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Journal Article Ppublish

PubMed: 33973994 DOI: 10.1590/2175-8239-JBN-2020-0174

Levels of angiotensin-converting enzyme 1 and 2 in serum and urine of children with Sickle Cell Disease.

J Bras Nefrol 43(3):303-310

Authors: Ho Chi Hsien, Dulce Elena Casarini, João Tomas de Abreu Carvalhaes, Fernanda Aparecida Ronchi, Lilian Caroline Gonçalves de Oliveira, Josefina Aparecida Pellegrini Braga

Affiliations

  • Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Pediatria, Disciplina de Nefrologia, São Paulo, SP, Brasil.
  • Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Medicina, Disciplina de Nefrologia, São Paulo, SP, Brasil.
  • Universidade Federal de São Paulo, Escola Paulista de Medicina, Departamento de Pediatria, Disciplina de Hematologia, São Paulo, SP, Brasil.

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.

MeSH

Enzymes, Anemia, Sickle Cell, Child, Angiotensins, Kidney Diseases, Cells, Peptidyl-Dipeptidase A, Serum, Creatinine