Additional B‐Lymphocyte Stimulator Inhibitors Treatment Facilitated Glucocorticoid Withdrawal in Lupus Nephritis Patients: A Real‐World Retrospective Observational Single‐Center Cohort Study
- 1Peking University First Hospital, Peking University
Abstract
Glucocorticoid (GC) withdrawal remains a major challenge for lupus nephritis (LN). In this 20-year retrospective cohort, we evaluated whether B-lymphocyte stimulator (BLyS) inhibitors facilitated GC discontinuation. Among 702 LN patients, 553 were treated with standard-of-care alone, and 149 received add-on BLyS inhibitors (belimumab or telitacicept). Patients receiving BLyS inhibitors achieved a higher rate of GC withdrawal than those receiving standard-of-care alone (10.7% vs. 5.61%, p = 0.026). Kaplan-Meier analysis confirmed a higher cumulative incidence of GC withdrawal in the BLyS inhibitor group (p = 0.001). After adjusting for age, sex, Systemic Lupus Erythematosus Disease Activity Index, acute kidney injury, nephrotic syndrome, and renal histopathology, time-dependent Cox regression revealed that BLyS inhibitor therapy was independently associated with a higher GC withdrawal rate (hazard ratio [HR] = 7.97, 95% confidence interval [CI]: 4.11-15.5, p < 0.001). Exploratory subgroup analyses indicated that among GC‑discontinued patients, Class IV LN predominated in the BLyS inhibitor group, whereas Class V LN was more prevalent in controls. During follow-up, no renal flares occurred in BLyS inhibitor-treated patients who discontinued GCs, though there was no significant between-group difference. In conclusion, add-on BLyS inhibitor therapy may serve as a potential steroid withdrawal-permissive approach for LN, pending further prospective validation of its clinical applicability.
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BibTeX
@article{jin2026additional,
title = {{Additional B‐Lymphocyte Stimulator Inhibitors Treatment Facilitated Glucocorticoid Withdrawal in Lupus Nephritis Patients: A Real‐World Retrospective Observational Single‐Center Cohort Study}},
author = {Jingjing Jin and Meng Tan and Minghui Zhao and Ying Tan},
journal = {MedComm},
year = {2026},
month = oct,
doi = {10.1002/mco2.71113},
url = {https://europepmc.org/article/PMC/PMC13718938},
note = {CC BY},
}
RIS
TY - JOUR
TI - Additional B‐Lymphocyte Stimulator Inhibitors Treatment Facilitated Glucocorticoid Withdrawal in Lupus Nephritis Patients: A Real‐World Retrospective Observational Single‐Center Cohort Study
AU - Jingjing Jin
AU - Meng Tan
AU - Minghui Zhao
AU - Ying Tan
PY - 2026
DA - 2026/10/29
JO - MedComm
DO - 10.1002/mco2.71113
UR - https://europepmc.org/article/PMC/PMC13718938
AB - Glucocorticoid (GC) withdrawal remains a major challenge for lupus nephritis (LN). In this 20-year retrospective cohort, we evaluated whether B-lymphocyte stimulator (BLyS) inhibitors facilitated GC discontinuation. Among 702 LN patients, 553 were treated with standard-of-care alone, and 149 received add-on BLyS inhibitors (belimumab or telitacicept). Patients receiving BLyS inhibitors achieved a higher rate of GC withdrawal than those receiving standard-of-care alone (10.7% vs. 5.61%, p = 0.026). Kaplan-Meier analysis confirmed a higher cumulative incidence of GC withdrawal in the BLyS inhibitor group (p = 0.001). After adjusting for age, sex, Systemic Lupus Erythematosus Disease Activity Index, acute kidney injury, nephrotic syndrome, and renal histopathology, time-dependent Cox regression revealed that BLyS inhibitor therapy was independently associated with a higher GC withdrawal rate (hazard ratio [HR] = 7.97, 95% confidence interval [CI]: 4.11-15.5, p < 0.001). Exploratory subgroup analyses indicated that among GC‑discontinued patients, Class IV LN predominated in the BLyS inhibitor group, whereas Class V LN was more prevalent in controls. During follow-up, no renal flares occurred in BLyS inhibitor-treated patients who discontinued GCs, though there was no significant between-group difference. In conclusion, add-on BLyS inhibitor therapy may serve as a potential steroid withdrawal-permissive approach for LN, pending further prospective validation of its clinical applicability.
SN - 2688-2663
ER -