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Minimal Change Disease

1. Disease Information

2026-04-14
Falcon MONDO:0006835 Model: Edison Scientific Literature 26 citations

1. Disease Information

Overview (current understanding)

Minimal change disease (MCD) is a glomerular disorder/podocytopathy that classically presents with acute nephrotic syndrome (heavy proteinuria with edema) and shows minimal or absent changes on light microscopy, but diffuse podocyte foot-process effacement on electron microscopy. (gauckler2023diagnostikundtherapie pages 1-2, son2023outcomesofminimal pages 1-2)

Synonyms and alternative names (as used in retrieved sources)

Key identifiers

The following standard identifiers were not retrievable from the provided tool context in this run and therefore are not reported: MONDO ID, MeSH ID, Orphanet ID, OMIM entry, ICD-10/ICD-11 code.

Evidence source type

The report is derived from aggregated disease-level resources (consensus statements/guidelines, trial protocols, registry studies) and primary clinical/translational studies (cohorts, mechanistic antibody study). (gauckler2023diagnostikundtherapie pages 1-2, hengel2024autoantibodiestargetingnephrin pages 1-3, nakagawa2023demographicsandtreatment pages 1-2)

2. Etiology

Disease causal factors (primary vs secondary)

MCD is widely treated as an immune-mediated podocytopathy based on its typical responsiveness to immunosuppression (particularly glucocorticoids) and emerging autoantibody evidence. (gauckler2023diagnostikundtherapie pages 1-2, hengel2024autoantibodiestargetingnephrin pages 1-3)

A key recent etiologic advance is the identification of circulating anti-nephrin autoantibodies in a substantial subset of patients with MCD, supporting an autoimmune subset in which antibodies bind a podocyte slit diaphragm protein (nephrin) and are associated with disease activity. (hengel2024autoantibodiestargetingnephrin pages 1-3)

Secondary/trigger-associated MCD is recognized clinically; adult consensus emphasizes that secondary causes should be actively evaluated in adults. Specific secondary causes were not enumerated in the retrieved excerpts, so they are not itemized here. (gauckler2023diagnostikundtherapie pages 1-2)

Risk factors

Genetic susceptibility loci and gene–environment interaction evidence were not retrievable from the provided excerpts and are not reported.

Protective factors

Protective genetic or environmental factors were not retrievable from the provided excerpts.

3. Phenotypes

Core phenotypes (clinical and laboratory)

  • Nephrotic syndrome presentation: MCD is characterized by edema and nephrotic-range proteinuria in typical presentations. (son2023outcomesofminimal pages 1-2)
  • Adult biopsy cohort features: in a cohort of 79 adults with biopsy-proven primary MCD, outcomes were evaluated in patients with and without nephrotic-range proteinuria at biopsy; acute kidney injury occurred more often in those with nephrotic-range proteinuria (59.3% vs 5.0%). (son2023outcomesofminimal pages 1-2)

Phenotype ontology suggestions (HPO)

Formal HPO mappings were not directly provided in the retrieved excerpts. Suggested candidate terms based on described phenotypes (requires independent HPO verification before knowledge-base ingestion): - Nephrotic syndrome; Proteinuria; Edema; Hypoalbuminemia; Acute kidney injury.

Quality of life impact

Nephrotic syndrome was described as having “debilitating oedema” in an adult trial protocol, consistent with substantial symptom burden and functional limitation. (willcocks2024arandomisedtwoarm pages 1-2)

4. Genetic/Molecular Information

Causal genes and pathogenic variants

Monogenic causes/variants, modifier genes, and allele frequencies were not retrievable from the provided excerpts.

Key molecular findings and biomarkers

Anti-nephrin autoantibodies (major 2024 development): - In a multicenter NEJM study (Aug 2024), anti-nephrin autoantibodies were detected in 44% (46/105) of adults with MCD and 52% (94/182) of children with idiopathic nephrotic syndrome; positivity reached 69% in untreated active adult MCD and 90% in untreated active children. (hengel2024autoantibodiestargetingnephrin pages 1-3) - Antibody levels correlated with disease activity and decreased with remission, supporting their use as activity biomarkers (not yet established as routine clinical tests). (hengel2024autoantibodiestargetingnephrin pages 1-3)

