📋 Key Information Summary
- Primary membranous nephropathy (MN) is the most common cause of nephrotic syndrome in non-diabetic Caucasian adults aged 40–60 years
- Anti-PLA2R antibodies are detectable in ~70–80% of primary MN and are both diagnostic and prognostic; anti-THSD7A antibodies account for a further 3–5%
- Clinical presentation: insidious nephrotic syndrome (oedema, heavy proteinuria >3.5 g/day, hypoalbuminaemia, hypercholesterolaemia)
- The classic "Rule of Thirds": ~⅓ spontaneous remission, ⅓ persistent proteinuria, ⅓ progressive to ESKD over 10 years
- All patients require supportive care with RAAS blockade, diuretics, SGLT2 inhibitors, and statins regardless of immunosuppression decision
- Immunosuppressive therapy is indicated for patients at high risk of progressive disease per the KDIGO risk algorithm (persistent proteinuria >3.5 g/day despite 6 months supportive therapy)
- Rituximab has emerged as a preferred first-line immunosuppressive agent, supported by the MENTOR trial, replacing the older Ponticelli regimen in many centres
- The modified Ponticelli regimen (alternating corticosteroids + cyclophosphamide over 6 months) remains an effective alternative where rituximab is unavailable or contraindicated
- Calcineurin inhibitors (tacrolimus, ciclosporin) are second-line options; cyclophosphamide is PBS Authority Required for nephrotic syndrome
- Anti-PLA2R antibody titre correlates with disease activity — serial monitoring guides treatment response and relapse detection
- Renal biopsy remains the gold standard: shows diffuse capillary wall thickening with sub-epithelial immune complex deposits; immunofluorescence shows granular IgG4 ± C3
- Thromboembolism risk is significantly elevated in MN — consider prophylactic anticoagulation if albumin <25 g/L
- Screen for secondary causes (malignancy, autoimmune disease, hepatitis B/C, medications) in all patients before diagnosing primary MN
- Aboriginal and Torres Strait Islander peoples may present later, have reduced access to specialist nephrology care, and require culturally safe management pathways
Introduction & Australian Epidemiology
Primary membranous nephropathy (MN) is an autoimmune glomerulonephritis characterised by the formation of immune complexes along the glomerular basement membrane (GBM), resulting in thickening of the capillary wall and progressive podocyte injury. It is the leading cause of nephrotic syndrome in non-diabetic Caucasian adults and the second most common primary glomerulopathy diagnosed on renal biopsy in Australia after IgA nephropathy.
The discovery of anti-phospholipase A2 receptor (PLA2R) antibodies in 2009 revolutionised the understanding and management of primary MN, providing a serological biomarker for diagnosis, prognostication, and treatment monitoring. Subsequent identification of anti-thrombospondin type-1 domain-containing 7A (THSD7A) antibodies has further refined the immunopathological classification.
Australian Epidemiology
- Incidence in Australia: estimated at 8–12 per million population per year, with higher rates in Caucasian populations
- Peak incidence: 40–60 years of age; male-to-female ratio approximately 2:1
- Primary MN accounts for approximately 20–25% of all nephrotic syndrome biopsies in Australian adults
- The Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry reports MN as a significant contributor to incident ESKD, though outcomes have improved with modern immunosuppression
- Secondary MN (related to malignancy, lupus, hepatitis B, medications) must be excluded in all cases — particularly important given the higher burden of hepatitis B in Aboriginal and Torres Strait Islander communities
- Anti-PLA2R antibody testing is available through major Australian pathology services (Sullivan Nicolaides, Douglass Hanly Moir, SA Pathology) and is MBS-rebatable
Clinical Pearl: Approximately 20–30% of primary MN is seronegative for both PLA2R and THSD7A antibodies. In these patients, renal biopsy with electron microscopy remains essential for definitive diagnosis. Always consider secondary causes in seronegative patients.
