podocytes/ pedicels were higher in the MCD group than in the FSGS group. The number of autophagosomes correlated positively with the estimated glomerular filtration rate in cases of MCD. The density of caspase-3-labeled podocytes in FSGS and MCD was higher than control group, and a higher number of podocytes with an evidence of necrosis was detected in FSGS cases than in MCD and control cases. Podocytes from patients diagnosed with FSGS showed more morphological and functional alterations resulting from a larger number of lesions and reduced cell adaptation.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0241745PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641434PMC
December 2020

Renal expression of cytokines and chemokines in diabetic nephropathy.

BMC Nephrol 2020 07 28;21(1):308. Epub 2020 Jul 28.

Discipline of General Pathology, Institute of Biological and Natural Sciences of Federal University of Triângulo Mineiro, Praça Manoel Terra, 330, Nossa Senhora da Abadia, Uberaba, Minas Gerais, 38025-015, Brazil.

Background: Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide. Inflammatory mediators have been implicated in the pathogenesis of DN, thus considered an inflammatory disease. However, further studies are required to assess the renal damage caused by the action of these molecules. Therefore, the objective of this study was to analyze the expression of cytokines and chemokines in renal biopsies from patients with DN and to correlate it with interstitial inflammation and decreased renal function.

Methods: Forty-four native renal biopsies from patients with DN and 23 control cases were selected. In situ expression of eotaxin, MIP-1α (macrophage inflammatory protein-1α), IL-8 (interleukin-8), IL-4, IL-10, TNF-α (tumor necrosis factor-α), TNFR1 (tumor necrosis factor receptor-1), IL-1β, and IL-6 were evaluated by immunohistochemistry.

Results: The DN group showed a significant increase in IL-6 (p < 0.0001), IL-1β (p < 0.0001), IL-4 (p < 0.0001) and eotaxin (p = 0.0012) expression, and a decrease in TNFR1 (p = 0.0107) and IL-8 (p = 0.0262) expression compared to the control group. However, there were no significant differences in IL-10 (p = 0.4951), TNF-α (p = 0.7534), and MIP-1α (p = 0.3816) expression among groups. Regarding interstitial inflammation, there was a significant increase in IL-6 in scores 0 and 1 compared to score 2 (p = 0.0035), in IL-10 in score 2 compared to score 0 (p = 0.0479), and in eotaxin in score 2 compared to scores 0 and 1 (p < 0.0001), whereas IL-8 (p = 0.0513) and MIP-1α (p = 0.1801) showed no significant differences. There was a tendency for negative correlation between eotaxin and estimated glomerular filtration rate (eGFR) (p = 0.0566).

Conclusions: Our results indicated an increased in situ production of cytokines and chemokines in DN, including IL-6, IL-1β, IL-4, and eotaxin. It was observed that, possibly, eotaxin may have an important role in the progression of interstitial inflammation in DN and in eGFR decrease of these patients.
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http://dx.doi.org/10.1186/s12882-020-01960-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7389446PMC
July 2020

Analysis of serum inflammatory mediators in type 2 diabetic patients and their influence on renal function.

PLoS One 2020 4;15(3):e0229765. Epub 2020 Mar 4.

Discipline of General Pathology, Institute of Biological and Natural Sciences of Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil.

Aim: To evaluate the serum concentrations of inflammatory mediators in patients with type 2 diabetes mellitus (T2DM) with or without renal alteration (RA) function.

Methods: Serum samples from 76 patients with T2DM and 24 healthy individuals were selected. Patients with T2DM were divided into two groups according to eGFR (> or < 60mL/min/1.73m2). Cytokines, chemokines and adipokines levels were evaluated using the Multiplex immunoassay and ELISA.

Results: TNFR1 and leptin were higher in the T2DM group with RA than in the T2DM group without RA and control group. All patients with T2DM showed increased resistin, IL-8, and MIP-1α compared to the control group. Adiponectin were higher and IL-4 decreased in the T2DM group with RA compared to the control group. eGFR positively correlated with IL-4 and negatively with TNFR1, TNFR2, and leptin in patients with T2DM. In the T2DM group with RA, eGFR was negatively correlated with TNFR1 and resistin. TNFR1 was positively correlated with resistin and leptin, as well as resistin with IL-8 and leptin.

Conclusion: Increased levels of TNFR1, adipokines, chemokines and decrease of IL-4 play important role in the inflammatory process developed in T2DM and decreased renal function. We also suggest that TNFR1 is a strong predictor of renal dysfunction in patients with T2DM.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0229765PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7055870PMC
June 2020

Mast cells in the kidney biopsies of pediatric patients with lupus nephritis.

J Bras Nefrol 2020 03 31;42(1):59-66. Epub 2020 Jan 31.

Departamento de Patologia Genética e Evolução, Instituto de Ciências Biológicas e Naturais, Universidade Federal do Triângulo Mineiro, Uberaba, MG, Brasil.

Introduction: Mast cells may be involved in inflammation and contribute to the onset of fibrosis in lupus nephritis (LN).

Objective: This study aimed to correlate the presence of mast cells in kidney biopsy specimens of pediatric patients with LN with activity (AI) and chronicity (CI) indices and assess how effectively mast cells may be used as a prognostic factor.

Method: The study included 40 patients aged 6-18 years diagnosed with LN at the Renal Disease Service of the Federal University of Triângulo Mineiro between 1996 and 2015. Workup and epidemiological data were evaluated vis-à-vis AI, CI, and mast cell counts (MCC).

