Skip to main content
NCBI home page
Medicine logoLink to Medicine
. 2025 Sep 12;104(37):e44127. doi: 10.1097/MD.0000000000044127

Efficacy and safety of rituximab in Chinese patients of glomerular kidney diseases: An observational study

Jiadan Ye a,b, Chunyan Zhang a,*, Xiaolei Ren a, Lin Huang a, Xiaohong Zhang a
PMCID: PMC12440482  PMID: 40958232

Abstract

This study investigates the efficacy and safety of rituximab (RTX) in glomerular kidney diseases. Patients treated with RTX for glomerular kidney diseases in a tertiary hospital in 2021 and 2023 were selected. Clinical data were collected and reviewed before treatment and at 1, 2, 3, 6, and 12 months after initial treatment. Changes in white blood cells, hemoglobin, 24-hour urinary protein, creatinine, estimated glomerular filtration rate, albumin, B-cell count, remission rate, and adverse reaction rate were analyzed. A total of 30 patients were included, and during the follow-up period, 26 patients achieved clinical remission, including 8 cases of complete remission, 4 cases of no remission, and 5 cases of relapse. Compared to before treatment, albumin and 24-hour urinary protein significantly improved at 2, 3, 6, and 12 months after treatment (P < .05). In the high-dose group (14 patients) and low-dose group (16 patients), the time to achieve remission showed no significant difference (P > .05). No serious adverse reactions occurred during the follow-up period. In glomerular kidney diseases, RTX can deplete B-cell counts, improve 24-hour urinary protein and albumin levels, and low-dose RTX is as effective as high-dose RTX.

Keywords: Chinese, efficacy, glomerular kidney diseases, rituximab, safety

1. Introduction

Rituximab (RTX) is a human/mouse chimeric monoclonal antibody with established efficacy in various lymphatic system malignancies expressing CD20 and it has good safety profiles. Intravenous RTX received regulatory approval from the US Food and Drug Administration in 1997 and the European Medicines Agency in 1998 for relapsed/refractory indolent non-Hodgkin lymphoma. Subsequently, it was approved in 2009 and 2010 for chronic lymphocytic leukemia.[1] Following these approvals and with ongoing clinical trials, the indications for RTX and its off-label uses have expanded. In recent years, B-cell-targeted biologics have become effective strategies for treating various immune-mediated diseases, and RTX is one of the most important drugs in this category.[2] Multiple glomerular kidney diseases are immune-related, such as lupus nephritis, primary membranous nephropathy, and cold agglutinin disease kidney injury. Approximately 70% to 80% of patients with primary membranous nephropathy have phospholipase A2 receptor antibodies.[3] This makes the use of immunosuppressive drugs like RTX more rational. RTX is currently a first-line immunosuppressive therapy for patients with primary membranous nephropathy.[4]

2. Materials and methods

2.1. Data source

The patient data were obtained from Peking University People’s Hospital’s medical records system. Patients treated with RTX standard therapy (four RTX doses within 30 days or RTX cumulative dosage 2.0 g within 30 days) for glomerular kidney diseases from January 2021 to December 2023, with a follow-up period of more than 6 months were included. A total of 30 patients were included, and their basic information and laboratory indicators were collected.

2.2. Treatment protocol

All 30 patients received premedication, including dexamethasone injection 5 mg via intravenous injection, pheniramine injection 20 mg via intramuscular injection. RTX was provided by Roche Pharmaceuticals, with 2 specifications: 10 mL: 100 mg and 50 mL: 500 mg, approved with batch numbers J20170034 and J20170005, respectively. The patients were categorized into a high-dose group (single dose of 500 mg) and a low-dose group (single dose of 100 mg or 200 mg) based on the RTX single-dose amount.

2.3. Observation indicators

2.3.1. Characteristics

Patient Characteristics included gender, age, medical history, history of harmful habits, duration of glomerular kidney disease, and previous treatment plans. White blood cells, hemoglobin, 24-hour urinary protein, creatinine, estimated glomerular filtration rate, albumin, and B-cell count changes were recorded before treatment, and at 1, 2, 3, 6, and 12 months after treatment.