IL-33/ST2 axis: A 2023 translational study examined 49 biopsy-proven MCD patients and reported elevated soluble ST2 (sST2) at diagnosis with reductions after remission; podocyte IL-33 expression was increased by immunofluorescence, and patient serum induced IL-33 secretion from podocytes in vitro, suggesting IL-33–related immune response involvement. (zhong2025emergingroleof pages 1-2)

5. Environmental Information

Environmental exposures, lifestyle factors, and specific infectious triggers were not retrievable from the provided excerpts. Adult consensus notes possible triggering by viral infections or allergens, but detailed exposure-level evidence was not extractable from the excerpted text. (gauckler2023diagnostikundtherapie pages 1-2)

6. Mechanism / Pathophysiology

Current mechanistic model (evidence-based chain)

Podocyte injury → foot-process effacement → heavy proteinuria → edema/nephrotic syndrome is the central pathophysiologic chain, supported by diagnostic electron microscopy findings and clinical nephrotic syndrome presentation. (son2023outcomesofminimal pages 1-2, willcocks2024arandomisedtwoarm pages 1-2)

Autoantibody-mediated subset (anti-nephrin): The NEJM 2024 study provides a mechanistic link in which anti-nephrin antibodies bind at the slit diaphragm, track with activity, and in an experimental mouse immunization model induce nephrotic syndrome with slit-diaphragm IgG localization, nephrin phosphorylation, and severe cytoskeletal changes. (hengel2024autoantibodiestargetingnephrin pages 1-3)

Upstream vs downstream mechanisms (as supported here)

Cell types involved (CL suggestions)

Direct Cell Ontology (CL) mappings were not provided in the excerpts; evidence strongly implicates: - Podocytes (glomerular epithelial cells) as the primary injured cell type. (son2023outcomesofminimal pages 1-2, hengel2024autoantibodiestargetingnephrin pages 1-3) - B cells are implicated indirectly by anti-nephrin antibodies and rituximab responsiveness. (hengel2024autoantibodiestargetingnephrin pages 1-3, mirioglu2024managementofadult pages 5-6)

GO biological process suggestions

Not explicitly enumerated in excerpts; candidate processes (require GO verification): immune response, humoral immune response, antigen–antibody response, regulation of actin cytoskeleton.

Omics / single-cell / spatial transcriptomics

These were not retrievable from the provided excerpts.

7. Anatomical Structures Affected

Organ/tissue/cell levels

Suggested UBERON terms (require verification): kidney; glomerulus; renal corpuscle.

8. Temporal Development

Onset and course

9. Inheritance and Population

Epidemiology (selected recent statistics)

  • Adult cohort introduction: MCD comprises approximately 11–20% of adult primary nephrotic syndrome; one cited South Korean biopsy series reported 9.17% of biopsies as MCD. (son2023outcomesofminimal pages 1-2)
  • Japanese national registry of primary nephrotic syndrome (2015–2018): MCD constituted 56.2% (3394/6036) of recorded primary nephrotic syndrome cases. (nakagawa2023demographicsandtreatment pages 1-2)

Population incidence for MCD specifically was not directly extractable from available excerpts; however, an adult RCT protocol described primary MCD and FSGS as rare, “affecting about 10 per million population/year.” (willcocks2024arandomisedtwoarm pages 1-2)

Demographics

Japan registry: MCD median age of onset 31 years (IQR 16–49) and biopsy age 34 years (IQR 20–50), indicating frequent presentation in younger populations relative to membranous nephropathy. (nakagawa2023demographicsandtreatment pages 2-4)

10. Diagnostics

Clinical tests and biopsy findings

Adult diagnosis is based on kidney biopsy with characteristic pathology: - Light microscopy: absent/minimal changes; (gauckler2023diagnostikundtherapie pages 1-2, son2023outcomesofminimal pages 1-2) - Immunofluorescence: no immunoglobulin/complement deposition in primary MCD; (son2023outcomesofminimal pages 1-2) - Electron microscopy: diffuse podocyte foot-process effacement. (gauckler2023diagnostikundtherapie pages 1-2, willcocks2024arandomisedtwoarm pages 1-2)

Biomarkers

Differential diagnosis

The retrieved excerpts did not provide a structured differential diagnosis list. Practically, adult consensus and trial protocol framing places MCD in the umbrella of “podocytopathies,” particularly alongside primary FSGS, which can share nephrotic syndrome presentation but differs by focal/segmental scarring on pathology. (willcocks2024arandomisedtwoarm pages 1-2)

Genetic testing

Guidance on genetic testing (WES/WGS/panels) was not retrievable from the provided excerpts.