Pathophysiology — PLA2R & THSD7A Antibodies
Anti-PLA2R Antibodies
The M-type phospholipase A2 receptor (PLA2R) is a transmembrane glycoprotein expressed on the surface of glomerular podocytes. In approximately 70–80% of primary MN cases, IgG4 autoantibodies target the PLA2R antigen, forming sub-epithelial immune complexes in situ. This is distinct from secondary MN, where immune complexes are typically deposited from the circulation.
- Antigen: PLA2R — a 185 kDa transmembrane receptor belonging to the mannose receptor family
- Antibody subclass: Predominantly IgG4 (pathognomonic); IgG1 and IgG3 may co-exist and may indicate more active disease
- Target epitopes: Multiple epitope domains have been identified (CysR, CTLD1, CTLD7); epitope spreading is associated with disease persistence and poorer prognosis
- Mechanism: Anti-PLA2R IgG4 binds podocyte surface PLA2R → complement-independent podocyte injury (C5b-9 membrane attack complex may play a secondary role) → loss of glomerular permselectivity → proteinuria
- Genetic associations: HLA-DQA1 polymorphism confers susceptibility; environmental triggers (infections, malignancy) may initiate autoimmune response in genetically predisposed individuals
Anti-THSD7A Antibodies
Anti-thrombospondin type-1 domain-containing 7A (THSD7A) antibodies account for a further 3–5% of primary MN cases that are PLA2R-negative. THSD7A is also a transmembrane protein expressed on podocytes.
- Antigen: THSD7A — a 250 kDa transmembrane protein
- Antibody subclass: IgG4 (predominantly)
- Clinical significance: THSD7A-positive MN is associated with a higher incidence of concurrent or subsequent malignancy — thorough cancer screening is mandatory
- Mechanism: Similar in situ immune complex formation as PLA2R-mediated MN
Immune Complex Formation & Complement Activation
The pathogenic sequence in primary MN involves:
- Autoantibody production against podocyte surface antigens (PLA2R or THSD7A)
- In situ sub-epithelial immune complex formation along the GBM
- Activation of the complement cascade — primarily via the lectin pathway and C5b-9 membrane attack complex
- Podocyte injury and effacement of foot processes
- Loss of glomerular permselectivity leading to heavy proteinuria
- GBM thickening from immune complex incorporation ("spike" appearance on silver stain)
- Progressive podocyte depletion and tubulointerstitial fibrosis in advanced disease
Key distinction: Primary MN is predominantly IgG4-mediated and complement-independent in early stages. Secondary MN (e.g. lupus, hepatitis B) typically involves IgG1/IgG3 with prominent C3 and C1q deposition on immunofluorescence. This immunofluorescence pattern helps differentiate primary from secondary MN on biopsy.
Clinical Features & Natural History — Rule of Thirds
Clinical Presentation
Primary MN typically presents insidiously with the full nephrotic syndrome, though the degree of proteinuria varies considerably at presentation. Key clinical features include:
- Oedema: Peripheral, periorbital, and/or generalised (anasarca in severe cases) — often the presenting complaint
- Proteinuria: Nephrotic-range (>3.5 g/day or >200 mg/mmol on urine PCR) — may be sub-nephrotic at presentation in some cases
- Hypoalbuminaemia: Serum albumin <30 g/L (often <20 g/L in severe nephrotic syndrome)
- Hypercholesterolaemia: Due to hepatic lipoprotein synthesis in response to hypoalbuminaemia
- Frothy urine: Due to heavy proteinuria
- Haematuria: Microscopic haematuria in ~30% of cases; gross haematuria is uncommon and should prompt consideration of other diagnoses
- Hypertension: Present in approximately 30–50% at diagnosis
- Renal function: Often preserved at presentation; declining eGFR suggests advanced or progressive disease
The Classic "Rule of Thirds"
The natural history of untreated primary MN is classically described by the "Rule of Thirds":
⅓ of patients
Spontaneous Remission
Complete or partial remission of proteinuria without immunosuppressive therapy. Most remissions occur within 2–3 years of diagnosis. Favourable prognostic indicators include female sex, younger age, sub-nephrotic proteinuria, and preserved eGFR.