Results: Significant positive correlations were found between mast cell counts (MCC) and AI (p = 0.003; r: 0.66) and MCC and CI (p = 0.048; r: 0.48). The ROC curve showed that mast cells were highly sensitive and specific in the differentiation of patients with an AI > 12 from individuals with an AI ≤ 12. Serum creatinine levels were higher in individuals with class IV LN than in patients with class V disease [1.50 (0.40-20.90) vs. 0.70 (0.62-0.90), p = 0.04]. Blood urea nitrogen had a positive significant correlation with MCC (p = 0.002; r: 0.75). A trend toward a negative correlation was observed between MCC and serum albumin (p = 0.06; r: -0.5459). Kidney biopsies of patients with nephrotic syndrome had higher MCC [2.12 (0.41-5.140) vs. 0.53 (0.0-3.94), p = 0.07].

Conclusion: Inflammatory cell infiltration and morphological differences between cell types in the inflammatory infiltrate are relevant factors in the assessment of the LN. Mast cell analysis and AI/CI assessment may be relevant prognostic indicators for pediatric patients with LN.
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http://dx.doi.org/10.1590/2175-8239-jbn-2018-0222DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7213939PMC
March 2020

Cardiac Chagas Disease: MMPs, TIMPs, Galectins, and TGF- as Tissue Remodelling Players.

Dis Markers 2019 25;2019:3632906. Epub 2019 Nov 25.

Institute of Tropical Pathology and Public Health, Federal University of Goiás, 74605-450 Goiânia, GO, Brazil.

A century after the discovery of Chagas disease, studies are still needed to establish the complex pathophysiology of this disease. However, it is known that several proteins and molecules are related to the establishment of this disease, its evolution, and the appearance of its different clinical forms. Metalloproteinases and their tissue inhibitors, galectins, and TGF- are involved in the process of infection and consequently the development of myocarditis, tissue remodeling, and fibrosis upon infection with . Thus, considering that the heart is one of the main target organs in Chagas disease, knowledge regarding the mechanisms of action of these molecules is essential to understand how they interact and trigger local and systemic reactions and, consequently, determine whether they contribute to the development of Chagas' heart disease. In this sense, it is believed that the inflammatory microenvironment caused by the infection alters the expression of these proteins favoring progression of the host-parasite cycle and thereby stimulating cardiac tissue remodeling mechanisms and fibrosis. The aim of this review was to gather information on metalloproteinases and their tissue inhibitors, galectins, and TGF- and discuss how these molecules and their different interrelationships contribute to the development of Chagas' heart disease.
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http://dx.doi.org/10.1155/2019/3632906DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6899287PMC
May 2020

A novel single amino acid deletion impairs fibronectin function and causes familial glomerulopathy with fibronectin deposits: case report of a family.

BMC Nephrol 2019 08 16;20(1):322. Epub 2019 Aug 16.

Divisions of Nephrology and Molecular Medicine, University of São Paulo School of Medicine, São Paulo, SP, Brazil.

Background: Glomerulopathy with fibronectin deposits is an autosomal dominant disease associated with proteinuria, hematuria, hypertension and renal function decline. Forty percent of the cases are caused by mutations in FN1, the gene that encodes fibronectin.

Case Presentation: This report describes two cases of Glomerulopathy with fibronectin deposits, involving a 47-year-old father and a 14-year-old son. The renal biopsies showed glomeruli with endocapillary hypercellularity and large amounts of mesangial and subendothelial eosinophilic deposits. Immunohistochemistry for fibronectin was markedly positive. Whole exome sequencing identified a novel FN1 mutation that leads to an amino-acid deletion in both patients (Ile1988del), a variant that required primary amino-acid sequence analysis for assessment of pathogenicity. Our primary sequence analyses revealed that Ile1988 is very highly conserved among relative sequences and is positioned in a C-terminal FN3 domain containing heparin- and fibulin-1-binding sites. This mutation was predicted as deleterious and molecular mechanics simulations support that it can change the tertiary structure and affect the complex folding and its molecular functionality.

Conclusion: The current report not only documents the occurrence of two GFND cases in an affected family and deeply characterizes its anatomopathological features but also identifies a novel pathogenic mutation in FN1, analyzes its structural and functional implications, and supports its pathogenicity.
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http://dx.doi.org/10.1186/s12882-019-1507-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6697944PMC
August 2019

Is it possible to predict parameters of the Oxford classification of primary IgA Nephropathy from clinical laboratory data? Focus on the role of segmental glomerulosclerosis subtypes.

Pathol Res Pract 2019 Oct 12;215(10):152533. Epub 2019 Jul 12.

Federal University of Triângulo Mineiro, Praça Manoel Terra, 330, 38015-050, Uberaba, MG, Brazil. Electronic address:

Introduction: IgA nephropathy (IgAN) is the most common primary glomerulonephritis in the world and has a broad range of histological and clinical manifestations, ranging from morphologically normal to globally sclerotic glomeruli with clinical manifestations varying from isolated hematuria to end stage renal disease. This study aims to assess sensitivity, specificity and accuracy of clinical data at the time of biopsy in predicting 2017 updated Oxford classification parameters and to investigate if subtypes of segmental sclerosis (FSGS) influence clinical presentation.

Material And Methods: Renal biopsies from 103 patients with IgAN were analyzed. Oxford classification was updated and FSGS lesions were subclassified. ROC curves, univariate and multivariate logistic regression were used.

