Evidence for interactions between inflammatory markers and renin-angiotensin system molecules in the occurrence of albuminuria in children with sickle cell anemia

Belisário, André Rolim; Vieira, Érica Leandro Marciano; Almeida, Jéssica Alves de; Mendes, Fabíola Gomes; Miranda, Aline Silva de; Rezende, Paulo V.; Viana, Marcos Borato; Silva, Ana Cristina Simões e

doi:10.1016/j.cyto.2019.154800

Cited by 12 publications

(8 citation statements)

References 46 publications

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“…CXCL10 is elevated in HbSS-compared to HbAA-and independently discriminated between HbAA-and HbSS-, and was also significantly elevated in HbSC-compared to HbAA- (Figure 4, Supplement Figure 1). Previous studies have reported an important role of CXCL10 in SCD pathogenesis (29)(30)(31). A study assessing cytokine levels in SCA patients with and without albuminuria reported higher levels of CXCL10, CCL2, and IL-8 (also known as C-X-C motif ligand 8 CXCL8) in urine samples of children with albuminuria (31).…”

Section: Discussionmentioning

confidence: 99%

Hemoglobin Genotypes Modulate Inflammatory Response to Plasmodium Infection

et al. 2020

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In 2018, 228 million cases and 405,000 malaria-associated deaths were reported worldwide with a majority being in Africa. A wide range of factors, including parasitemia, host immunity, inflammatory responses to infection, and host hemoglobin genotype, mediate the severity of malaria. Among the hemoglobinopathies, hemoglobin S (HbS) is caused by a single amino acid substitution of Glutamic Acid replaced by Valine at the sixth position of the beta-globin chain (E6V). Hemoglobin C (HbC) on the other hand, involves a single amino acid substitution of Glutamic Acid by a Lysine (E6K), which has received the most attention. These substitutions alter the stability of Hb leading to wide-ranging hematological disorders. The homozygous state of hemoglobin S (HbSS) results in sickle cell anemia (SCA) whereas the heterozygous state (HbAS) results in sickle cell trait (SCT). Both mutations are reported to mediate the reduction in the severity and fatality of Plasmodium falciparum malaria. The mechanism underlying this protection is poorly understood. Since both malaria and sickle cell disease (SCD) are associated with the destruction of erythrocytes and widespread systemic inflammation, identifying which inflammatory factor(s) mediate susceptibility of individuals with different hemoglobin genotypes to Plasmodium infection could result in the discovery of new predictive markers and interventions against malaria or SCD severity. We hypothesized that hemoglobin genotypes modulate the inflammatory response to Plasmodium infection. We conducted a cross-sectional study in Ghana, West Africa, between 2014 and 2019 to ascertain the relationships between blood inflammatory cytokines, Plasmodium infection, and hemoglobin genotype. A total of 923 volunteers were enrolled in the study. A total of 74, age and sex-matched subjects were identified with various genotypes including HbAS, HbAC, HbSS, HbSC, HbCC, or HbAA. Complete blood counts and serum inflammatory cytokine expression levels were assessed. The results indicate that differential expression of CXCL10, TNF-α, CCL2, IL-8, and IL-6 were tightly linked to hemoglobin genotype and severity of Plasmodium infection and that these cytokine levels may be predictive for susceptibility to severe malaria or SCD severity.

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Section: Discussionmentioning

confidence: 99%

Hemoglobin Genotypes Modulate Inflammatory Response to Plasmodium Infection

et al. 2020

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“…In turn, IL-8 and IL-10 are important inflammatory molecules and their levels have been reported to be increased in patients with SCA during the VOE 22 and albuminuria. 23 Recently, Domingos et al demonstrated an association between increased IL-8 levels and LU occurrence in individuals with SCA followed up at a northeastern Brazilian reference center. 24 It has been suggested that the IL-8 acts as an activator for the epithelial to mesenchymal transition in the wound healing of diabetic foot ulcers, 25 in addition to its principal role as a chemokine for neutrophils.…”

Section: Discussionmentioning

confidence: 99%

Association between inflammatory molecules, nitric oxide metabolites and leg ulcers in individuals with sickle cell anemia

Belisário

Mendes-Oliveira

Souza

et al. 2022

Hematology, Transfusion and Cell Therapy

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“…There is a clear association between albuminuria in children with SCN and urinary levels of cytokines and chemokines, including IL-6, TNF, and MCP-1/CCL2. These molecules might be possible biomarkers for poorer outcomes in SCN [121]. In addition, high hemoglobin F and platelet levels were also associated with increased estimated glomerular filtration rate and albuminuria, respectively [122].…”

Section: Systemic Diseases Affecting the Kidneymentioning

confidence: 99%

2020 update on the renin–angiotensin–aldosterone system in pediatric kidney disease and its interactions with coronavirus

et al. 2020

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The last decade was crucial for our understanding of the renin-angiotensin-aldosterone system (RAAS) as a two-axis, counterregulatory system, divided into the classical axis, formed by angiotensin-converting enzyme (ACE), angiotensin II (Ang II), and the angiotensin type 1 receptor (AT1R), and the alternative axis comprising angiotensin-converting enzyme 2 (ACE2), angiotensin-(1-7) (Ang-(1-7)), and the Mas receptor. Breakthrough discoveries also took place, with other RAAS endopeptides being described, including alamandine and angiotensin A. In this review, we characterize the two RAAS axes and the role of their components in pediatric kidney diseases, including childhood hypertension (HTN), pediatric glomerular diseases, congenital abnormalities of the kidney and urinary tract (CAKUT), and chronic kidney disease (CKD). We also present recent findings on potential interactions between the novel coronavirus, SARS-CoV-2, and components of the RAAS, as well as potential implications of coronavirus disease 2019 (COVID-19) for pediatric kidney diseases.

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Evidence for interactions between inflammatory markers and renin-angiotensin system molecules in the occurrence of albuminuria in children with sickle cell anemia

Cited by 12 publications

References 46 publications

Hemoglobin Genotypes Modulate Inflammatory Response to Plasmodium Infection

Hemoglobin Genotypes Modulate Inflammatory Response to Plasmodium Infection

Association between inflammatory molecules, nitric oxide metabolites and leg ulcers in individuals with sickle cell anemia

2020 update on the renin–angiotensin–aldosterone system in pediatric kidney disease and its interactions with coronavirus

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