Setting: Supportive care only; serial monitoring
⅓ of patients
Persistent Proteinuria
Ongoing nephrotic-range proteinuria without progressive renal decline. These patients remain at risk of complications (thromboembolism, infection, hyperlipidaemia) and may eventually require immunosuppression if proteinuria persists beyond 6–12 months.
Setting: Optimise supportive care; consider immunosuppression per KDIGO risk algorithm
⅓ of patients
Progressive to ESKD
Gradual decline in renal function over 5–10 years progressing to end-stage kidney disease requiring dialysis or transplantation. Poor prognostic indicators include older age, male sex, persistent heavy proteinuria >8 g/day, declining eGFR, and tubulointerstitial fibrosis on biopsy.
Setting: Aggressive immunosuppression; RRT planning
Complications
- Thromboembolism: MN confers the highest thrombotic risk among glomerulonephritides. Renal vein thrombosis occurs in ~10–30%; pulmonary embolism in ~5–10%. Risk is highest when serum albumin <25 g/L
- Infection: Urinary tract infections, peritonitis (in ascites), and spontaneous bacterial peritonitis due to immunoglobulin loss and oedema
- Cardiovascular disease: Accelerated atherosclerosis from dyslipidaemia; volume overload
- Acute kidney injury: May occur from severe intravascular volume depletion, intercurrent illness, or use of nephrotoxic agents
- Malignancy: MN may be a paraneoplastic phenomenon — screen for malignancy especially in THSD7A-positive and older patients
Anticoagulation threshold: Consider prophylactic anticoagulation with warfarin (target INR 2.0–2.5) or LMWH in patients with serum albumin <25 g/L, particularly if additional thrombotic risk factors exist (immobility, obesity, prior VTE). Direct oral anticoagulants (DOACs) may not provide adequate antithrombotic efficacy in nephrotic syndrome due to urinary loss of antithrombin III and altered pharmacokinetics.
Investigations
Laboratory Investigations
Essential
Serum anti-PLA2R antibodies
Sensitivity 70–80%, specificity ~99% for primary MN. Available via ELISA or indirect immunofluorescence (IIF). MBS-rebatable through specialist request. Serial titres guide treatment response — falling titres predict remission; rising titres predict relapse.
Available
Serum anti-THSD7A antibodies
Test if PLA2R-negative. Available at reference laboratories (IMVS Adelaide, Westmead). Positive result warrants enhanced malignancy screening.
Essential
Renal biopsy — light microscopy
Diffuse thickening of glomerular capillary walls. Jones silver stain shows "spikes" (Stage I–II) or "domes" (Stage III–IV) corresponding to GBM material projecting between immune deposits. Masson trichrome shows sub-epithelial "red" deposits.
Essential
Immunofluorescence
Granular capillary wall staining. Primary MN: IgG4 dominant (± IgG1), C3 variable (30–50%), C1q usually negative. Secondary MN (lupus): IgG1/IgG3, C3, C1q all strongly positive.
Essential
Electron microscopy
Gold standard for staging. Sub-epithelial electron-dense deposits with podocyte foot process effacement. Staging (Ehrenreich-Churg): Stage I — small deposits, normal GBM thickness; Stage II — spikes between deposits; Stage III — deposits surrounded by GBM; Stage IV — lucent deposits with GBM thickening.
Available
Urine protein creatinine ratio (uPCR)
Quantifies proteinuria. Nephrotic-range: >350 mg/mmol (>3.5 g/day equivalent). Monitor serially as primary outcome marker. Available at all Australian pathology services; MBS-rebatable.
Available
Serum albumin, lipid profile, eGFR
Baseline and serial monitoring. Serum albumin correlates with thromboembolic risk. Lipid panel for cardiovascular risk assessment and statin initiation.
Available
Hepatitis B & C serology, ANA, dsDNA, complement (C3/C4)
Essential to exclude secondary causes. Lupus nephritis class V (membranous) must be excluded by ANA, dsDNA, and complement studies. Hepatitis B is particularly relevant in Aboriginal and Torres Strait Islander populations.