2.3.2. Efficacy

Clinical effectiveness was evaluated according to the “Chinese Expert Consensus on Immunotherapy for Adult Nephrotic Syndrome.”[5] Remission was divided into complete remission, partial remission, no remission, and relapse.

2.3.3. Safety

Short-term infusion reactions and long-term adverse reactions were recorded.

2.3.4. Statistical analysis

Excel 2016 and SPSS 27.0 were used to analyze statistical data. Data are expressed as mean ± standard deviation. Data comparison was done using one-way analysis of variance, with P < .05 indicating statistical significance.

3. Results

3.1. Characteristics

A total of 30 patients were included, including 20 males (66.7%) and 10 females (33.3%). The average age was 46.25 ± 13.25 years, and the disease duration was 2.35 ± 2.48 years. Sixteen patients (53.3%) had a history of tobacco and alcohol dependence. Only 3 patient (10%) used RTX as initial treatment. Among the 30 patients, 14 (46.7%) received a single dose of 500 mg of RTX. Pathological classification revealed that 21 patients (70%) had membranous nephropathy. Characteristics of the 30 included patients were shown in Table 1.

Table 1.

Characteristics of the 20 included patients.

Characteristics (%)
Male 20 (66.7%)
Age (yr) 46.25 ± 13.25
History of hypertension 17 (56.7%)
History of diabetes 4 (13.3%)
History of hyperlipidemia 16 (53.3%)
History of coronary heart disease 1 (3.3%)
Smoking history 9 (30%)
Drinking history 7 (23.3%)
Family history of kidney disease 2 (6.7%)
Duration of illness (yr) 2.35 ± 2.48
Prior hormonal and/ or immunosuppressive therapy 27 (90%)
RTX as initial treatment 3 (10%)
High dose group (RTX single dose) 14 (46.7%)
Membranous nephropathy 21 (70%)
Membrane nephropathy 3 (10%)
AAV 2 (6.7%)
Endocapillary hyperplasia nephropathy 1 (3.3%)
FSGS 1 (3.3%)
Others 2 (6.7%)
Open in a new tab

AAV = antineutrophil cytoplasmic antibody-associated small vessel vasculitis, FSGS = focal segmental glomerulosclerosis.

3.2. Efficacy analysis

3.2.1. Laboratory indicators

Compared to before treatment, there was no significant difference in white blood cells, hemoglobin, creatinine, and estimated glomerular filtration rate after treatment (P > .05). However, B-cell absolute values significantly decreased from the 1st month after treatment (P < .05). The 1st month albumin and 24-hour urinary protein did not significantly improve compared to before treatment (P > .05), but albumin and 24-hour urinary protein significantly improved at 2, 3, 6, and 12 months after treatment (P < .05). Compared to the 2nd month after treatment, there was no significant increase in albumin at the 3rd month (P > .05), but there was a significant difference in albumin between the 6th and 12th months after treatment compared to the 2nd month (P < .05). There was no significant decrease in 24-hour urinary protein at the 3rd, 6th, and 12th months after treatment compared to the 2nd month (P > .05), shown in Table 2.

Table 2.

Laboratory indices of patients at base line and during follow-up.

