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Vol. 42. Issue S2.
Pages 324 (November 2020)
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Vol. 42. Issue S2.
Pages 324 (November 2020)
537
Open Access
PANEL OF NOVEL KIDNEY INJURY BIOMARKERS IN A LARGE COHORT OF CHILDREN WITH SICKLE CELL ANEMIA
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A.R. Belisárioa,b, R.S. Filhab, J.A. Almeidab, F.G. Mendesb, P.V. Rezendea, E.L.M. Vieirab, A.C.S.E. Silvab
a Fundação Centro de Hematologia e Hemoterapia do Estado de Minas Gerais (Hemominas), Belo Horizonte, MG, Brazil
b Universidade Federal de Minas Gerais (UFMG), Belo Horizonte, MG, Brazil
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Introduction: Patients with sickle cell anemia (SCA) suffer from structural and functional kidney abnormalities. Subclinical kidney dysfunction is common in patients with SCA, and routine laboratory tests for chronic kidney disease (CKD) screening are not able to detect early changes in kidney function. Thus, there is a need for additional biomarkers to early recognize which children are at highest risk for CKD and end-stage renal disease (ESRD). Aim: The aim of this study was to compare novel kidney injury biomarkers in urine samples of health controls and SCA children with and without albuminuria. Methods: A cross-sectional study of children selected from the Minas Gerais state cohort were assigned to three groups: 1) children with SCA who had albuminuria (n = 104); 2) children with SCA and normal albuminuria (n = 262); 3) healthy control children (n = 13). Fifteen kidney injury biomarkers in urine were measured using multilplex xMAP® assays. Albuminuria was defined as urine albumin/creatinine ratio >30 mg/g. The estimated glomerular filtration rate (eGFR) was calculated using the updated pediatric Schwartz formula. Results: Participants with SCA were recruited from a wide age range (1.9-18.9 years; median, 10.7 years), and 189 (51.6%) were female. Nearly two thirds of the participants were under hydroxyurea (HU) therapy (57.1%), and 12% were on both chronic transfusion and HU therapy. No children were receiving angiotensin converting enzyme inhibitors or angiotensin receptor blockers at the time of urine sampling. All biomarkers levels were significantly higher in urine samples of children with SCA when compared with health controls. After adjustment for age, we found eleven urine kidney injury biomarkers associated with albuminuria [Epidermal Growth Factor (EGF), Neutrophil gelatinase-associated lipocalin (LIPOCALIN-2/NGAL), Clusterin, Cystatin C, Alpha-1-microglobulin, Calbindin, Osteoactivin, TIMP Metalloproteinase inhibitor 1 (TIMP-1), Kidney Injury Molecule-1 (KIM-1), Fatty Acid-Binding Protein 1 (FABP-1), and Collagen IV] and ten biomarkers associated with glomerular hyperfiltration (EGF, LIPOCALIN-2/NGAL, Clusterin, Cystatin C, Alpha-1-microglobulin, Osteoactivin, TIMP-1, KIM-1, Renin, and Collagen IV). Discussion: In our study, we found eleven urine kidney injury biomarkers associated with albuminuria and ten biomarkers associated with glomerular hyperfiltration. These biomarkers are indicators of functional or structural impairment that are linked to an ongoing pathophysiology and thus may also provide information and insights into the underlying mechanisms of sickle cell nephropathy. Conclusion: In summary, levels of novel kidney injury biomarkers were associated with albuminuria and glomerular hyperfiltration in Brazilian children with SCA, suggesting concomitant structural and functional abnormalities. Our results highlight the importance of early detection of sickle cell nephropathy and provide insight into the use of novel kidney injury biomarkers.

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Hematology, Transfusion and Cell Therapy
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