Secondary Cause Screening
| Category | Tests | Notes |
|---|---|---|
| Autoimmune | ANA, dsDNA, anti-Smith, C3/C4 | Lupus nephritis class V; both ANA and dsDNA positive → consider lupus |
| Infection | Hepatitis B (HBsAg, anti-HBc, HBV DNA), Hepatitis C (anti-HCV, HCV RNA) | Especially important in ATSI populations |
| Malignancy | Age-appropriate cancer screening (CT chest/abdomen/pelvis, colonoscopy if age >50) | Mandatory in THSD7A-positive, age >65, or clinical suspicion |
| Medications | Medication review | NSAIDs, gold, penicillamine, captopril, mercury exposure |
Renal Biopsy — Staging (Ehrenreich-Churg)
| Stage | Light Microscopy | Electron Microscopy | Prognosis |
|---|---|---|---|
| I (Early) | Normal GBM thickness; subtle sub-epithelial deposits | Small, discrete sub-epithelial deposits; intact GBM | Best prognosis; most responsive to therapy |
| II (Spike) | GBM thickening; "spike" projections on silver stain | GBM material grows between deposits creating spikes | Good prognosis with treatment |
| III (Dome) | GBM surrounds deposits; "dome" appearance | Deposits incorporated within GBM | Moderate; partial response to immunosuppression |
| IV (Sclerosis) | GBM thickened, lucent deposits, sclerosis | Lucent, degraded deposits; GBM irregularly thickened | Poor prognosis; irreversible damage |
MBS note: Renal biopsy (MBS item 13700 series) and anti-PLA2R antibody testing (specialist-requested serology) are rebatable in Australia. Anti-PLA2R testing is typically performed at reference laboratories and may require a nephrology referral for access.
Management
KDIGO Risk Stratification
Treatment decisions in MN follow the KDIGO 2021 algorithm, which categorises patients into risk groups based on proteinuria and eGFR trajectory:
Low Risk
Supportive Care
Proteinuria <3.5 g/day with normal eGFR. OR partial remission (proteinuria 0.3–3.5 g/day with >50% reduction from peak and stable/improving eGFR).
Setting: 6–12 months supportive therapy; monitor serially
Moderate Risk
Consider Immunosuppression
Persistent proteinuria 3.5–6 g/day for >6 months with stable eGFR. OR proteinuria 3.5–6 g/day for >6 months with rising anti-PLA2R titres.
Setting: Shared decision-making; rituximab or modified Ponticelli
High Risk
Immunosuppression Indicated
Persistent proteinuria >6 g/day for >6 months despite optimised supportive care. OR rising anti-PLA2R titres >150 RU/mL. OR declining eGFR. OR life-threatening complications.
Setting: Urgent immunosuppression; rituximab preferred first-line
Supportive / Conservative Therapy
All patients with MN — regardless of immunosuppression decision — require comprehensive supportive care:
- RAAS blockade: ACE inhibitor (e.g. perindopril 4–8 mg PO daily) or ARB (e.g. irbesartan 150–300 mg PO daily). Titrate to maximum tolerated dose. Reduces proteinuria by 30–50% and controls blood pressure.
- SGLT2 inhibitor: Dapagliflozin 10 mg PO daily (Forxiga®) — now PBS-listed for CKD regardless of diabetes status. Reduces proteinuria and slows CKD progression (DAPA-CKD, EMPA-KIDNEY trials).
- Diuretics: Loop diuretics (furosemide 20–80 mg PO daily) for oedema management. Combination with thiazide for resistant oedema.
- Statin: Atorvastatin 10–40 mg PO daily or rosuvastatin 5–20 mg PO daily for dyslipidaemia. PBS General Benefit.