Time Leucocyte (109 g L−1) Creatinine (μmol L−1) Glomerular filtration rate (mL min−1 1.73 m−2) Albumin (g L−1) 24-hour urine protein (g 24 h−1) Absolute value of B cells (cell μL−1)
Before treatment (n = 30) 7.49 ± 2.39 147.28 ± 83.65 60.58 ± 33.42 26.88 ± 7.98 5.83 ± 4.35 32035 ± 105.80
1 mo after treatment (n = 30) 9.29 ± 2.95a 130.30 ± 70.56a 68.78 ± 36.12a 31.73 ± 6.10a 3.95 ± 2.98a 2.98 ± 2.12b
2 mo after treatment (n = 28) 10.01 ± 3.08a 124.38 ± 69.72a 66.75 ± 34.02a 35.08 ± 5.28b 3.53 ± 2.72b 12.88 ± 21.56b,e
3 mo after treatment (n = 26) 7.72 ± 2.61a,c 121.21 ± 85.30a,c 76.25 ± 34.58a,c 36.16 ± 6.34b,c 2.61 ± 2.08b,c 20.00 ± 38.48b,e
6 mo after treatment (n = 28) 6.49 ± 1.71a,c 114.84 ± 63.58a,c 74.74 ± 32.72a,c 40.42 ± 6.91b,d 1.68 ± 1.12b,c 10.10 ± 9.12b,e
9 mo after treatment (n = 15) 7.59 ± 1.58a,c 112.23 ± 40.05a,c 69.21 ± 25.37a,c 43.07 ± 5.98b,d 1.70 ± 2.43b,c 26.95 ± 33.48b,e
Open in a new tab

Based on one-way analysis of variance, compared to before treatment: aP > .05, bP < .05. Compared to the 2nd month after treatment: cP > .05, dP < .05. Compared to the 1st month after treatment: eP > .05.

3.2.2. Clinical efficacy

Of the 30 patients, 26 achieved clinical remission, including 8 cases of complete remission, 4 cases of no remission, and 3 cases of partial remission followed by a relapse (24-hour urinary protein exceeding 3.5 g again). The time to partial remission in 26 patients was (1.89 ± 1.58) months, complete remission in 8 patients occurred at (7.65 ± 3.90) months, and relapse in 3 patients happened at (6.88 ± 3.95) months. The effectiveness of RTX treatment is detailed in Table 3.

Table 3.

Clinical remission during follow-up.

Time CR PR NR Relapse
1 mo after treatment (n = 30) 0 (0.00%) 19 (63.33%) 11 (36.67%) 0 (0.00%)
2 mo after treatment (n = 28) 0 (0.00%) 19 (67.85%) 8 (28.57%) 1 (3.57%)
3 mo after treatment (n = 26) 2 (7.69%) 20 (76.92%) 4 (15.38%) 0 (0.00%)
6 mo after treatment (n = 28) 3 (10.71%) 22 (78.57%) 1 (3.57%) 2 (7.14%)
12 mo after treatment (n = 11) 4 (36.36%) 5 (45.45%) 0 (0.00%) 2 (18.18%)
Open in a new tab

CR = complete remission, NR = no remission, PR = partial remission, RTX = rituximab.

3.2.3. Impact of single RTX dose on efficacy

Among the 30 patients, 14 received a high dose of RTX (single dose of 500 mg), while the other 16 patients received a single dose of 100 mg or 200 mg. Each patient’s single-dose amount and dosing interval varied, and some patients received additional RTX based on B-cell absolute count recovery or disease relapse. The average cumulative RTX dose for the 30 patients was 1.70 ± 0.56 g, with the high-dose group at 2.48 ± 0.62 g and the low-dose group at 1.23 ± 0.54 g. The time to remission was 2.39 ± 1.45 months in the high-dose group and 1.85 ± 1.23 months in the low-dose group, with no significant difference between the 2 groups (P > .05).

3.2.4. Safety

During treatment, 2 patients experienced transient elevation of liver enzymes, but the levels did not exceed 3 times of the normal value. After hepatoprotective treatment, the liver enzyme levels returned to normal. None of the 30 patients experienced infusion reactions, and no other adverse reactions occurred during the follow-up period.

