# Successful Bridging to Rituximab With Plasma Exchange in a Pediatric Patient With Severe Lupus Nephritis

**Authors:** Taro Yoshida, Hiroshi Sugahara, Keisuke Oikawa, Chinatsu Onodera, Manami Akasaka

PMC · DOI: 10.7759/cureus.102373 · Cureus · 2026-01-27

## TL;DR

A 14-year-old girl with severe lupus nephritis improved after plasma exchange and a combination of immunosuppressive treatments, including rituximab.

## Contribution

Demonstrates the effectiveness of early plasma exchange in enabling rituximab treatment for severe pediatric lupus nephritis.

## Key findings

- Plasma exchange reduced autoantibodies and improved renal function in a pediatric lupus nephritis patient.
- The patient achieved complete remission with normalization of serologic markers and urinary findings.
- Combination therapy allowed successful discontinuation of corticosteroids after 18 months.

## Abstract

We report a case of a 14-year-old girl diagnosed with class IV-G (A) lupus nephritis (LN), presenting with severe clinical manifestations, including nephrotic syndrome, acute kidney injury, and life-threatening hyperkalemia. The condition was managed with early initiation of plasma exchange (PE), followed by a combination of immunosuppressive therapies: high-dose corticosteroids, mycophenolate mofetil, rituximab, tacrolimus, and hydroxychloroquine. PE was promptly introduced after methylprednisolone pulse therapy to reduce circulating pathogenic autoantibodies and mitigate renal inflammation. Renal function gradually improved, accompanied by a marked decline in antibody levels. During recovery, the patient developed deep vein thrombosis and pulmonary embolism, which were managed with anticoagulation therapy. Belimumab was subsequently added to facilitate steroid tapering and maintain long-term disease control. Over an 18-month follow-up period, the patient achieved complete remission, with normalization of serologic markers and urinary findings, and corticosteroids were successfully discontinued. This case highlights the potential utility of early PE in enabling effective rituximab treatment for severe pediatric LN and underscores the importance of individualized, multimodal strategies to optimize outcomes in high-risk patients.

## Linked entities

- **Chemicals:** methylprednisolone (PubChem CID 6741), mycophenolate mofetil (PubChem CID 5281078), tacrolimus (PubChem CID 445643), hydroxychloroquine (PubChem CID 3652)
- **Diseases:** lupus nephritis (MONDO:0005556), nephrotic syndrome (MONDO:0005377), acute kidney injury (MONDO:0002492), pulmonary embolism (MONDO:0005279)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, TRIM21 (tripartite motif containing 21) [NCBI Gene 6737] {aka RNF81, RO52, Ro/SSA, SSA, SSA1, TRIM21/Ro52}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, SSB (small RNA binding exonuclease protection factor La) [NCBI Gene 6741] {aka LARP3, La, La/SSB, SSB/La}, OGA (O-GlcNAcase) [NCBI Gene 10724] {aka MEA5, MGEA5, NCOAT}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, MMP3 (matrix metallopeptidase 3) [NCBI Gene 4314] {aka CHDS6, MMP-3, SL-1, STMY, STMY1, STR1}, C3 (complement C3) [NCBI Gene 718] {aka AHUS5, ARMD9, ASP, C3a, C3b, CPAMD1}, ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}, GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}
- **Diseases:** thrombosis (MESH:D013927), anemia (MESH:D000740), glomerulonephritis (MESH:D005921), PE (MESH:D054219), cytopenias (MESH:D006402), end-stage kidney disease (MESH:D007676), thrombocytopenia (MESH:D013921), antiphospholipid antibodies (MESH:D016736), deep vein thrombosis (MESH:D020246), cough (MESH:D003371), toxicities (MESH:D064420), impaired renal function (MESH:D007674), thrombotic microangiopathy (MESH:D057049), thromboembolic complications (MESH:D013923), fibrosis (MESH:D005355), fluid overload (MESH:D019190), inflammatory (MESH:D007249), nephrotic (MESH:D009404), hyperkalemia (MESH:D006947), hematuria (MESH:D006417), LN (MESH:D008181), ear erythema (MESH:D004427), edema (MESH:D004487), facial rash (MESH:D005076), iliac vein thrombosis (MESH:D062108), hypoalbuminemia (MESH:D034141), acute kidney injury (MESH:D058186), Proteinuria (MESH:D011507), urinary casts (MESH:D013478), pulmonary artery embolism (MESH:D011655), Fibrinoid necrosis (MESH:D038261), SLE (MESH:D008180)
- **Chemicals:** prednisolone (MESH:D011239), Anti- (-), tacrolimus (MESH:D016559), HCQ (MESH:D006886), Rituximab (MESH:D000069283), steroid (MESH:D013256), rivaroxaban (MESH:D000069552), heparin (MESH:D006493), creatinine (MESH:D003404), Belimumab (MESH:C511911), Pro (MESH:D011392), MMF (MESH:D009173), bilirubin (MESH:D001663), methylprednisolone (MESH:D008775), RTX (MESH:C024353), cyclophosphamide (MESH:D003520)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12937027/full.md

## References

15 references — full list in the complete paper: https://tomesphere.com/paper/PMC12937027/full.md

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Source: https://tomesphere.com/paper/PMC12937027