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      Levels of angiotensin-converting enzyme 1 and 2 in serum and urine of children with Sickle Cell Disease Translated title: Níveis de enzima conversora da angiotensina 1 e 2 no soro e na urina de crianças com Doença Falciforme

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          Abstract

          Introduction:

          Sickle cell nephropathy begins in childhood and presents early increases in glomerular filtration, which, over the long term, can lead to chronic renal failure. Several diseases have increased circulating and urinary angiotensin-converting enzyme (ACE) activity, but there is little information about changes in ACEs activity in children with sickle cell disease (SCD).

          Objective:

          We examined circulating and urinary ACE 1 activity in children with SCD.

          Methods:

          This cross-sectional study compared children who were carriers of SCD with children who comprised a control group (CG). Serum and urinary activities of ACE were evaluated, as were biochemical factors, urinary album/creatinine rates, and estimated glomerular filtration rate.

          Results:

          Urinary ACE activity was significantly higher in patients with SCD than in healthy children (median 0.01; range 0.00-0.07 vs median 0.00; range 0.00-0.01 mU/mL·creatinine, p < 0.001. No significant difference in serum ACE activities between the SCD and CG groups was observed (median 32.25; range 16.2-59.3 vs median 40.9; range 18.0-53.4) mU/m`L·creatinine, p < 0.05.

          Conclusion:

          Our data revealed a high urinary ACE 1 activity, different than plasmatic level, in SCD patients suggesting a dissociation between the intrarenal and systemic RAAS. The increase of urinary ACE 1 activity in SCD patients suggests higher levels of Ang II with a predominance of classical RAAS axis, that can induce kidney damage.

          Resumo

          Introdução:

          A nefropatia falciforme começa na infância e apresenta aumentos precoces na filtração glomerular, que, em longo prazo, podem levar à insuficiência renal crônica. Várias doenças têm aumentado a atividade da enzima conversora da angiotensina (ECA) urinária e circulante, mas há pouca informação sobre alterações na atividade das ECAs em crianças com doença falciforme (DF).

          Objetivo:

          Examinamos a atividade da ECA-1 circulante e urinária em crianças com DF.

          Métodos:

          Este estudo transversal comparou crianças que eram portadoras de DF com crianças que compunham um Grupo Controle (GC). As atividades séricas e urinárias da ECA foram avaliadas, assim como os fatores bioquímicos, a relação albumina/creatinina urinária e a taxa de filtração glomerular estimada.

          Resultados:

          A atividade urinária da ECA foi significativamente maior em pacientes com DF do que em crianças saudáveis (mediana 0,01; intervalo 0,00-0,07 vs mediana 0,00; intervalo 0,00-0,01 mU/mL·creatinina, p < 0,001. Não foi observada diferença significativa nas atividades séricas da ECA entre os grupos DF e GC (mediana 32,25; intervalo 16,2-59,3 vs mediana 40,9; intervalo 18,0-53,4) mU/mL·creatinina, p < 0,05.

          Conclusão:

          Nossos dados revelaram uma alta atividade urinária da ECA-1, diferente do nível plasmático, em pacientes com DF, sugerindo uma dissociação entre o Sistema Renina Angiotensina Aldosterona (SRAA) intra-renal e sistêmico. O aumento da atividade urinária da ECA-1 em pacientes com DF sugere níveis mais elevados de Ang II com predominância do eixo clássico do SRAA, que pode induzir lesão renal.

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          Most cited references43

          • Record: found
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          Evaluation and management of chronic kidney disease: synopsis of the kidney disease: improving global outcomes 2012 clinical practice guideline.

          The Kidney Disease: Improving Global Outcomes (KDIGO) organization developed clinical practice guidelines in 2012 to provide guidance on the evaluation, management, and treatment of chronic kidney disease (CKD) in adults and children who are not receiving renal replacement therapy. The KDIGO CKD Guideline Development Work Group defined the scope of the guideline, gathered evidence, determined topics for systematic review, and graded the quality of evidence that had been summarized by an evidence review team. Searches of the English-language literature were conducted through November 2012. Final modification of the guidelines was informed by the KDIGO Board of Directors and a public review process involving registered stakeholders. The full guideline included 110 recommendations. This synopsis focuses on 10 key recommendations pertinent to definition, classification, monitoring, and management of CKD in adults.
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            The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents

            (2004)
            PEDIATRICS, 114(2), 555-576
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              Glomerular hyperfiltration: definitions, mechanisms and clinical implications.

