Article Text
Abstract
Introduction Chronic kidney disease (CKD) is a common comorbidity of rheumatoid arthritis (RA). The association of longitudinal RA disease activity with long-term kidney function has remained uncertain.
Method We analysed a multicentre prospective RA registry in the USA from 2001 to 2022. The exposure was updated time-averaged Clinical Disease Activity Index (TA-CDAI) categories from study enrolment. The primary outcome was a longitudinal estimated glomerular filtration rate (eGFR) change. Secondary outcomes included developments of CKD stage G3a (eGFR<60 mL/min/1.73 m2) and stage G3b (eGFR<45 mL/min/1.73 m2). Results were adjusted for relevant time-fixed and time-varying covariates.
Results 31 129 patients (median age: 58.0 years, female: 76.3%, median eGFR: 90.7 mL/min/1.73 m2) contributed 234 973 visits and 146 778 person-years of follow-up. Multivariable mixed-effect linear model showed an average annual eGFR decline during follow-up in the TA-CDAI-remission group of −0.83 mL/min/1.73 m2 and estimated additional annual declines (95% CI) of –0.09 (–0.15 to –0.03) in low, –0.17 (−0.23 to –0.10) in moderate and −0.18 (–0.27 to –0.08) mL/min/1.73 m2 in high disease activity patients. Compared with TA-CDAI remission, adjusted HRs (95% CI) for CKD stage G3a during follow-up were 1.15 (1.01 to 1.30) in low, 1.22 (1.06 to 1.40) in moderate and 1.27 (1.05 to 1.52) in high disease activity; for CKD stage G3b, 1.22 (0.84 to 1.76) in low, 1.66 (1.12 to 2.45) in moderate and 1.93 (1.16 to 3.20) in high disease activity.
Conclusions Higher RA disease activity was associated with accelerated eGFR decline and increased risk of clinically relevant kidney dysfunction. Future intervention studies should attempt to replicate the association between RA disease activity and eGFR.
- Rheumatoid Arthritis
- Epidemiology
- Arthritis, Rheumatoid
- Atherosclerosis
Data availability statement
No data are available. Data are not available publicly.
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Data availability statement
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Footnotes
Handling editor Josef S Smolen
Contributors SF and DHS contributed to the original conception and design of this study, which WCW, SKT, JM, LH, HJL and TS reviewed and corrected. SF and HG collected data. SF performed data analysis with supervision from LH, HJL, TS and DHS. SF, WCW, SKT, JM and DHS initially interpreted the data, and other authors advised on the interpretation. SF drafted the original manuscript, which was critically reviewed and revised by all other authors. All authors have read and approved the final version of the manuscript. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted. SF is the guarantor.
Funding This study was supported by funding from National Institute of Arthritis and Musculoskeletal and Skin Diseases P30 AR072577 (PI: DHS).
Competing interests WCW reports having served as a scientific advisor or consultant to Actos, Akebia, Ardelyx, AstraZeneca, Bayer, Cadrenal, GlaxoSmithKline, Lilly, Merck, Natera, Pharmacosmos, Unicycive, Vera and Zydus. SKT reports consulting fees from Novartis. LH reports employment of CorEvitas, consultant to AbbVie, Bristol Myers Squibb, Pfizer, Roche and speakers bureau for Bristol Myers Squibb. DHS reports salary support through research contracts to his institution from CorEvitas, Janssen and Novartis.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Provenance and peer review Not commissioned; externally peer reviewed.
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