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Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs
BACKGROUND: We investigated the incidence of chronic kidney disease (CKD) progression and its factors relevant to patients with stable rheumatoid arthritis (RA). METHODS: We enrolled consecutive patients with RA who had initiated treatment with a biologic disease-modifying anti-rheumatic drug (bDMAR...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9217658/ https://www.ncbi.nlm.nih.gov/pubmed/35756739 http://dx.doi.org/10.1093/ckj/sfac036 |
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author | Hanaoka, Hironari Kikuchi, Jun Hiramoto, Kazuoto Saito, Shuntaro Kondo, Yasushi Kaneko, Yuko |
author_facet | Hanaoka, Hironari Kikuchi, Jun Hiramoto, Kazuoto Saito, Shuntaro Kondo, Yasushi Kaneko, Yuko |
author_sort | Hanaoka, Hironari |
collection | PubMed |
description | BACKGROUND: We investigated the incidence of chronic kidney disease (CKD) progression and its factors relevant to patients with stable rheumatoid arthritis (RA). METHODS: We enrolled consecutive patients with RA who had initiated treatment with a biologic disease-modifying anti-rheumatic drug (bDMARD) at our institution and continued the same drug for >5 years between 2001 and 2016. Patients with CKD at bDMARD initiation were excluded. C-reactive protein (CRP) level, Clinical Disease Activity Index (CDAI) score and estimated glomerular filtration rate were measured every 6 months. RESULTS: We included 423 patients, with 196 on tumour necrosis factor inhibitors, 190 on tocilizumab and 37 on abatacept. Among these patients, 34 (8.0%) progressed to CKD within 5 years. The mean CRP level and CDAI score over 5 years were significantly lower in patients without CKD progression than in those with CKD progression (P < .001 and P = .008, respectively). Multivariable analysis revealed that age at bDMARD initiation [odds ratio (OR) 1.05, P = .002], non-steroidal anti-inflammatory drug use (OR 3.47, P = .004) and mean CRP >0.14 mg/dL (OR 5.89, P = .015) were independently associated with CKD progression, while tocilizumab use was associated with a decreased risk of CKD progression (OR 0.31, P = .027). CONCLUSIONS: Controlling inflammation contributes to the inhibition of CKD progression in RA patients. |
format | Online Article Text |
id | pubmed-9217658 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-92176582022-06-23 Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs Hanaoka, Hironari Kikuchi, Jun Hiramoto, Kazuoto Saito, Shuntaro Kondo, Yasushi Kaneko, Yuko Clin Kidney J Original Article BACKGROUND: We investigated the incidence of chronic kidney disease (CKD) progression and its factors relevant to patients with stable rheumatoid arthritis (RA). METHODS: We enrolled consecutive patients with RA who had initiated treatment with a biologic disease-modifying anti-rheumatic drug (bDMARD) at our institution and continued the same drug for >5 years between 2001 and 2016. Patients with CKD at bDMARD initiation were excluded. C-reactive protein (CRP) level, Clinical Disease Activity Index (CDAI) score and estimated glomerular filtration rate were measured every 6 months. RESULTS: We included 423 patients, with 196 on tumour necrosis factor inhibitors, 190 on tocilizumab and 37 on abatacept. Among these patients, 34 (8.0%) progressed to CKD within 5 years. The mean CRP level and CDAI score over 5 years were significantly lower in patients without CKD progression than in those with CKD progression (P < .001 and P = .008, respectively). Multivariable analysis revealed that age at bDMARD initiation [odds ratio (OR) 1.05, P = .002], non-steroidal anti-inflammatory drug use (OR 3.47, P = .004) and mean CRP >0.14 mg/dL (OR 5.89, P = .015) were independently associated with CKD progression, while tocilizumab use was associated with a decreased risk of CKD progression (OR 0.31, P = .027). CONCLUSIONS: Controlling inflammation contributes to the inhibition of CKD progression in RA patients. Oxford University Press 2022-01-31 /pmc/articles/PMC9217658/ /pubmed/35756739 http://dx.doi.org/10.1093/ckj/sfac036 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of the ERA. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Original Article Hanaoka, Hironari Kikuchi, Jun Hiramoto, Kazuoto Saito, Shuntaro Kondo, Yasushi Kaneko, Yuko Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs |
title | Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs |
title_full | Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs |
title_fullStr | Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs |
title_full_unstemmed | Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs |
title_short | Decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs |
title_sort | decreased chronic kidney disease in rheumatoid arthritis in the era of biologic disease-modifying anti-rheumatic drugs |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9217658/ https://www.ncbi.nlm.nih.gov/pubmed/35756739 http://dx.doi.org/10.1093/ckj/sfac036 |
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