              Glomerular hyperfiltration is a phenomenon that can occur in various clinical conditions including kidney disease. No single definition of glomerular hyperfiltration has been agreed upon, and the pathophysiological mechanisms, which are likely to vary with the underlying disease, are not well explored. Glomerular hyperfiltration can be caused by afferent arteriolar vasodilation as seen in patients with diabetes or after a high-protein meal, and/or by efferent arteriolar vasoconstriction owing to activation of the renin-angiotensin-aldosterone system, thus leading to glomerular hypertension. Glomerular hypertrophy and increased glomerular pressure might be both a cause and a consequence of renal injury; understanding the renal adaptations to injury is therefore important to prevent further damage. In this Review, we discuss the current concepts of glomerular hyperfiltration and the renal hemodynamic changes associated with this condition. A physiological state of glomerular hyperfiltration occurs during pregnancy and after consumption of high-protein meals. The various diseases that have been associated with glomerular hyperfiltration, either per nephron or per total kidney, include diabetes mellitus, polycystic kidney disease, secondary focal segmental glomerulosclerosis caused by a reduction in renal mass, sickle cell anemia, high altitude renal syndrome and obesity. A better understanding of the mechanisms involved in glomerular hyperfiltration could enable the development of new strategies to prevent progression of kidney disease.
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                Author and article information

                Journal
                J Bras Nefrol
                J Bras Nefrol
                jbn
                Jornal Brasileiro de Nefrologia
                Sociedade Brasileira de Nefrologia
                0101-2800
                2175-8239
                03 May 2021
                Jul-Sep 2021
                : 43
                : 3
                : 303-310
                Affiliations
                [1 ]Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Pediatria, Disciplina de Nefrologia, São Paulo, SP, Brasil.
                [2 ]Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Medicina, Disciplina de Nefrologia, São Paulo, SP, Brasil.
                [3 ]Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Pediatria, Disciplina de Hematologia, São Paulo, SP, Brasil.
                Author notes
                Correspondence to: Ho Chi Hsien. E-mail: hochihsien@ 123456gmail.com

                Authors’ Contributions

                All authors approved the final manuscript as submitted and agreed to be accountable for all aspects of the work.

                Ho Chi Hsien: Participated in the concept and design, analysis and interpretation of data, and drafting or revising of the manuscript, and approved the manuscript as submitted.

                Dulce Elena Casarini: Participated in the concept and design, analysis and interpretation of data, and drafting or revising of the manuscript, and approved the manuscript as submitted.

                João Tomas de Abreu Carvalhaes: Participated in the concept and design, analysis and interpretation of data, and drafting or revising of the manuscript, and approved the manuscript as submitted.

                Fernanda Aparecida Ronchi: Participated in the concept and design, analysis and interpretation of data, and drafting or revising of the manuscript, and approved the manuscript as submitted.

                Lilian Caroline Gonçalves de Oliveira: Participated in the analysis and interpretation of data, and drafting or revising of the manuscript, and approved the manuscript as submitted.

                Josefina Aparecida Pellegrini Braga: Participated in the concept and design, analysis and interpretation of data, and drafting or revising of the manuscript, and approved the manuscript as submitted.

                Conflict Of Interest

                The authors have no conflict of interest relevant to this article to disclose.

                Author information
                http://orcid.org/0000-0003-3355-4221
                http://orcid.org/0000-0003-1912-4292
                http://orcid.org/0000-0003-2991-1820
                http://orcid.org/0000-0002-0024-9602
                http://orcid.org/0000-0001-5117-6979
                http://orcid.org/0000-0001-7839-6904
                Article
                10.1590/2175-8239-JBN-2020-0174
                8428630
                33973994
                b8b214a8-ab0c-45d4-8d17-d4e53b261e69

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 08 August 2020
                : 11 January 2021
                Categories
                Original Article

                anemia,peptidyl-dipeptidase a,kidney,glomerular filtration rate,peptidil dipeptidase a,rim,taxa de filtração glomerular

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