Serum hepcidin is increased in ANCA-associated vasculitis and correlates with activity markers
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
30204470
DOI
10.33549/physiolres.933765
PII: 933765
Knihovny.cz E-resources
- MeSH
- Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis blood diagnosis MeSH
- Anemia blood diagnosis MeSH
- Biomarkers blood MeSH
- Renal Insufficiency, Chronic blood diagnosis MeSH
- Adult MeSH
- Hepcidins blood MeSH
- Middle Aged MeSH
- Humans MeSH
- Aged MeSH
- Lupus Erythematosus, Systemic blood diagnosis MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Biomarkers MeSH
- Hepcidins MeSH
Hepcidin is a key regulator of iron metabolism and plays an important role in many pathologies. It is increased by iron administration and by inflammation, while erythropoiesis downregulates its expression. It decreases iron availability and thus contributes to anemia of chronic diseases. The aim of the study was to measure hepcidin as a marker and pathogenetic factor in ANCA-associated vasculitis (AAV). Hepcidin plasma concentration was measured by the immunological method in 59 patients with AAV and compared to patients with non-vasculitic etiology of chronic kidney disease, patients on hemodialysis (HD), with systemic lupus erythematodes (SLE) and to healthy controls and blood donors, and was correlated with the parameters of iron metabolism, inflammation, activity of the process and kidney function. Hepcidin concentration was increased in patients with AAV, SLE and HD and correlated positively with C-reactive protein, serum ferritin and creatinine, and negatively with hemoglobin and serum transferrin. In active form of AAV it correlated with the clinical scoring system (BVAS). Hepcidin can thus be considered as a pathogenetic factor of anemia in AAV and can be used for evaluation of inflammation in AAV and as an additional marker in active forms of the disease.
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