Results: In Oxford classification, the majority of patients had mesangial hypercellularity in less than a half of glomeruli (M0), did not have endocapillary hypercellularity (E0), had segmental glomerulosclerosis (S1), had interstitial fibrosis and tubular atrophy in more than a half of the sample (T2) and had no crescents (C0). Hypertension increases the chance of M1 in 2.54x (p = 0.02). For each unit of increased creatinine, 2.6x more chances of E1 (p = 0.001). S1 is predicted by proteinuria with 75% sensitivity and 90.9% specificity (p < 0.0001). For each unit of increase in GFR, there is a reduction of 6% in the chance of T2 in relation to T0 (p = 0.0001). If hypertension, there is 5x more chances of T2 than T0 (p = 0.01). For each unit of increase in creatinine, there are 2.8x more chances of crescents- C (p = 0.003). Creatinine also showed 75.8% sensitivity and 75% specificity for prediction of C (p = 0.002). Inversely, for each unit of GFR, the chance of C is reduced by 4% (p = 0.007). Other clinical data related with C are hypertension (p = 0.03) and proteinuria (p = 0.02). To determine the role of FSGS subtypes in clinical presentation, we divided patients in S0 and S1 groups. Proteinuria was the only clinical parameter with significative difference, respectively, 0.3 (0-2.1) and 1.6 (0.02-16.2) g/24 h (p < 0.0001). FSGS subtypes related to proteinuria were cellular (p = 0.03) and peri-hilar (p = 0.02). Subtypes classically related to podocytopathies showed no correlation with clinical data.

Conclusion: In the future, with noninvasive methods for diagnosis of IgAN, it will be essential to predict Oxford classification parameters using clinical laboratory data for establishment of prognosis and therapeutics. We showed that Oxford classification parameters correspond to some clinical laboratory data, making this approach possible. FSGS lesions not specifically related to podocytopathies may also influence clinical parameters that affect renal disease progression.
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http://dx.doi.org/10.1016/j.prp.2019.152533DOI Listing
October 2019

Evaluation of the Diagnostic Potential of uPAR as a Biomarker in Renal Biopsies of Patients with FSGS.

Dis Markers 2019 2;2019:1070495. Epub 2019 May 2.

Discipline of General Pathology, Institute of Biological and Natural Sciences of Federal University of Triângulo Mineiro, Praça Manoel Terra, 330, Nossa Senhora da Abadia, 38025-015 Uberaba, Minas Gerais, Brazil.

Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are primary glomerulopathies leading to proteinuria, known as podocytopathies, which share syndromic and morphological similarities. Morphological similarity occurs in cases of FSGS in which the sclerotic lesion was not sampled in renal biopsy, due to the focal nature of the disease. Differentiating these entities is very important, especially in cases of suspected FSGS but with sclerotic lesion not sampled, as they are diseases that apparently have different pathogenic mechanisms and prognosis. The difference in uPAR expression in situ among these two entities may be related to a distinct molecular mechanism involved in pathogenesis. Thus, finding biomarkers involved in the pathogenesis and that can also help in differential diagnosis is very relevant. The aim of this work was to evaluate the potential of urokinase-type plasminogen activator receptor (uPAR) as a biomarker in renal biopsies of patients with podocytopathies ( = 38). Immunohistochemistry showed that FSGS ( = 22) had increased uPAR expression in podocytes compared with both the MCD group ( = 16; = 0.0368) and control group ( = 21; = 0.0076). ROC curve ( = 0.008) showed that this biomarker has 80.95% of specificity in biopsies of patients with FSGS. Therefore, uPAR presented a high specificity in cases of podocytopathies associated with sclerosis and it can be considered a potential biomarker for FSGS.
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http://dx.doi.org/10.1155/2019/1070495DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6525920PMC
December 2019

Podocin and uPAR are good biomarkers in cases of Focal and segmental glomerulosclerosis in pediatric renal biopsies.

PLoS One 2019 12;14(6):e0217569. Epub 2019 Jun 12.

Institute of Biological and Natural Sciences, Discipline of General Pathology, Federal University of Triangulo Mineiro, Uberaba, Minas Gerais, Brazil.

There are controversies whether Minimal Change Disease (MCD) and Focal and Segmental Glomerulosclerosis (FSGS) are distinct glomerular lesions or different manifestations within the same spectrum of diseases. The uPAR (urokinase-type plasminogen activator receptor) and some slit diaphragm proteins may be altered in FSGS glomeruli and may function as biomarkers of the disease in renal biopsies. Thus, this study aims to evaluate the diagnostic potential of uPAR and glomerular proteins for differentiation between MCD and FSGS in renal pediatric biopsy. Renal biopsies from 50 children between 2 and 18 years old were selected, with diagnosis of MCD (n = 29) and FSGS (n = 21). Control group consisted of pediatric autopsies (n = 15) from patients younger than 18 years old, with no evidences of renal dysfunction. In situ expressions of WT1, nephrin, podocin and uPAR were evaluated by immunoperoxidase technique. Renal biopsy of patients with MCD and FSGS expressed fewer WT1 (p≤0.0001, F = 19.35) and nephrin (p<0.0001; H = 21.54) than patients in the control group. FSGS patients expressed fewer podocin than control (p<0.0359, H = 6.655). FSGS cases expressed more uPAR than each of control and MCD (p = 0.0019; H = 12.57) and there was a positive and significant correlation between nephrin and podocin (p = 0.0026, rS = 0.6502) in these cases. Podocin had sensitivity of 73.3% and specificity of 86.7% (p = 0.0068) and uPAR had sensitivity of 78.9% and specificity of 73.3% (p = 0.0040) for diagnosis of FSGS patients. The main limitation of the study is the limited number of cases due to the difficulty in performing biopsy in pediatric patients. Podocin and uPAR are good markers for FSGS and differentiate these cases from MCD, reinforcing the theory of distinct glomerular diseases. These findings suggest that podocin and uPAR can be used as biomarkers in the routine analysis of renal biopsies in cases of podocytopathies when the lesion (sclerosis) is not sampled.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0217569PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6561567PMC
February 2020

Focal and Segmental Glomerulosclerosis and Membranous Nephropathy overlapping in a patient with Nephrotic Syndrome: a case report.