4. Discussion

Immune-mediated glomerular structural damage is a major cause of most glomerular kidney diseases related to pathology.[6] Factors in both innate and adaptive immune systems can cause cellular damage in glomerular kidney diseases.[7] Glomerular damage has both inflammatory and noninflammatory immune mechanisms.[8] The formation of immune complexes within the glomerulus typically leads to a cell-mediated inflammatory response. The main mediators and effector cells of the inflammatory response include complement and T cells.[6,9] Moreover, multiple immune mediators can directly induce podocyte functional disorders sufficient to cause proteinuria, even in the absence of inflammation, including T-cell-derived factors and vascular endothelial growth factor, among others.[10] For idiopathic nephrotic syndrome (INS), including 2 major histological diseases, minimal change disease (MCD) and primary focal segmental glomerulosclerosis (FSGS), the absence of immunoglobulin deposits in renal biopsy did not originally suggest that INS was an antibody-mediated disease.[11] However, some studies have shown that immunomodulatory factors in INS patients altered the glomerular permeability, leading to proteinuria.[10] In primary FSGS, it is also postulated that certain circulating factors lead to extensive podocyte functional impairment, manifested as widespread foot process fusion.[12]

B cells play a central role in the pathogenesis of many autoimmune diseases.[13,14] As a human/murine chimeric monoclonal antibody, RTX specifically binds to the B-cell surface antigen CD20.[15] This anti-CD20 monoclonal antibody has immunosuppressive effects by depleting B cells, reducing the production of antibodies and cytokines, and altering the antigen presentation process. RTX depletes B cells through 3 mechanisms: antibody-dependent cell-mediated cytotoxicity, complement-dependent cell-mediated cytotoxicity, and apoptosis.[16] Therefore, for immune-related glomerular kidney diseases, the rational use of rituximab is justified from a pathogenic perspective. For example, the characteristic of primary membranous nephropathy is the formation of autoantibodies and immune complex deposits, and RTX is currently the first-line immunosuppressive therapy for patients with primary membranous nephropathy.[4] The 2021 KDIGO guidelines also recommend RTX for the initial alternative treatment of antineutrophil cytoplasmic antibody-associated vasculitis.[4] Studies have shown that RTX induces remission in patients with frequently relapsing nephrotic syndrome secondary to MCD in both adults and children and in patients with steroid-dependent nephrotic syndrome, which may be due to the depletion of B cells that activate T cells in MCD and primary FSGS.[17,18]

The results of this study show that the albumin level significantly increased from the 2nd month after treatment, and 24-hour urinary protein significantly decreased from before treatment (P < .05), indicating that RTX is effective in treating glomerular kidney diseases and works relatively quickly, consistent with the literature. Zhao et al[19] found that albumin significantly increased in patients with primary IgA nephropathy 3 months after RTX treatment, and 24-hour urinary protein significantly decreased 1 month after treatment. Li Yanmei[20] study shows that for refractory kidney disease patients, there is a trend of remission in 24-hour urinary protein and albumin 1 month after RTX treatment. Creatinine levels and estimated glomerular filtration rate did not significantly differ during the follow-up period (P > .05), but creatinine levels showed a decreasing trend over time (144.30 ± 89.61 vs 114.11 ± 35.95), similar to the results of Sun et al[21] study. B cells significantly decreased from the 1st month after treatment (P < .05). Among all the indicators, B-cell depletion was the earliest to appear. Research has found that most patients experience a rapid decline in B-cell absolute count and percentage 4 days after RTX administration.[22] Clinical trials by Stone et al[23] found that peripheral blood CD19+ B-cell counts dropped to below 10 cells/mm3 after 2 infusions of rituximab and remained at that level for 6 months in most patients, which is consistent with the results of this study. There was no significant difference in white blood cells compared to before treatment, and no severe infections occurred during the follow-up period, indicating the safety of RTX.