- Anticoagulation: Consider prophylactic warfarin (INR 2.0–2.5) or LMWH if serum albumin <25 g/L with additional risk factors
- Sodium restriction: <2 g/day sodium intake
- Dietary protein: Avoid high-protein diets; aim for 0.8 g/kg/day unless malnourished
- Pneumococcal and influenza vaccination: Annual influenza; pneumococcal (Prevenar 13 then Pneumovax 23)
First-Line Immunosuppression — Rituximab
Rituximab has emerged as the preferred first-line immunosuppressive agent for moderate-to-high risk primary MN, based on the landmark MENTOR trial (Fervenza et al., 2019) and subsequent GEMRITUX trial.
Rituximab
MabThera® · Riximyo® · Anti-CD20 monoclonal antibody
Adult dose
1000 mg IV on day 1 and day 15 (2-dose induction); repeat 1000 mg IV at month 6 if incomplete remission or rising PLA2R titres
Alternative dose
375 mg/m² IV weekly × 4 doses (lymphoma protocol); some Australian centres use this regimen
Paediatric dose
375 mg/m² IV weekly × 4 doses (limited data in paediatric MN)
Route & frequency
IV infusion; induction at 0 and 2 weeks; reassess at 6 months
Renal adjustment
No dose adjustment required
Hepatic adjustment
No dose adjustment required
Key monitoring
Pre-treatment: HBV screening (HBsAg, anti-HBc), quantitative immunoglobulins, hepatitis B prophylaxis if HBV-positive. Monitor CD19+ B-cells, anti-PLA2R titres q3 months
PBS status
⚠ PBS Restricted Benefit — Authority Required for ANCA vasculitis; off-label for MN requires private script or hospital authority
MENTOR Trial (2019): Rituximab achieved complete or partial remission in 60% of patients vs 20% with cyclosporine at 24 months. Rituximab group had superior sustained remission rates and fewer adverse events. Anti-PLA2R titres declined earlier and more consistently in the rituximab group.
Alternative Immunosuppression — Modified Ponticelli Regimen
The modified Ponticelli regimen (alternating corticosteroids with alkylating agent) remains an effective alternative, particularly where rituximab is unavailable, contraindicated, or unaffordable.
Modified Ponticelli Regimen
Corticosteroid + Cyclophosphamide alternating protocol
Month 1, 3, 5
Methylprednisolone 1 g IV daily × 3 days, then oral prednisolone 0.4 mg/kg/day × 27 days
Month 2, 4, 6
Cyclophosphamide 2.0–2.5 mg/kg/day PO (adjusted to age and renal function)
Total duration
6 months (3 cycles of alternating therapy)
Renal adjustment
Reduce cyclophosphamide dose by 25% if eGFR <30 mL/min
Key monitoring
FBC fortnightly (neutropenia risk), urinalysis (haemorrhagic cystitis), fertility counselling, mesna if IV cyclophosphamide used
PBS status — Cyclophosphamide
⚠ PBS Authority Required — Restricted Benefit for nephrotic syndrome
PBS status — Prednisolone
✔ PBS General Benefit
Cyclophosphamide toxicity: Cumulative dose-related risks include gonadal toxicity (offer fertility preservation), haemorrhagic cystitis (use mesna with IV dosing), myelosuppression, increased infection risk, and long-term bladder malignancy risk. Limit cumulative dose where possible and avoid repeat courses.