J Bras Nefrol 2020 Mar 25;42(1):113-117. Epub 2019 Feb 25.

Instituto de Ciências Biológicas e Naturais, Universidade Federal do Triângulo Mineiro, Uberaba, MG, Brasil.

Introduction: Some cases of membranous nephropathy (MGN) present focal segmental glomerulosclerosis (FSGS) typically associated with disease progression. However, we report a case of a patient who seemed to have MGN and FSGS, both primary.

Case Presentation: A 17-year-old female, Caucasian, presenting lower extremity edema associated with episodes of foamy urine and high blood pressure, had physical and laboratorial exams indicating nephrotic syndrome. A renal biopsy was performed and focal and segmental glomerulosclerosis were observed under light microscopy in some glomeruli presented as tip lesion, and in others it was accompanied by podocyte hypertrophy and podocyte detachment in urinary space, compatible with podocytopathy FSGS. Besides, there were thickened capillary loops with basement membrane irregularities due to "spikes" compatible with MGN stage II. Immunofluorescence showed finely granular IgG, IgG4, and PLA2R deposits in capillary loops and, in electron microscopy, subepithelial deposits and foot process effacement. These morphological findings are compatible with FSGS and MGN stage II.

Conclusions: In the present case, clinical and morphological characteristics showed a possible overlap of primary FSGS and MGN as focal and segmental glomerulosclerosis does not seem to be related with MGN progression but with the podocytopathy FSGS.
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http://dx.doi.org/10.1590/2175-8239-JBN-2018-0239DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7213925PMC
March 2020

Melatonin treatment in fetal and neonatal diseases.

Pathol Res Pract 2018 Dec 23;214(12):1940-1951. Epub 2018 Oct 23.

Discipline of General Pathology, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil. Electronic address:

This literature review aims to address the main scientific findings on oxidative stress activity in different gestational disorders, as well as the function and application of melatonin in the treatment of fetal and neonatal changes. Oxidative stress has been associated with the etiopathogenesis of recurrent miscarriages, preeclampsia, intrauterine growth restriction, and stillbirth. Both, the exacerbated consumption of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, and the increased synthesis of reactive oxygen species, such as superoxide, peroxynitrite, and hydrogen peroxide, induce phospholipid peroxidation and endothelial dysfunction, impaired invasion and death of trophoblast cells, impaired decidualization, and remodeling of maternal spiral arteries. It has been postulated that melatonin induces specific biochemical responses that regulate cell proliferation in fetuses, and that its antioxidant action promotes bioavailability of nitric oxide and, thus, placental perfusion and also fetal nutrition and oxygenation. Therefore, the therapeutic action of melatonin has been the subject of major studies that aim to minimize or prevent different injuries affecting this pediatric age group, such as intrauterine growth restriction, encephalopathy, chronic lung diseases, retinopathy of prematurity Conclusion: the results antioxidant and indicate that melatonin is an important therapy for the clinical treatment of these diseases.
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http://dx.doi.org/10.1016/j.prp.2018.10.016DOI Listing
December 2018

Is arterial calcification in children and adolescents with end-stage renal disease a rare finding?

Nephrology (Carlton) 2019 Jul 25;24(7):696-702. Epub 2019 Apr 25.

Department of Pediatrics, UNIFESP, Sao Paulo, Brazil.

Aim: To investigate if calcification and intimal media thickness (IMT) of arteries are present in children and adolescents with end-stage renal disease and to describe the risk factors associated with these alterations.

Methods: In an observational, cross-sectional prospective study, 68 patients were evaluated at the time of renal transplantation. A fragment of the inferior epigastric artery was removed during surgery for histopathological analysis to verify the presence or not of arterial calcification. Two outcomes were considered: the presence of calcium deposition and the measurement of the IMT of the artery. The potential exposure variables were: age, chronic kidney disease aetiology, diagnosis time, systolic blood pressure (SBP), use of oral active vitamin D, homocysteine and C-reactive protein.

Results: No arterial calcification was observed in the studied sample. The median value of the IMT of the inferior epigastric artery was 166 μm (interquartile range = 130-208). SBP standard deviation score and age were the only factors associated with this outcome. There was no statistical interaction between SBP and age with the IMT (P = 0.280).

Conclusion: Arterial calcification is rare in children and adolescents with end-stage renal disease. The factors associated with IMT were age and SBP.
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http://dx.doi.org/10.1111/nep.13480DOI Listing
July 2019

TLR2 and TLR4 play opposite role in autophagy associated with cisplatin-induced acute kidney injury.

Clin Sci (Lond) 2018 08 22;132(16):1725-1739. Epub 2018 Aug 22.