About 63.33% of patients achieved partial remission after 1 month of treatment, and the rate of partial remission increased over time from 1 to 6 months (63.33% vs 78.57%), as shown in Table 3. Li Bin et al[21] study found that the remission rate was 41.67% at 3 months, 75.00% at 6 months, and 83.3% at 12 months in adults with atypical membranous nephropathy. In comparison, this study showed quicker effectiveness, but the remission rate was similar at 6 months. The criteria for partial remission used in this study refer to the “Expert Consensus on Immunotherapy for Adult Kidney Disease Syndromes in China,”[5] which defines partial remission as a 24-hour urinary protein between 0.3 and 3.5 g or a 50% reduction in 24-hour urinary protein compared to baseline, with stable renal function (creatinine increase <20% compared to baseline). In contrast, the KDIGO guidelines[4] require both criteria to be met for partial remission, so the remission rate in this study may be slightly higher. Five patients achieved partial remission 1 month after RTX treatment, but relapsed during the follow-up period at different times (2, 6, and 12 months). The overall relapse rate during the follow-up period was 16.7%. Reported relapse rates vary among published studies, ranging from 0%[21] to 33%.[24]

In patients who achieved complete response after RTX-treatment, the highest B-cell counts was 82 and the lowest was 1. In patients with partial response, the highest B-cell counts was 103 and the lowest was 0. The highest B-cell counts was 33 and the lowest was 0 in patients without remission. The highest B-cell counts in patients with recurrence was 5 and the lowest was 3. The results of this study did not show the correlation between clinical remission and B-cell counts, mainly due to the following 2 reasons: firstly, the number of patients was small, and not all patients were regularly monitored during treatment; secondly, the observation time was relatively short, and the correlation between clinical remission and B-cell counts has not been fully demonstrated.

Regarding the impact of the single RTX dose on efficacy and safety, most studies pertain to primary membranous nephropathy and antineutrophil cytoplasmic antibody-associated vasculitis, and results are controversial. Most studies support the efficacy and safety of low-dose RTX.[25–28] However, in Moroni et al study,[29] despite achieving B-cell depletion in all patients, low-dose RTX was less effective in IMN. In this study, the low-dose group had a higher remission rate at 3 months (89.5% vs 76.8%), but the high-dose group had a higher remission rate at 6 months (100% vs 91.8%). The low-dose group achieved remission faster than the high-dose group (1.21 vs 3.15 months), but the difference was not statistically significant (P > .05). The average cumulative dose of the low-dose group was lower than the high-dose group (1.23 vs 2.39 g), which is consistent with the literature. Moroni et al[29] also found that the average cumulative dose in the low-dose group was significantly lower than in the high-dose group (0.5 vs 1 g). The average cumulative dose in Tu et al[30] study was also lower in the low-dose group. There was no significant difference in the occurrence of relapse during the follow-up period between the low-dose and high-dose groups, as found in Tu et al[30] study. In this study, 2 patients in the low-dose group and 1 patient in the high-dose group experienced transient elevation of liver enzymes, but the levels did not exceed 3 times the normal value. After hepatoprotective treatment, the liver enzyme levels returned to normal. There were no reports of serious adverse reactions. Previous studies reported that the safety of the 2 doses was similar, with some studies showing that the low-dose group had a lower frequency of infusion reactions,[25,26] while other studies showed that the high-dose group had a lower frequency of infections.[27,28]

In terms of the limitations of this study, the sample size was small and heterogeneous in terms of disease spectrum and treatment regimen. In the future, with the wide application of RTX in China, we’ll collect more data and stratify the study by disease, set a control group or use a matched cohort design to strengthen the conclusions about RTX’s efficacy. There were many factors influencing the dose of RTX. Although patients were divided into 2 groups based on the single-dose amount, the dosing interval varied among patients, and some patients received additional RTX treatment based on the B-cell absolute count recovery or disease relapse. The results might be different if the disease spectrum, treatment plan, and disease activity were uniform. Although there are some clinical reports that high-dose RTX therapy leads to deeper B-cell depletion than low-dose therapy, the current study did not analyze the changes in B-cell percentage and absolute count between the high-dose and low-dose groups because of the small sample size.

5. Conclusion

In glomerular kidney diseases, RTX can deplete B-cell counts, improve 24-hour urinary protein and albumin levels, and low-dose RTX is as effective as high-dose RTX. RTX is a relatively safe treatment with no severe infections reported during the follow-up period. Large-scale prospective clinical trials are needed to further explore the optimal single dose and dosing interval of RTX and its safety. Research on the rational application of RTX in glomerular kidney diseases is still in its infancy and will provide more possibilities for the treatment of glomerular kidney diseases in the future.