11. Outcome/Prognosis

Short- and medium-term outcomes (available quantitative data)

Mortality and long-term kidney survival specific to MCD were not directly extractable from the retrieved excerpts.

12. Treatment

Guideline-concordant initial therapy (adults)

An ERA Immunonephrology Working Group update summarizing KDIGO 2021 recommends high-dose glucocorticoids for adult MCD with an upper bound of 16 weeks at high dose and tapering after remission. The excerpted KDIGO-based regimen is: “1 mg/kg/d (max. 80 mg/d) or 2 mg/kg every other day (max. 120 mg/d) for a minimum of 4 weeks, and a maximum of 16 weeks. Taper might be started 2 weeks after CR is obtained.” (mirioglu2024managementofadult pages 5-6)

The same source notes a KDIGO stopping rule concept: “a patient with no proteinuria response at 16 weeks is unlikely to benefit from continuing high-dose glucocorticoid therapy.” (mirioglu2024managementofadult pages 3-5)

Steroid-sparing and relapse-prevention strategies

Adult consensus and ERA update identify calcineurin inhibitors, cyclophosphamide, mycophenolic acid, and rituximab as options for steroid-dependent, steroid-resistant, and/or frequently relapsing disease, reflecting real-world practice to reduce relapse and cumulative steroid toxicity. (gauckler2023diagnostikundtherapie pages 1-2, mirioglu2024managementofadult pages 5-6)

Rituximab (real-world evidence and trials)

  • Low-dose rituximab retrospective study (Apr 2023, BMC Nephrology): 33 adults with MCD; relapse-treatment group (n=22) receiving 200 mg weekly ×4 then 200 mg q6 months had 95.45% remission and 90.90% relapse-free during follow-up; relapse-prevention group (n=11) receiving 200 mg q6 months had no relapses during median 12 months. (zhang2023efficacyoflowdose pages 1-2)
  • TURING trial protocol (Aug 2024): phase III, double-blind, placebo-controlled adult RCT recruiting 130–150 participants with de novo or relapsing MCD/FSGS; rituximab 1 g ×2 two weeks apart (and optional week-26 dose if in remission), with standardized steroid taper; primary endpoint is time from remission to relapse. (willcocks2024arandomisedtwoarm pages 1-2, willcocks2024arandomisedtwoarm pages 4-5)

Real-world implementations and algorithms (visual evidence)

The ERA update includes a visual management summary (flowchart) for adult MCD and a table of steroid regimens (KDIGO vs MINTAC/TURING). (mirioglu2024managementofadult media 6fdf5a00, mirioglu2024managementofadult media fcda3580)

MAXO suggestions (treatments)

MAXO terms were not provided in excerpts; candidate actions (require MAXO verification): glucocorticoid therapy; B-cell depletion therapy (rituximab); calcineurin inhibitor therapy; cyclophosphamide therapy.

13. Prevention

Primary prevention strategies were not retrievable from the provided excerpts. The main preventable burdens reflected here are relapse- and treatment-related complications; trial and consensus documents emphasize steroid-sparing approaches to reduce cumulative toxicity. (willcocks2024arandomisedtwoarm pages 1-2)

14. Other Species / Natural Disease

Not retrievable from the provided excerpts.

15. Model Organisms

A mechanistic mouse model was created in which active immunization with recombinant murine nephrin induced a nephrotic syndrome and MCD-like phenotype, supporting pathogenicity of anti-nephrin autoimmunity. (hengel2024autoantibodiestargetingnephrin pages 1-3)

Key 2023–2024 Developments (executive synthesis)

  1. Autoimmune subset defined by anti-nephrin antibodies (NEJM 2024): high prevalence in MCD and correlation with activity; experimental model supports causality. (hengel2024autoantibodiestargetingnephrin pages 1-3)
  2. Adult management refinement and trial pipeline (ERA update 2024 + TURING 2024): codifies KDIGO-based steroid regimens/limits and highlights rituximab-focused adult RCTs. (mirioglu2024managementofadult pages 5-6, willcocks2024arandomisedtwoarm pages 1-2)
  3. Real-world rituximab minimization strategies (BMC Nephrol 2023): suggests low-dose schedules may maintain remission with steroid-sparing in selected adults (retrospective evidence). (zhang2023efficacyoflowdose pages 1-2)