Department of Immunology, Universidade de São Paulo, São Paulo, Brazil

Acute kidney injury (AKI) is considered an inflammatory disease in which toll-like receptors (TLRs) signaling pathways play an important role. The activation of TLRs results in production of several inflammatory cytokines leading to further renal damage. In contrast, TLRs are key players on autophagy induction, which is associated with a protective function on cisplatin-induced AKI. Hence, the present study aimed to evaluate the specific participation of TLR2 and TLR4 molecules on the development of cisplatin-induced AKI. Complementarily, we also investigated the link between TLRs and heme oxygenase-1 (HO-1), a promisor cytoprotective molecule. First, we observed that only the absence of TLR2 but not TLR4 in mice exacerbated the renal dysfunction, tissue injury and mortality rate, even under an immunologically privileged microenvironment. Second, we demonstrated that TLR2 knockout (KO) mice presented lower expression of autophagy-associated markers when compared with TLR4 KO animals. Similar parameter was confirmed , using tubular epithelial cells derived from both KO mice. To test the cross-talking between HO-1 and TLRs, hemin (an HO-1 internal inducer) was administrated in cisplatin-treated TLR2 and TLR4 KO mice and it was detected an improvement in the global renal tissue parameters. However, this protection was less evident at TLR2 KO mice. In summary, we documented that TLR2 plays a protective role in cisplatin-induced AKI progression, in part, by a mechanism associated with autophagy up-regulation, considering that its interplay with HO-1 can promote renal tissue recover.
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http://dx.doi.org/10.1042/CS20170262DOI Listing
August 2018

Complement System and C4d expression in cases of Membranous nephropathy.

J Bras Nefrol 2017 Oct-Dec;39(4):370-375

Universidade Federal do Triângulo Mineiro, Serviço de Patologia Geral e Nefropatologia, Uberaba - MG, Brazil.

Introduction: Membranous nephropathy (MN) is one of the major causes of nephrotic syndrome. The complement system plays a key role in the pathophysiology of MN.

Objectives: To identify the complement pathway possibly activated in MN cases and correlate the presence of C4d with more severe clinical and histological markers.

Methods: Sixty nine cases from renal biopsy with membranous nephropathy were investigated. The presence of C1q was analyzed by direct immunofluorescence; and expression of C4d by immunohistochemistry. Clinical and epidemiological data were obtained upon biopsy request.

Results: The presence of focal segmental glomerulosclerosis, global glomerulosclerosis, vascular lesions and tubulointerstitial fibrosis were collected by anatomopathological report. C4d(+) was found in 58 (84%), and C1q(+) was found in 12 (17%) of the cases. Twelve patients had C4d(+)/C1q(+), 46 had C4d(+)/C1q(-), and 11 patients had C4d(-)/C1q(-), probably indicating the activation of the classical, lectin and alternative pathways, respectively.

Conclusion: C4d was associated with increased interstitial fibrosis, but not with clinical markers of poor prognosis. Through the deposition of C4d and C1q we demonstrated that all complement pathways may be involved in MN, highlighting the lectin pathway. The presence of C4d has been associated with severe tubulointerstitial lesions, but not with clinical markers, or can be taken as a universal marker of all cases of MN.
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http://dx.doi.org/10.5935/0101-2800.20170068DOI Listing
September 2018

Angiogenic and antiangiogenic factors in preeclampsia.

Pathol Res Pract 2018 Jan 31;214(1):7-14. Epub 2017 Oct 31.

Discipline of General Pathology, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil. Electronic address:

Background: Pre-eclampsia is a multifactorial hypertensive disorder that is triggered by placental insufficiency and that accounts for up to 15% of maternal deaths. In normal pregnancies, this process depends on the balance between the expression of angiogenic factors and antiangiogenic factors, which are responsible for remodeling the spiral arteries, as well as for neoangiogenesis and fetal development.

Purpose: The aim of this review is to discuss the main scientific findings regarding the role of angiogenic and antiangiogenic factors in the etiopathogenesis of preeclampsia.

Methods: An extensive research was conducted in the Pubmed database in search of scientific manuscripts discussing potential associations between angiogenic and antiangiogenic factors and preeclampsia. Ninety-one papers were included in this review.

Results: There is an increased expression of soluble fms-like tyrosine kinase receptor and soluble endoglin in pre-eclampsia, as well as reduced placental expression of vascular endothelial growth factor and placental growth factor. Systemic hypertension, proteinuria and kidney injury - such as enlargement and glomerular fibrin deposit, capillary occlusion due to edema, and hypertrophy of endocapillary cells - are some of these changes. The complex etiopathogenesis of preeclampsia instigates research of different biomarkers that allow for the early diagnosis of this entity, such as vascular endothelial growth factor, placental growth factor, soluble fms-like tyrosine kinase receptor, soluble endoglin, placental glycoprotein pregnancy-associated plasma protein-A and protein 13.

Conclusion: Even though it is possible to establish an efficient and effective diagnostic tool, three key principles must be observed in the management of preeclampsia: prevention, early screening and treatment.
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http://dx.doi.org/10.1016/j.prp.2017.10.021DOI Listing
January 2018

Ultrastructural deposits appearing as "zebra bodies" in renal biopsy: Fabry disease?- comparative case reports.

BMC Nephrol 2017 May 12;18(1):157. Epub 2017 May 12.

Nephropathology Service, Federal University of Triângulo Mineiro, Praça Manoel Terra, 330, Uberaba, MG, CEP: 38015-050, Brazil.