Author contributions

Conceptualization: Chunyan Zhang.

Validation: Xiaolei Ren.

Writing – original draft: Jiadan Ye, Chunyan Zhang.

Writing – review & editing: Lin Huang, Xiaohong Zhang.

Abbreviations:

FSGS
focal segmental glomerulosclerosis
INS
idiopathic nephrotic syndrome
MCD
minimal change disease
RTX
rituximab

The studies involving human participants were reviewed and approved by 2021PHB207-001 (Ethical review approval of Peking University People’s Hospital).

The authors have no funding and conflicts of interest to disclose.

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

How to cite this article: Ye J, Zhang C, Ren X, Huang L, Zhang X. Efficacy and safety of rituximab in Chinese patients of glomerular kidney diseases: An observational study. Medicine 2025;104:37(e44127).

Contributor Information

Jiadan Ye, Email: yejia@163.com.

Xiaolei Ren, Email: renxiaolei@126.com.

Lin Huang, Email: Huangli@peuph.edu.cn.

Xiaohong Zhang, Email: zhangxiaohon@pkuph.edu.cn.

References

  • [1].Ly S, Nedosekin D, Wong HK. Review of an anti-CD20 monoclonal antibody for the treatment of autoimmune diseases of the skin. Am J Clin Dermatol. 2023;24:247–73. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [2].Salles G, Barrett M, Foà R, et al. Rituximab in B-cell hematologic malignancies: a review of 20 years of clinical experience. Adv Ther. 2017;34:2232–73. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [3].Debiec H, Ronco P. PLA2R autoantibodies and PLA2R glomerular deposits in membranous nephropathy. N Engl J Med. 2011;364:689–90. [DOI] [PubMed] [Google Scholar]
  • [4].Kidney Disease: Improving Global Outcomes Glomerular Diseases Work Group. KDIGO 2021 clinical practice guideline for the management of glomerular diseases. Kidney Int. 2021;100:S1–S276. [DOI] [PubMed] [Google Scholar]
  • [5].China adult nephrotic syndrome immunosuppressive treatment expert group. China adult nephrotic syndrome immunosuppressive treatment expert consensus. Chin J Nephrol. 2014;30:467–74. [Google Scholar]
  • [6].Dickinson BL. Unraveling the immunopathogenesis of glomerular disease. Clin Immunol. 2016;169:89–97. [DOI] [PubMed] [Google Scholar]
  • [7].Santos JE, Fiel D, Santos R, et al. Rituximab use in adult glomerulopathies and its rationale. J Bras Nefrol. 2020;42:77–93. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [8].Couser WG. Basic and translational concepts of immune-mediated glomerular diseases. J Am Soc Nephrol. 2012;23:381–99. [DOI] [PubMed] [Google Scholar]
  • [9].Ooi JD, Kitching AR, Holdsworth SR. Review: T helper 17 cells: their role in glomerulonephritis. Nephrology (Carlton). 2010;15:513–21. [DOI] [PubMed] [Google Scholar]
  • [10].Maas RJ, Deegens JK, Wetzels JF. Permeability factors in idiopathic nephrotic syndrome: historical perspectives and lessons for the future. Nephrol Dial Transplant. 2014;29:2207–16. [DOI] [PubMed] [Google Scholar]
  • [11].Maas RJ, Deegens JK, Smeets B, Moeller MJ, Wetzels JF. Minimal change disease and idiopathic FSGS: manifestations of the same disease. Nat Rev Nephrol. 2016;12:768–76. [DOI] [PubMed] [Google Scholar]
