Authors
Lucia Zhu, Evelyne Vinet, Arielle Mendel, Christian A Pineau, Fares Kalache, Louis-Pierre Grenier, Thao Huynh, Karim Sacre, Sasha Bernatsky
Published in
The Journal of rheumatology. Oct 15, 2026. Epub Oct 15, 2026.
Abstract
We evaluated patterns of N-terminal prohormone of n-terminal brain natriuretic peptide (NT-proBNP, a biomarker of cardiac disease) in SLE, and associations with demographic and clinical characteristics.
We analyzed data from the McGill SLE Research Cohort, including yearly serum NTproBNP. We assessed prevalence of baseline elevated NT-proBNP (≥133 ng/L) , and associations with baseline variables: age, sex, race/ethnicity, age at SLE diagnosis, SLE duration, smoking, and SLE International Collaborating Clinics Damage Index. Patients were classified into four NT-proBNP patterns: abnormal at baseline and remaining abnormal; abnormal and normalizing; normal and becoming abnormal; normal and remaining normal. We compared baseline characteristics across patterns using multivariate logistic regressions.
We studied 294 patients with ≥2 measurements. At baseline, 101 (34.4%) had elevated NT-proBNP. Higher levels were associated with older age at SLE diagnosis, longer SLE duration, cardiovascular damage, pulmonary hypertension, and renal damage. Of 101 individuals with abnormal baseline NT-proBNP, 79 (78.2%) remained abnormal. Of the 193 with normal baseline levels, 30 (15.5%) became abnormal. No patient with a baseline level ≥350 normalized to <133. High-risk patterns (abnormal-remaining-abnormal and normal-becoming-abnormal) were more likely to have cardiovascular damage (OR 3.90, 95% CI 1.49-12.5, renal damage (OR 2.87, 95% CI 1.61-5.51), and pulmonary hypertension (OR 32.0, 95% CI 4.59-651.1).
Over one-third of SLE patients had abnormal baseline NT-proBNP; most (78%) remained abnormal. Over 15% of those with an initially normal value became abnormal. Higher levels were associated with age, SLE duration, and organ damage. Levels ≥350 ng/L did not normalize over our evaluation.
PMID:
42880891
Bibliographic data and abstract were imported from PubMed on 16 Oct 2026.
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