Second-Line & Adjunctive Agents
Tacrolimus
Prograf® · Calcineurin inhibitor
Adult dose
0.05–0.075 mg/kg/day PO in 2 divided doses; target trough 5–10 ng/mL
Duration
12–24 months; taper gradually over 6–12 months after remission
Key side effects
Nephrotoxicity (monitor eGFR closely), new-onset diabetes, hypertension, neurotoxicity
PBS status
⚠ PBS Authority Required — transplant indication; off-label for MN
Ciclosporin
Neoral® · Calcineurin inhibitor
Adult dose
3.5–5.0 mg/kg/day PO in 2 divided doses; target trough 100–200 ng/mL
Duration
12–24 months with low-dose prednisolone; taper after remission
PBS status
✔ PBS General Benefit (for approved indications)
Treatment Response Criteria
| Response | Definition | Significance |
|---|---|---|
| Complete remission | uPCR <50 mg/mmol (proteinuria <0.3 g/day) × 2 consecutive measurements | Best long-term renal outcome; 10-year renal survival >95% |
| Partial remission | uPCR 50–350 mg/mmol (0.3–3.5 g/day) with >50% reduction from peak | Good prognosis; 10-year renal survival ~80–90% |
| No response | <50% reduction in proteinuria after 6 months of therapy | Consider alternative agent or second-line therapy |
| Relapse | uPCR returns to >350 mg/mmol after prior complete/partial remission | May require re-treatment with rituximab or alternative agent |
Anti-PLA2R Guided Treatment Monitoring
Serial anti-PLA2R antibody titres are now the cornerstone of treatment monitoring in primary MN:
- Check anti-PLA2R at baseline, then every 3 months during and after treatment
- Serological remission (PLA2R negativity) typically precedes clinical remission by 6–12 months
- Rising PLA2R titres after treatment cessation predict clinical relapse — consider pre-emptive re-treatment
- Persistent high titres despite therapy may indicate treatment-resistant disease; consider switching agent
- In PLA2R-negative MN, rely on proteinuria and eGFR for monitoring
Australian practice note: Rituximab access for MN in Australia currently requires private prescription or hospital authority application, as it is PBS-listed only for ANCA vasculitis, rheumatoid arthritis, and haematological malignancies. Discuss costs with patients and consider state-based compassionate access programmes. The modified Ponticelli regimen using PBS-listed cyclophosphamide and prednisolone remains a cost-effective alternative.
Relapsed or Refractory Disease
- First relapse after rituximab: Re-induction with rituximab 1000 mg × 2 doses; most patients respond to re-treatment
- Rituximab-refractory: Consider switch to modified Ponticelli regimen or combination rituximab + low-dose ciclosporin
- Cyclophosphamide-refractory: Rituximab is the preferred alternative
- Maintenance therapy: Some centres use low-dose rituximab (500 mg every 6 months) as maintenance in relapsing patients
- Novel agents: Ongoing clinical trials with ofatumumab (anti-CD20), obinutuzumab, and complement inhibitors (iptacopan, narsoplimab) show promise
Special Populations
Pregnancy
Rituximab
Contraindicated in pregnancy — crosses placenta and depletes fetal B-cells. Avoid conception for 12 months after last dose. Effective contraception required during treatment.
Cyclophosphamide
Teratogenic (FDA Category D) — absolutely contraindicated in pregnancy. Fertility preservation discussion mandatory before treatment.
ACE inhibitors / ARBs
Contraindicated in pregnancy (teratogenic — renal agenesis, oligohydramnios). Switch to labetalol, nifedipine, or methyldopa for BP control.
Tacrolimus
Can be used cautiously in pregnancy if indicated — monitor levels closely. Limited safety data in MN specifically.
LMWH (enoxaparin)
Preferred anticoagulant in pregnancy with nephrotic syndrome. Dose-adjust for renal function. PBS General Benefit.
Paediatrics
MN in children
Rare in paediatrics — MN accounts for <2% of childhood nephrotic syndrome. More common in adolescents. Higher rate of secondary causes (lupus, hepatitis B) in children. PLA2R testing may be less sensitive; biopsy essential.
Immunosuppression
Rituximab 375 mg/m² IV weekly × 4 doses — limited paediatric MN data extrapolated from adult trials. Calcineurin inhibitors (tacrolimus) used as second-line. Cyclophosphamide should be avoided if possible due to gonadotoxicity.
Elderly (>65 years)
Malignancy screening
Mandatory comprehensive malignancy screening in all elderly patients with MN — CT CAP, colonoscopy, age-appropriate cancer screening. THSD7A positivity mandates enhanced screening.
Treatment considerations
Rituximab preferred over cyclophosphamide due to lower toxicity in elderly. Higher infection risk with immunosuppression — ensure vaccinations up to date before treatment. Consider more conservative approach if limited life expectancy.