  • [12].Rosenberg AZ, Kopp JB. Focal segmental glomerulosclerosis. Clin J Am Soc Nephrol. 2017;12:502–17. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [13].Duarte I, Oliveira J, Outerelo C, et al. Rituximab in glomerular diseases: a case series and narrative review. J Bras Nefrol. 2022;44:187–95. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [14].Ejaz AA, Asmar A, Alsabbagh MM, Ahsan N. Rituximab in immunologic glomerular diseases. MAbs. 2012;4:198–207. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [15].AlSahow A, Al-Muhaiteeb A, Nawar H, et al. Use of rituximab as an off-label medication in glomerular diseases: clinical perspective. Med Princ Pract. 2022;31:133–41. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [16].Marinaki S, Skalioti C, Boletis JN. B cell depletion: rituximab in glomerular disease and transplantation. Nephron Extra. 2013;3:125–30. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [17].King C, Logan S, Smith SW, Hewins P. The efficacy of rituximab in adult frequently relapsing minimal change disease. Clin Kidney J. 2017;10:16–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [18].Salvadori M, Tsalouchos A. How immunosuppressive drugs may directly target podocytes in glomerular diseases. Pediatr Nephrol. 2022;37:1431–41. [DOI] [PubMed] [Google Scholar]
  • [19].Ying Z, Lijie Z, Shuang M, Xinyu P, Shenghua S, Jing X. Efficacy and safety analysis of rituximab in the treatment of primary IgA nephropathy. Pract Pharm Clin Remed. 2023;26:516–21. [Google Scholar]
  • [20].Haiyan L. Efficacy and Safety Analysis of Rituximab in the Treatment of Primary IgA Nephropathy. Shandong University; 2022. [Google Scholar]
  • [21].Bin S, Dongyang H, Qianqian X, et al. Efficacy analysis of rituximab in the treatment of atypical membranous nephropathy in adults. Chin J New Drugs Clin Rem. 2022;41:612–7. [Google Scholar]
  • [22].Maloney DG, Grillo-López AJ, White CA, et al. IDEC-C2B8 (Rituximab) anti-CD20 monoclonal antibody therapy in patients with relapsed low-grade non-Hodgkin’s lymphoma. Blood. 1997;90:2188–95. [PubMed] [Google Scholar]
  • [23].Stone JH, Merkel PA, Spiera R, et al. Rituximab versus cyclophosphamide for ANCA-associated vasculitis. N Engl J Med. 2010;363:221–32. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [24].Carranza-Enriquez F, Meade-Aguilar JA, Hinojosa-Azaola A. Rituximab treatment in ANCA-associated vasculitis patients: outcomes of a real-life experience from an observational cohort. Clin Rheumatol. 2022;41:2809–16. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [25].Bagchi S, Subbiah AK, Bhowmik D, et al. Low-dose rituximab therapy in resistant idiopathic membranous nephropathy: single-center experience. Clin Kidney J. 2018;11:337–41. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [26].Wang YW, Wang X-H, Wang H-X, Yu R-H. Successful treatment of patients with refractory idiopathic membranous nephropathy with low-dose rituximab: a single-center experience. World J Clin Cases. 2023;11:566–75. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [27].Liu L, Lu H, Zou G, et al. Efficacy and safety of low-dose rituximab as induction therapy for antineutrophil cytoplasmic antibody-associated vasculitis with renal involvement: a Chinese case series. BMC Nephrol. 2023;24:28. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • [28].Fenoglio R, Baldovino S, Sciascia S, et al. Efficacy of low or standard rituximab-based protocols and comparison to Ponticelli’s regimen in membranous nephropathy. J Nephrol. 2021;34:565–71. [DOI] [PubMed] [Google Scholar]
  • [29].Moroni G, Depetri F, Del Vecchio L, et al. Low-dose rituximab is poorly effective in patients with primary membranous nephropathy. Nephrol Dial Transplant. 2017;32:1691–6. [DOI] [PubMed] [Google Scholar]
  • [30].Zhihui T, Dingping Y. Efficacy and safety of two dose regimens of rituximab for idiopathic membranous nephropathy. J Clin Nephrol. 2024;24:89–95. [Google Scholar]

Articles from Medicine are provided here courtesy of Wolters Kluwer Health

RESOURCES