Background: Fabry Disease (FD) is a genetic disorder caused by alpha-galactosidase A deficiency. Certain drugs, such as hydroxychloroquine, can produce renal deposits that mimic morphological findings seen in FD, characterizing a type of drug-induced renal phospholipidosis.

Case Presentation: Case 1: A 28-year-old female patient with systemic lupus erythematosus who had been using hydroxychloroquine for 14 months presented subnephrotic proteinuria. Renal biopsy showed deposits compatible with FD. Neither activity analysis of alpha-galactosidase A nor genetic analysis were available and were not performed. These deposits were not detected in a subsequent renal biopsy three years after withdrawal of the medication, characterizing a possible hydroxychloroquine-induced renal phospholipidosis. Case 2: A 29-year-old male patient presented with acroparesthesia, angiokeratomas, cornea verticillata and subnephrotic proteinuria. Deposits compatible with FD were detected upon renal biopsy. The evaluation of alpha-galactosidase A showed no activity in both blood and leukocytes. Genetic analysis identified an M284 T mutation in exon 6, and such mutation was also found in other family members.

Conclusion: Clinical investigation is necessary in suspected cases of Fabry Disease upon renal biopsy in order to confirm diagnosis. Drug-induced renal phospholipidosis should be considered in differential diagnosis in cases with intracellular osmiophilic, lamellar inclusions in electron microscopy.
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http://dx.doi.org/10.1186/s12882-017-0571-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5427530PMC
May 2017

Intrauterine infection, immune system and premature birth.

J Matern Fetal Neonatal Med 2018 May 20;31(9):1227-1233. Epub 2017 Apr 20.

a Department of General Pathology , Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro , Minas Gerais , Brazil.

Preterm birth accounts for nearly one million deaths among children under five years of age, and although its etiopathogenesis is not fully elucidated, ascending intrauterine infection and fetal inflammatory response seem to be the main triggers. The intense inflammatory response mediated by IL-1β, TNF-α, PAF, IFN-γ and IL-6, PGE and MMP-1 and MMP-9 causes fetal membrane damage and rupture, increased uterine contractions and biochemical and structural changes in the cervix. Furthermore, preterm neonates have deficient innate and adaptive immune responses characterized by reduced levels of IgG, opsonization and phagocytosis, as well as increased activation of Th1 cells in relation to Th2 cells. Therefore, this triad is favors the occurrence of neonatal complications, such as respiratory distress syndrome, necrotizing enterocolitis, retinopathy of prematurity and bronchopulmonary dysplasia. Due to serious maternal and child health complications of intrauterine infection, several studies have tried to identify biomarkers for the early diagnosis of this entity. This literature review aims to discuss the main scientific findings regarding the association between ascending intrauterine infection, immune system and preterm birth.
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http://dx.doi.org/10.1080/14767058.2017.1311318DOI Listing
May 2018

A Regulatory miRNA-mRNA Network Is Associated with Tissue Repair Induced by Mesenchymal Stromal Cells in Acute Kidney Injury.

Front Immunol 2016 3;7:645. Epub 2017 Jan 3.

Departamento de Medicina, Divisão de Nefrologia, Universidade Federal de São Paulo, São Paulo, Brazil; Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.

Mesenchymal stromal cells (MSCs) orchestrate tissue repair by releasing cell-derived microvesicles (MVs), which, presumably by small RNA species, modulate global gene expression. The knowledge of miRNA/mRNA signatures linked to a reparative status may elucidate some of the molecular events associated with MSC protection. Here, we used a model of cisplatin-induced kidney injury (acute kidney injury) to assess how MSCs or MVs could restore tissue function. MSCs and MVs presented similar protective effects, which were evidenced and by modulating apoptosis, inflammation, oxidative stress, and a set of prosurvival molecules. In addition, we observed that miRNAs (i.e., miR-880, miR-141, miR-377, and miR-21) were modulated, thereby showing active participation on regenerative process. Subsequently, we identified that MSC regulates a particular miRNA subset which mRNA targets are associated with Wnt/TGF-β, fibrosis, and epithelial-mesenchymal transition signaling pathways. Our results suggest that MSCs release MVs that transcriptionally reprogram injured cells, thereby modulating a specific miRNA-mRNA network.
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http://dx.doi.org/10.3389/fimmu.2016.00645DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5206861PMC
January 2017

Influence of the Expression of Inflammatory Markers on Kidney after Fetal Programming in an Experimental Model of Renal Failure.

J Immunol Res 2016 28;2016:9151607. Epub 2016 Nov 28.

Discipline of General Pathology, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, MG, Brazil.

To evaluate the expression of inflammatory markers in experimental renal failure after fetal programming. The offspring aged two and five months were divided into four groups: CC (control dams, control offspring); DC (diabetic dams, control offspring); CFA (control dams, folic acid offspring, 250 mg/Kg); and DFA (diabetic dams, folic acid offspring). Gene expression of inflammatory markers MCP-1, IL-1, NOS3, TGF-, TNF-, and VEGF was evaluated by RT-PCR. MCP-1 was increased in the CFA and DFA groups at two and five months of age, as well as in DC5 when compared to CC5. There was a higher expression of IL-1 in the CFA2, DFA2, and DC2 groups. There was a decrease in NOS3 and an increase in TNF- in DFA5 in relation to CFA5. The gene expression of TGF- increased in cases that had received folic acid at two and five months, and VEGF decreased in the CFA5 and DFA5 groups. DC5 showed increased VEGF expression in comparison with CC5. Gestational diabetes mellitus and folic acid both change the expression of inflammatory markers, thus demonstrating that the exposure to harmful agents in adulthood has a more severe impact in cases which underwent fetal reprogramming.
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http://dx.doi.org/10.1155/2016/9151607DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5149704PMC
March 2017

Nodular glomerulosclerosis in a non-diabetic hypertensive, dyslipidemic, smoker patient: a case report.