Structured summary table

Table (click to expand)
Category Summary Key sources (URL; publication date) Evidence IDs
Identifiers & synonyms Disease: Minimal Change Disease (MCD); also called minimal change nephropathy, minimal change glomerulopathy, and minimal change nephrotic syndrome (MCNS) in cited sources. ICD-10: not retrieved. MeSH: not retrieved. MONDO: not retrieved. Gauckler et al., Diagnostik und Therapie der Minimal Change Glomerulopathie beim Erwachsenen – 2023 — https://doi.org/10.1007/s00508-023-02258-5; Aug 2023. Willcocks et al., TURING trial protocol — https://doi.org/10.1186/s12882-024-03576-0; Aug 2024. (gauckler2023diagnostikundtherapie pages 1-2, willcocks2024arandomisedtwoarm pages 1-2)
Core definition & pathology hallmarks MCD is a podocytopathy/glomerular disease that typically presents with acute nephrotic syndrome. Diagnostic hallmarks in adults are near-normal or absent light-microscopic changes, absence of immune-complex/electron-dense deposits, and diffuse podocyte foot-process effacement on electron microscopy; biopsy is generally required in adults. Son et al., PLOS ONE — https://doi.org/10.1371/journal.pone.0289870; Aug 2023. Gauckler et al. — https://doi.org/10.1007/s00508-023-02258-5; Aug 2023. (gauckler2023diagnostikundtherapie pages 1-2, son2023outcomesofminimal pages 1-2)
Epidemiology & outcomes In adults, MCD accounts for about 11–20% of primary nephrotic syndrome; a South Korean biopsy series cited by Son et al. found 9.17% of biopsies were MCD. Japanese registry data: 56.2% of primary nephrotic syndrome cases were MCD (3394/6036). Relapse is common: ~75% relapse as glucocorticoids are withdrawn; approximately two-thirds have at least one relapse after remission, and up to one-third become frequently relapsing/steroid-dependent. Steroid response is usually high: in Son et al., remission after steroids was 100% in non-nephrotic-range proteinuria and 92.3% in nephrotic-range disease; complete remission at final visit was 73.4%. Japanese registry: 70.2% steroid-dependent/frequently relapsing; 6.4% steroid-resistant. Son et al. — https://doi.org/10.1371/journal.pone.0289870; Aug 2023. Mirioglu et al., Nephrol Dial Transplant — https://doi.org/10.1093/ndt/gfae025; Feb 2024. Nakagawa et al., Scientific Reports — https://doi.org/10.1038/s41598-023-41909-5; Sep 2023. Willcocks et al. — https://doi.org/10.1186/s12882-024-03576-0; Aug 2024. (mirioglu2024managementofadult pages 3-5, son2023outcomesofminimal pages 1-2, nakagawa2023demographicsandtreatment pages 1-2, nakagawa2023demographicsandtreatment pages 2-4, willcocks2024arandomisedtwoarm pages 1-2)
Mechanistic advances (2023–2024) Anti-nephrin autoantibodies: major 2024 advance supporting an autoimmune subset of MCD. In adults, anti-nephrin antibodies were found in 44% (46/105) of MCD patients; in children with idiopathic nephrotic syndrome 52% (94/182) were positive; prevalence rose to 69% in active untreated adult MCD and 90% in untreated active children. Levels correlated with disease activity/remission, and experimental immunization induced an MCD-like nephrotic phenotype with slit-diaphragm IgG localization, nephrin phosphorylation, and cytoskeletal change. Gauckler notes an earlier cited study with ~30% positivity. IL-33/ST2 axis: serum sST2 was elevated in MCD at diagnosis, correlated inversely with total protein and positively with creatinine, fell with remission, and podocyte IL-33 expression was increased—supporting a type-2/alarmin-related immune pathway. Hengel et al., NEJM — https://doi.org/10.1056/NEJMoa2314471; Aug 2024. Gauckler et al. — https://doi.org/10.1007/s00508-023-02258-5; Aug 2023. (gauckler2023diagnostikundtherapie pages 1-2, hengel2024autoantibodiestargetingnephrin pages 1-3)
Treatment: glucocorticoids (guideline dosing) KDIGO-based initial adult regimen: prednisone/prednisolone 1 mg/kg/day (max 80 mg/day) or 2 mg/kg every other day (max 120 mg) for a minimum of 4 weeks and maximum of 16 weeks; taper may start 2 weeks after complete remission. Lack of proteinuria response by 16 weeks suggests continued high-dose steroids are unlikely to help. Trial regimens summarized by ERA IWG: MINTAC prednisolone arm achieved 84% remission at 8 weeks and 92% at 16 weeks. Mirioglu et al. — https://doi.org/10.1093/ndt/gfae025; Feb 2024. (mirioglu2024managementofadult pages 5-6)
Treatment: rituximab low-dose evidence Retrospective adult low-dose RTX study (33 biopsy-proven MCD cases): relapse-treatment cohort n=22 received 200 mg weekly ×4, then 200 mg every 6 months; 95.45% remitted (86.36% CR, 9.09% PR), 90.90% remained relapse-free, median sustained remission 16.3 months. Relapse-prevention cohort n=11 received 200 mg every 6 months and had 0 relapses during median 12-month follow-up. Prednisone dose fell significantly after RTX. Zhang et al., BMC Nephrology — https://doi.org/10.1186/s12882-023-03092-7; Apr 2023. (zhang2023efficacyoflowdose pages 1-2)
Treatment: TURING trial / real-world implementation TURING is a phase III, double-blind, placebo-controlled, 1:1 randomized adult trial of rituximab for de novo or relapsing MCD/FSGS, planned enrollment 130–150. Regimen: rituximab 1 g ×2 infusions two weeks apart (plus optional week-26 dose if in remission) versus placebo, with all patients receiving glucocorticoids per KDIGO and tapering after remission. Primary endpoint: time from remission to relapse. This reflects current real-world movement toward steroid-sparing, B-cell–targeted therapy while adult RCT evidence is still being generated. Willcocks et al. — https://doi.org/10.1186/s12882-024-03576-0; Aug 2024. (willcocks2024arandomisedtwoarm pages 1-2)
Clinical interpretation Overall, current evidence supports MCD as a mostly steroid-sensitive but relapse-prone autoimmune podocytopathy, with emerging biomarker-defined subgroups (especially anti-nephrin-positive disease) and increasing use of rituximab to reduce steroid exposure and prevent relapse. Synthesized from cited 2023–2024 studies above. (mirioglu2024managementofadult pages 3-5, gauckler2023diagnostikundtherapie pages 1-2, hengel2024autoantibodiestargetingnephrin pages 1-3, mirioglu2024managementofadult pages 5-6, zhang2023efficacyoflowdose pages 1-2)

