# Opportunities and challenges in the treatment of IgA nephropathy

**Authors:** Yang Yang, Gaosi Xu

PMC · DOI: 10.3389/fphar.2025.1559593 · 2025-07-30

## TL;DR

This review discusses new treatment options and challenges in managing IgA nephropathy, a chronic kidney disease.

## Contribution

The paper highlights emerging therapies and the need for personalized treatment strategies in IgA nephropathy.

## Key findings

- New therapies like complement inhibitors and endothelin receptor antagonists show promise in IgAN treatment.
- Combination therapies may offer greater benefits for IgAN patients.
- Personalized precision therapy is a key challenge in IgAN management.

## Abstract

The treatment paradigm of immunoglobulin A nephropathy (IgAN) is shifting, and traditional therapeutic strategies are insufficient to meet clinical needs. Based on the increasing understanding of the pathogenesis of IgAN, current treatment goals concentrate on anti-inflammatory and targeted therapy, as well as optimizing therapy. New therapeutic approaches are being developed, including complement inhibitors, B-cell activating factor and a proliferation-inducing ligand inhibitor, and endothelin receptor antagonists. Further supportive care showed promising prospects and combination therapy such as sodium-glucose cotransporter 2 inhibitor with endothelin receptor antagonists are also being investigated, which may provide greater benefit. IgAN is a disease that requires lifelong management, the treatment choices faced may be inconsistent at different ages and periods. With the emerging opportunities in IgAN treatment, achieving individualized precision therapy is a key challenge currently facing research institues. This review summarizes recent advances in the treatment of IgAN and discusses possible therapeutic strategies for IgAN patients.

## Linked entities

- **Diseases:** IgA nephropathy (MONDO:0005342)

## Full-text entities

- **Genes:** CD38 (CD38 molecule) [NCBI Gene 952] {aka ADPRC 1, ADPRC1, cADPR1}, C5AR1 (complement C5a receptor 1) [NCBI Gene 728] {aka C5A, C5AR, C5R1, CD88}, TNFSF13B (TNF superfamily member 13b) [NCBI Gene 10673] {aka BAFF, BLYS, CD257, TALL-1, TALL1, THANK}, MFSD11 (major facilitator superfamily domain containing 11) [NCBI Gene 79157] {aka ET}, MBL2 (mannose binding lectin 2) [NCBI Gene 4153] {aka COLEC1, HSMBPC, MBL, MBL2D, MBP, MBP-C}, C1QA (complement C1q A chain) [NCBI Gene 712] {aka C1QD1}, TNFRSF13B (TNF receptor superfamily member 13B) [NCBI Gene 23495] {aka CD267, CVID, CVID2, IGAD2, RYZN, TACI}, CFD (complement factor D) [NCBI Gene 1675] {aka ADIPSIN, ADN, DF, PFD}, CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, TLR9 (toll like receptor 9) [NCBI Gene 54106] {aka CD289}, CD163 (CD163 molecule) [NCBI Gene 9332] {aka M130, MM130, SCARI1}, NPHS1 (NPHS1 adhesion molecule, nephrin) [NCBI Gene 4868] {aka CNF, NPHN, nephrin}, EDN1 (endothelin 1) [NCBI Gene 1906] {aka ARCND3, ET1, HDLCQ7, PPET1, QME}, AGT (angiotensinogen) [NCBI Gene 183] {aka ANHU, SERPINA8, hFLT1}, C3 (complement C3) [NCBI Gene 718] {aka AHUS5, ARMD9, ASP, C3a, C3b, CPAMD1}, TNFRSF13C (TNF receptor superfamily member 13C) [NCBI Gene 115650] {aka BAFF-R, BAFFR, BROMIX, CD268, CVID4, prolixin}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, MASP2 (MBL associated serine protease 2) [NCBI Gene 10747] {aka MAP-2, MAP19, MASP-2, MASP1P1, sMAP}, IGHA1 (immunoglobulin heavy constant alpha 1) [NCBI Gene 3493] {aka IgA1}, EDNRB (endothelin receptor type B) [NCBI Gene 1910] {aka ABCDS, ET-B, ET-BR, ETB, ETB1, ETBR}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, CFB (complement factor B) [NCBI Gene 629] {aka AHUS4, ARMD14, BF, BFD, CFAB, CFBD}, TNFRSF17 (TNF receptor superfamily member 17) [NCBI Gene 608] {aka BCM, BCMA, CD269, TNFRSF13A}, ERAL1 (Era like 12S mitochondrial rRNA chaperone 1) [NCBI Gene 26284] {aka CEGA, ERA, ERA-W, ERAL1A, ERAL1B, H-ERA}, EDNRA (endothelin receptor type A) [NCBI Gene 1909] {aka ET-A, ETA, ETA-R, ETAR, ETRA, MFDA}
- **Diseases:** autoimmune disease (MESH:D001327), inflammatory damage (MESH:D018746), glomerulonephritis (MESH:D005921), mesangial hyperplasia (MESH:D006965), Cushing syndrome (MESH:D003480), IgA nephropathy (MESH:D005922), cardiovascular and renal failure (MESH:D051437), proliferative (MESH:D009220), fibrosis (MESH:D005355), CKD (MESH:D051436), diabetes mellitus (MESH:D003920), eGFR (MESH:D007674), cytotoxicity (MESH:D064420), Infections (MESH:D007239), death (MESH:D003643), glomerular inflammation (MESH:D007249), hematuria (MESH:D006417), proteinuria (MESH:D011507), type 2 diabetes mellitus (MESH:D003924), ESRD (MESH:D007676), hypotension (MESH:D007022), impaired glucose tolerance (MESH:D018149), Gd-IgA1 (MESH:D005693), peripheral oedema (MESH:D010523), lupus nephritis (MESH:D008181), renal function decline (MESH:D060825)
- **Chemicals:** Finerenone (MESH:C576501), MMF (MESH:D009173), azathioprine (MESH:D001379), Narsoplimab (MESH:C000718989), HCQ (MESH:D006886), Eculizumab (MESH:C481642), N-acetylgalactosamine (MESH:D000116), carbohydrate (MESH:D002241), DAPA (MESH:C020269), sodium (MESH:D012964), Ravulizumab (MESH:C000629409), BION-1301 (-), Gd (MESH:D005682), cyclophosphamide (MESH:D003520), bortezomib (MESH:D000069286), creatinine (MESH:D003404), Sparsentan (MESH:C000634424), budesonide (MESH:D019819), aldosterone (MESH:D000450), irbesartan (MESH:D000077405), Atrasentan (MESH:D000077868), avacopan (MESH:C000620232), Felzartamab (MESH:C000709267), Leflunomide (MESH:D000077339)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12343601/full.md

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Source: https://tomesphere.com/paper/PMC12343601