J Bras Nefrol 2016 Dec;38(4):473-477

Universidade Federal do Triângulo Mineiro, Brazil.

Introduction: This is a case report of a patient with idiopathic nodular glomerulosclerosis whose pathogenesis and morphology are similar to diabetic nephropathy.

Case Presentation: A 64-year-old Brazilian man, leukoderma, dyslipidemic, obese with chronic obstructive pulmonary disease secondary to tobacco smoking, known to be hypertensive for five years and he had no history of diabetes. He was admitted with sudden anasarca, rapid loss of renal function and needed to start hemodialysis immediately. Renal biopsy was performed, and the sections were examined by light microscopy, immunofluorescence and electron microscopy. Morphological and ultrastructural findings showed that the profile of the disease studied herein strongly resembles diabetic nephropathy. However, the absence of diabetes mellitus, the presence of arteriolar hyalinosis in renal arterioles, tobacco smoking, and other clinical factors observed can play a significant role in nodular formation.

Conclusion: The clinical features of the patient, and most importantly, the fact that he is a smoker, favor the diagnosis of "nodular glomerulosclerosis associated with smoking", a nomenclature proposed by some authors as an alternative to the term idiopathic nodular glomerulosclerosis. This clinical case report highlights idiopathic nodular glomerulosclerosis as a rare disease of little known etiopathogenesis; thus, further studies are necessary in order to elucidate the causes of this disease.
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http://dx.doi.org/10.5935/0101-2800.20160076DOI Listing
December 2016

An overview of maternal and fetal short and long-term impact of physical activity during pregnancy.

Arch Gynecol Obstet 2017 Feb 19;295(2):273-283. Epub 2016 Oct 19.

Institute of Biological and Natural Sciences, Discipline of General Pathology, Federal University of Triângulo Mineiro, Rua Frei Paulino No. 30, Bairro Nossa Senhora da Abadia, Uberaba, MG, 38025-180, Brazil.

Purpose: To explore information available in the literature about the possible benefits resulting from physical activity (PA) in non-risky pregnant women, repercussion on maternal organism, fetal development, and on long-term offspring health.

Methods: Critical narrative review using online databases.

Results: Through critical discussion of studies focused on PA practiced during pregnancy, it was observed that some of the outcomes investigated on both mother and offspring showed conflicting findings. Considering the impact of maternal PA in certain offspring characteristics, due to the fact that their findings come from studies with small samples, they do not allow the stablishment of scientific evidence. However, a feature that shows broad consensus among studies is the view of PA during pregnancy as a safe intervention for mother and fetus. In situations where studies employing PA of moderate-intensity have not enough power to ensure a positive influence on certain clinical outcomes, what is observed is the lack of their influence, not negative impacts. Regarding epigenetic modulations measured late in the offspring, it has been attributed to PA a positive modulatory role on metabolic, hemodynamic and even on behavioral characteristics. However, possible mechanisms involved in these epigenetic changes have not been sufficiently explored.

Conclusion: Maternal PA appears to be safe for both mother and fetus, and additional studies are needed to confirm the real influence of this practice in the offspring, as well as the perpetuation and transfer of these features between generations.
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http://dx.doi.org/10.1007/s00404-016-4204-9DOI Listing
February 2017

Epithelial-mesenchymal transition in pediatric nephropathies.

Pathol Res Pract 2016 Dec 22;212(12):1157-1166. Epub 2016 Sep 22.

Department of General Pathology, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil.

Introduction: Epithelial-mesenchymal transition (EMT) is a process in which epithelial cells may express mesenchymal cell markers with subsequent change in their functions, and it may be part of the etiopathogenesis of kidney disease.

Objective: The aim of this study was to evaluate the immunexpression of some EMT inducers and markers in frequent nephropathies in pediatric patients.

Methods: 59 patients aged 2-18 years old were selected and divided into 6 groups of frequent nephropathies in children and adolescents, as well as one control group. Urea and creatinine data of the patients were recorded. TGF-β3, fibronectin, α-SMA and vimentin were evaluated by immunohistochemistry.

Results: Glomerular TGF-β3 was higher in the Lupus Nephritis and Acute Diffuse Glomerulonephritis (ADGN) groups than in the control group. Glomerular fibronectin was higher in the Podocytopathy, Lupus Nephritis, ADGN and Membranous Glomerulopathy patients than in control subjects. The expression of α-SMA was higher in the tubulointerstitial compartment of ADGN and Membranous Glomerulopathy groups than in the control group. Glomerular α-SMA was higher in ADGN patients than in control and Berger's Disease groups. Glomerular vimentin was higher in individuals with ADGN than in those with Podocytopathy, Lupus Nephritis, Berger's Disease and Thin Basement Membrane Disease/Alport Syndrome. There was a positive correlation between fibronectin in the tubulointerstitial compartment and creatinine levels, between α-SMA and vimentin in both tubulointerstitial and glomerular compartments, and between urea and creatinine levels of patients, regardless of their nephropathy (p<0.05 for all results).