Table: This table condenses key identifiers, pathology, epidemiology, mechanistic advances, and treatment evidence for minimal change disease using only the specified context IDs. It is designed as a compact reference for rapid knowledge-base population and citation tracing.

Notes on evidence gaps in this run

  • Standard identifiers (MONDO/MeSH/Orphanet/OMIM/ICD) and formal ontology mappings (HPO/GO/CL/UBERON/MAXO codes) were not available in retrieved excerpts; candidate terms are provided only as suggestions and should be verified against the corresponding ontology resources.
  • Detailed differential diagnosis lists, granular environmental risk factors, and comprehensive genetic testing guidance were not extractable from the present evidence set.

References

  1. (gauckler2023diagnostikundtherapie pages 1-2): Philipp Gauckler, Heinz Regele, Kathrin Eller, Marcus D. Säemann, Karl Lhotta, Emanuel Zitt, Irmgard Neumann, Michael Rudnicki, Balazs Odler, Andreas Kronbichler, and Martin Windpessl. Diagnostik und therapie der minimal change glomerulopathie beim erwachsenen – 2023. Wiener Klinische Wochenschrift, 135:628-637, Aug 2023. URL: https://doi.org/10.1007/s00508-023-02258-5, doi:10.1007/s00508-023-02258-5. This article has 0 citations and is from a peer-reviewed journal.

  2. (son2023outcomesofminimal pages 1-2): Hyung Eun Son, Giae Yun, Eun-Jeong Kwon, Seokwoo Park, Jong Cheol Jeong, Sejoong Kim, Ki Young Na, Jin Ho Paik, and Ho Jun Chin. Outcomes of minimal change disease without nephrotic range proteinuria. PLOS ONE, 18:e0289870, Aug 2023. URL: https://doi.org/10.1371/journal.pone.0289870, doi:10.1371/journal.pone.0289870. This article has 3 citations and is from a peer-reviewed journal.

