Key result
In children with systemic lupus erythematosus, those with lupus nephritis had higher median serum hepcidin and pulse wave velocity.
Why the study?
Children with systemic lupus erythematosus and lupus nephritis face increased cardiovascular risk, but whether hepcidin levels and arterial stiffness are higher in those with biopsy-proven nephritis was unknown.
Do children with systemic lupus erythematosus and lupus nephritis have higher hepcidin levels and pulse wave velocity compared to those without kidney disease?
Cross-Sectional (n=16)
No
Do children with systemic lupus erythematosus and lupus nephritis have higher hepcidin levels and pulse wave velocity compared to those without kidney disease?
Children with lupus nephritis demonstrate a trend toward higher serum hepcidin and pulse wave velocity compared to those with SLE alone, suggesting a potential link between hepcidin and cardiovascular risk in this population.
Answers are grounded in this paper and cite their sources.
No significant differences seen; leaves open possible links of nephritis with hepcidin and stiffness in pediatric SLE.
BACKGROUND: Cardiovascular disease is common in patients with systemic lupus erythematosis (SLE) and lupus nephritis (LN). Up to 80% of children with SLE develop kidney disease, which is also associated with increased risk for cardiovascular disease and death compared to those without renal involvement. Hepcidin is an iron-regulatory protein which may contribute to atherosclerosis and is elevated in autoimmune disease. Pulse wave velocity (PWV) is a validated indicator of arterial stiffness, an early marker of cardiovascular risk, and is increased in children with SLE versus healthy controls. Our objective was to quantify hepcidin and PWV in children with SLE and investigate if those with biopsy-proven LN have higher hepcidin levels and higher PWV compared to those without kidney disease. METHODS: Cross-sectional analysis with hepcidin was measured via ELISA assay in 16 children aged 10-21 years with SLE recruited from a single center. Subjects were classified as having LN if histologic evidence of the disease was documented on a clinical renal biopsy. Serum hepcidin was quantified using a validated competitive enzyme-linked immunoassay. Carotid-femoral PWV was measured using applanation tonometry. Wilcoxon rank sum testing was used to compare median levels of hepcidin, PWV, and other continuous variables by nephritis status. RESULTS: The cohort (n = 16) was 93.8% female and 68.8% African-American with mean (SD) 16 (3.6) years. 37.5% (n = 6) had LN. Overall median (IQR) hepcidin was 34.4 (18.9, 91.9) ng/ml, and PWV 4.4 (4, 4.6) meters/second. Although significance was limited by small sample size, both hepcidin and PWV were higher in the subjects with LN. Median (IQR) hepcidin in subjects with LN was 71.5 (26.4, 116.4) ng/ml compared to 27.9 (18.7, 59.7) ng/ml in those with SLE(p = 0.19). Similarly, median (IQR) PWV in those with LN was 4.4 (4.4, 4.9) meters/second compared to 3 (3.75, 4.55) meters/second in those with without kidney involvement (p = 0.10). CONCLUSION: PWV and serum hepcidin were higher in subjects with LN compared to those with SLE alone, suggesting that elevated hepcidin levels may be associated with morbid CV changes in children with LN. This association, along with identification of additional predictors of arterial stiffness in patients with LN, warrants further investigation.
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Atkinson et al. (2019) conducted a cross-sectional in Systemic lupus erythematosus and lupus nephritis (n=16). Lupus nephritis vs. Systemic lupus erythematosus without lupus nephritis was evaluated on Median serum hepcidin level (ng/ml) (p=0.19). In children with systemic lupus erythematosus, those with lupus nephritis had higher median serum hepcidin and pulse wave velocity.
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