Conclusion: These markers may possibly be used as indicators of renal functional impairment in various nephropathies in pediatric patients.
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http://dx.doi.org/10.1016/j.prp.2016.09.008DOI Listing
December 2016

Diagnosis of congenital and infantile nephrotic syndromes in renal biopsies in Minas Gerais, Brazil: Six case reports.

Ultrastruct Pathol 2016 Nov-Dec;40(6):311-316. Epub 2016 Sep 26.

a General Pathology Division, Biological and Natural Sciences Institute , Federal University of Triângulo Mineiro , Uberaba , Minas Gerais , Brazil.

Congenital or infantile nephrotic syndromes (CNS/INS) correspond to a heterogeneous group of rare diseases in which glomerular renal dysfunction and proteinuria are prominent. The aim of this study is to present six cases of possible CNS/INS with diagnoses based on clinical findings and especially histological, ultrastructural, and immunohistochemical characteristics of renal biopsies. Four cases are presented with diffuse mesangial sclerosis, one of them possibly part of Denys-Drash syndrome and two cases with CNS probably of the Finnish type in patients between 3 months old and 13 years old. The study focuses on the late evolution of Denys-Drash syndrome to end-stage renal disease in a 13-year-old patient and the diagnosis of diffuse mesangial sclerosis in an 8-year-old patient. Thus, it contributes to a better epidemiological characterization of these syndromes, demonstrating cases of CNS/INS in infrequent age groups.
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http://dx.doi.org/10.1080/01913123.2016.1221868DOI Listing
April 2018

Targeted Screening of Fabry Disease in Male Hemodialysis Patients in Brazil Highlights Importance of Family Screening.

Nephron 2016 31;134(4):221-230. Epub 2016 Aug 31.

Introduction: Fabry disease (FD) is a lysosomal storage disorder caused by enzyme α galactosidase A (α-Gal A) deficiency due to mutations in the galactosidase alpha (GLA) gene. It leads to damage several organs, such as the kidneys, due to progressive accumulation of glycosphingolipids.

Objective: To estimate the prevalence of FD among male hemodialysis (HD) patients in a northern state of Brazil.

Methods: Screening was performed using a dried blood spot on filter paper to identify patients with low α-Gal A enzyme activity (≤2.2 µmol/l/h). Those with low enzyme activity underwent genetic analysis of the GLA gene. Family screening was conducted in the index cases.

Results: 2,583 male HD patients (age: 52 (18-91 years)) were screened. The α-Gal A assay identified 72 males (2.78%) with low enzyme activity. Genotyping identified 3 patients with GLA mutations: W204X, A368T, both previously reported; and C52F, a novel missense mutation. Only the patient with W204X mutation had classic FD. The prevalence rate was 0.12%. Family screening of the index cases identified 23 family members with the same mutations.

Conclusions: The prevalence of FD amongst male HD patients found in the Northern of Brazil was low (0.12%). However, family screening of the 3 index cases identified family members at an early stage of the disease, which may benefit from earlier treatment.
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http://dx.doi.org/10.1159/000448740DOI Listing
March 2017

Renal involvement in Fabry disease.

J Bras Nefrol 2016 Jun;38(2):245-54

Universidade Federal do Triângulo Mineiro, Brazil.

Every cell in the human body has globotriaosylceramide accumulation (Gb3) in Fabry disease due to the mutation in gene of the enzyme α-galactosidase A. It is a disease linked to sex. The main clinical features are: cutaneous angiokeratomas; acroparestesias and early strokes; decreased sweating and heat intolerance; ocular changes; myocardial hypertrophy, arrhythmias; gastrointestinal disorders and renal involvement. Renal involvement occurs due to Gb3 accumulation in all types of renal cells. Therefore, patients may present glomerular and tubular function disorders. Podocytes are particularly affected, with pedicels effacement and development of proteinuria. The diagnosis is made by detection of reduced plasma or leukocyte α-galactosidase activity and genetic study for detecting the α-galactosidase gene mutation. Treatment with enzyme replacement contributes to delay the progression of kidney disease, especially if initiated early.
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http://dx.doi.org/10.5935/0101-2800.20160034DOI Listing
June 2016

Morphometric evaluation of the aortic root in stillborns.

Pathol Res Pract 2016 Aug 1;212(8):686-9. Epub 2016 Apr 1.

General Pathology Sector, Biological and Natural Sciences Institute (ICBN), Triângulo Mineiro Federal University (UFTM), Uberaba, MG, Brazil.

Objective: To describe the dimensions and amount of collagen in the aortic root of autopsied fetuses at different gestational ages.

Material And Methods: 40 samples of aortic roots were selected from autopsied fetuses with gestational ages ranging between 20 and 40 weeks. The thickness and the area of the aortic wall were analyzed on slides stained with Hematoxylin and Eosin, and the collagen was quantified on slides stained with Picrosirius, by using an image analyzing system.

Results: A positive correlation was observed between the thickness of the media layer of the aortic wall and the gestational age. There was a positive and significant correlation between the percentage of collagen in the aortic wall with gestational age and fetal weight. The correlation between gestational age and the area of the aortic root circumference was positive and significant. And the correlation between the aortic diameter and the gestational age as well as fetal length was positive and significant.

Conclusion: The thickness of the media layer, the amount of collagen in the aortic wall, the area of the aortic root circumference and the aortic diameter rose with the increase of the gestational age. Thus, the morphological analysis of the aortic root may help as a parameter during the follow-up of inter-uterine growth and fetal development.
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http://dx.doi.org/10.1016/j.prp.2016.03.012DOI Listing
August 2016