  3. (willcocks2024arandomisedtwoarm pages 1-2): Lisa C Willcocks, Wendi Qian, Ruzaika Cader, Katrina Gatley, Hira Siddiqui, Endurance Tabebisong, Karlena Champion, Andreas Kronbichler, Liz Lightstone, David Jayne, Edward Wilson, and Megan Griffith. A randomised, two-arm (1:1 ratio), double blind, placebo controlled phase iii trial to assess the efficacy, safety, cost and cost-effectiveness of rituximab in treating de novo or relapsing ns in patients with mcd/fsgs (turing). BMC Nephrology, Aug 2024. URL: https://doi.org/10.1186/s12882-024-03576-0, doi:10.1186/s12882-024-03576-0. This article has 5 citations and is from a peer-reviewed journal.

  4. (hengel2024autoantibodiestargetingnephrin pages 1-3): Felicitas E. Hengel, Silke Dehde, Moritz Lassé, Gunther Zahner, Larissa Seifert, Annabel Schnarre, Oliver Kretz, Fatih Demir, Hans O. Pinnschmidt, Florian Grahammer, Renke Lucas, Lea Maxima Mehner, Tom Zimmermann, Anja M. Billing, Jun Oh, Adele Mitrotti, Paola Pontrelli, Hanna Debiec, Claire Dossier, Manuela Colucci, Francesco Emma, William E. Smoyer, Astrid Weins, Franz Schaefer, Nada Alachkar, Anke Diemert, Julien Hogan, Elion Hoxha, Thorsten Wiech, Markus M. Rinschen, Pierre Ronco, Marina Vivarelli, Loreto Gesualdo, Nicola M. Tomas, and Tobias B. Huber. Autoantibodies targeting nephrin in podocytopathies. New England Journal of Medicine, 391:422-433, Aug 2024. URL: https://doi.org/10.1056/nejmoa2314471, doi:10.1056/nejmoa2314471. This article has 252 citations and is from a highest quality peer-reviewed journal.

  5. (nakagawa2023demographicsandtreatment pages 1-2): Naoki Nakagawa, Tomonori Kimura, Ryuichi Sakate, Takehiko Wada, Kengo Furuichi, Hirokazu Okada, Yoshitaka Isaka, and Ichiei Narita. Demographics and treatment of patients with primary nephrotic syndrome in japan using a national registry of clinical personal records. Scientific Reports, Sep 2023. URL: https://doi.org/10.1038/s41598-023-41909-5, doi:10.1038/s41598-023-41909-5. This article has 8 citations and is from a peer-reviewed journal.

  6. (mirioglu2024managementofadult pages 3-5): Safak Mirioglu, Lisa Daniel-Fischer, Ilay Berke, Syed Hasan Ahmad, Ingeborg M Bajema, Annette Bruchfeld, Gema M Fernandez-Juarez, Jürgen Floege, Eleni Frangou, Dimitrios Goumenos, Megan Griffith, Sarah M Moran, Cees van Kooten, Stefanie Steiger, Kate I Stevens, Kultigin Turkmen, Lisa C Willcocks, and Andreas Kronbichler. Management of adult patients with podocytopathies: an update from the era immunonephrology working group. Nephrology Dialysis Transplantation, 39:569-580, Feb 2024. URL: https://doi.org/10.1093/ndt/gfae025, doi:10.1093/ndt/gfae025. This article has 31 citations and is from a domain leading peer-reviewed journal.

  7. (nakagawa2023demographicsandtreatment pages 2-4): Naoki Nakagawa, Tomonori Kimura, Ryuichi Sakate, Takehiko Wada, Kengo Furuichi, Hirokazu Okada, Yoshitaka Isaka, and Ichiei Narita. Demographics and treatment of patients with primary nephrotic syndrome in japan using a national registry of clinical personal records. Scientific Reports, Sep 2023. URL: https://doi.org/10.1038/s41598-023-41909-5, doi:10.1038/s41598-023-41909-5. This article has 8 citations and is from a peer-reviewed journal.