Renal Impairment
Rituximab
No dose adjustment required for renal impairment. Safe in CKD stages 3–5.
Cyclophosphamide
Reduce dose by 25% if eGFR <30 mL/min. Increase monitoring frequency.
Tacrolimus
Monitor levels closely — nephrotoxicity risk compounded by underlying renal disease. Avoid if eGFR <30 mL/min if possible.
Dapagliflozin
Initiate if eGFR ≥20 mL/min (PBS criteria for CKD). Can continue until dialysis commencement. Monitor for volume depletion.
Hepatic Impairment
Rituximab
No dose adjustment required. Caution in active hepatitis B — risk of reactivation. Prophylactic entecavir or tenofovir required if HBV-positive.
Cyclophosphamide
Hepatically metabolised — reduce dose and monitor LFTs in severe hepatic impairment.
Immunocompromised
Pre-treatment screening
HBV screening mandatory before rituximab. Check quantitative immunoglobulins (IgG, IgA, IgM). Screen for latent TB (IGRA). Ensure varicella immunity.
Infection prophylaxis
Consider trimethoprim-sulfamethoxazole 480 mg PO daily for PJP prophylaxis if combining rituximab with corticosteroids. IVIg replacement if hypogammaglobulinaemia develops post-rituximab.
Aboriginal and Torres Strait Islander Health
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander peoples experience a higher burden of kidney disease compared to non-Indigenous Australians, with glomerulonephritis contributing significantly to the disparity. While membranous nephropathy is less common than IgA nephropathy or diabetic kidney disease in ATSI populations, specific considerations apply:
📚 References
- 1. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney International. 2021;100(4S):S1–S276.
- 2. Fervenza FC, Appel GB, Barbour SJ, et al. Rituximab or Cyclosporine in the Treatment of Membranous Nephropathy. New England Journal of Medicine. 2019;381(1):36–46. (MENTOR Trial)
- 3. Beck LH Jr, Bonegio RGB, Lambeau G, et al. M-type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. New England Journal of Medicine. 2009;361(1):11–21.
- 4. Tomas NM, Beck LH Jr, Meyer-Schwesinger C, et al. Thrombospondin type-1 domain-containing 7A in idiopathic membranous nephropathy. New England Journal of Medicine. 2014;371(24):2277–2287.
- 5. Dahan K, Debiec H, Plaisier E, et al. Rituximab for Severe Membranous Nephropathy: A 6-Center Trial. Journal of the American Society of Nephrology. 2017;28(8):2509–2518. (GEMRITUX Trial)
- 6. Rovin BH, Adler SG, Barratt J, et al. Executive summary of the KDIGO 2021 Guideline for the Management of Glomerular Diseases. Kidney International. 2021;100(4):753–779.
- 7. Ponticelli C, Zucchelli P, Passerini P, et al. A 10-year follow-up of a randomized study with methylprednisolone and chlorambucil in membranous nephropathy. Kidney International. 1995;48(5):1600–1604.
- 8. Australian Institute of Health and Welfare (AIHW). Chronic kidney disease: Australian facts. Cat. no. PHE 221. Canberra: AIHW; 2023.
- 9. Australia and New Zealand Dialysis and Transplant Registry (ANZDATA). 46th Annual Report. Adelaide: ANZDATA; 2023.
- 10. Australian Commission on Safety and Quality in Health Care (ACSQHC). National Safety and Quality Health Service Standards. 2nd ed. Sydney: ACSQHC; 2021.
- 11. Fernandez-Juarez G, Rojas-Rivera J, Logt AV, et al. The STARMEN trial indicates that alternating treatment with corticosteroids and cyclophosphamide is superior to sequential treatment with tacrolimus and rituximab in primary membranous nephropathy. Kidney International. 2021;99(4):986–998.
- 12. Ponticelli C, Glassock RJ. Glomerular diseases: membranous nephropathy — A modern view. Clinical Journal of the American Society of Nephrology. 2014;9(3):609–616.