  8. (zhong2025emergingroleof pages 1-2): Anni Zhong, Yi Yu, Tao Cao, Qijun Wan, and Ricong Xu. Emerging role of rituximab in adult minimal change disease: a narrative review of clinical evidence, biomarkers and future perspectives. BMC Nephrology, Mar 2025. URL: https://doi.org/10.1186/s12882-025-04086-3, doi:10.1186/s12882-025-04086-3. This article has 3 citations and is from a peer-reviewed journal.

  9. (mirioglu2024managementofadult pages 5-6): Safak Mirioglu, Lisa Daniel-Fischer, Ilay Berke, Syed Hasan Ahmad, Ingeborg M Bajema, Annette Bruchfeld, Gema M Fernandez-Juarez, Jürgen Floege, Eleni Frangou, Dimitrios Goumenos, Megan Griffith, Sarah M Moran, Cees van Kooten, Stefanie Steiger, Kate I Stevens, Kultigin Turkmen, Lisa C Willcocks, and Andreas Kronbichler. Management of adult patients with podocytopathies: an update from the era immunonephrology working group. Nephrology Dialysis Transplantation, 39:569-580, Feb 2024. URL: https://doi.org/10.1093/ndt/gfae025, doi:10.1093/ndt/gfae025. This article has 31 citations and is from a domain leading peer-reviewed journal.

  10. (zhang2023efficacyoflowdose pages 1-2): Jian Zhang, Hui Zhao, Xiaoli Li, Rui Qian, Peijuan Gao, Shou-Yan Lu, and Zhigang Ma. Efficacy of low-dose rituximab in minimal change disease and prevention of relapse. BMC Nephrology, Apr 2023. URL: https://doi.org/10.1186/s12882-023-03092-7, doi:10.1186/s12882-023-03092-7. This article has 18 citations and is from a peer-reviewed journal.

  11. (willcocks2024arandomisedtwoarm pages 4-5): Lisa C Willcocks, Wendi Qian, Ruzaika Cader, Katrina Gatley, Hira Siddiqui, Endurance Tabebisong, Karlena Champion, Andreas Kronbichler, Liz Lightstone, David Jayne, Edward Wilson, and Megan Griffith. A randomised, two-arm (1:1 ratio), double blind, placebo controlled phase iii trial to assess the efficacy, safety, cost and cost-effectiveness of rituximab in treating de novo or relapsing ns in patients with mcd/fsgs (turing). BMC Nephrology, Aug 2024. URL: https://doi.org/10.1186/s12882-024-03576-0, doi:10.1186/s12882-024-03576-0. This article has 5 citations and is from a peer-reviewed journal.

  12. (mirioglu2024managementofadult media 6fdf5a00): Safak Mirioglu, Lisa Daniel-Fischer, Ilay Berke, Syed Hasan Ahmad, Ingeborg M Bajema, Annette Bruchfeld, Gema M Fernandez-Juarez, Jürgen Floege, Eleni Frangou, Dimitrios Goumenos, Megan Griffith, Sarah M Moran, Cees van Kooten, Stefanie Steiger, Kate I Stevens, Kultigin Turkmen, Lisa C Willcocks, and Andreas Kronbichler. Management of adult patients with podocytopathies: an update from the era immunonephrology working group. Nephrology Dialysis Transplantation, 39:569-580, Feb 2024. URL: https://doi.org/10.1093/ndt/gfae025, doi:10.1093/ndt/gfae025. This article has 31 citations and is from a domain leading peer-reviewed journal.

  13. (mirioglu2024managementofadult media fcda3580): Safak Mirioglu, Lisa Daniel-Fischer, Ilay Berke, Syed Hasan Ahmad, Ingeborg M Bajema, Annette Bruchfeld, Gema M Fernandez-Juarez, Jürgen Floege, Eleni Frangou, Dimitrios Goumenos, Megan Griffith, Sarah M Moran, Cees van Kooten, Stefanie Steiger, Kate I Stevens, Kultigin Turkmen, Lisa C Willcocks, and Andreas Kronbichler. Management of adult patients with podocytopathies: an update from the era immunonephrology working group. Nephrology Dialysis Transplantation, 39:569-580, Feb 2024. URL: https://doi.org/10.1093/ndt/gfae025, doi:10.1093/ndt/gfae025. This article has 31 citations and is from a domain leading peer-reviewed journal.