Microscopic Polyangiitis (MPA)

Table of Contents

  1. Overview
  2. Pathogenesis and ANCA Immunology
  3. Clinical Features: Renal Manifestations
  4. Clinical Features: Pulmonary and Systemic
  5. MPA vs. GPA: Key Distinctions
  6. Diagnosis
  7. Treatment
  8. Prognosis and Monitoring
  9. Key Research Papers
  10. Connections
  11. Featured Videos

1. Overview

Microscopic Polyangiitis (MPA) is an ANCA-associated small-vessel necrotizing vasculitis (AAV) — one of the three major AAV subtypes alongside Granulomatosis with Polyangiitis (GPA) and Eosinophilic Granulomatosis with Polyangiitis (EGPA). The name reflects its defining feature: inflammation of microscopic vessels — capillaries, venules, and arterioles — that are too small to be seen with the naked eye during surgery or conventional angiography.

The single most important distinguishing feature of MPA is the absence of granulomas. This is not a minor histological footnote — it is definitional in the Chapel Hill Consensus Conference classification of AAV. GPA is a granulomatous necrotizing vasculitis; EGPA is an eosinophilic granulomatous vasculitis; MPA is non-granulomatous necrotizing vasculitis. This distinction drives differences in affected organs, ANCA specificity, and some aspects of management.

MPA predominantly affects small vessels — capillaries, venules, arterioles — but also involves small arteries. The kidneys and lungs are the most critically affected organs. Rapidly progressive glomerulonephritis (RPGN) is the defining renal manifestation; diffuse alveolar hemorrhage (DAH) causes the most life-threatening pulmonary emergencies. Mononeuritis multiplex, palpable purpura, and constitutional symptoms round out the clinical picture.

A 2022 meta-analysis of 25 studies estimated a worldwide pooled MPA prevalence of 39.2 per million people and an incidence of 5.9 per million person-years, against 96.8 per million and 9.0 per million person-years for GPA, with ANCA-associated vasculitis more frequent in the northern hemisphere and rising over time (Redondo-Rodriguez 2022). A 2015 review describes a slight male predominance (Greco 2015); a French cohort of 85 patients included 47 men and 38 women, with a mean age of 56.8 years (Guillevin 1999). The balance between subtypes differs by region: in a population-based comparison using the same case definitions, MPA made up 83% of ANCA-associated vasculitis cases in Miyazaki, Japan, while GPA was more frequent in Norfolk, UK; most Japanese patients were p-ANCA/anti-MPO positive and two-thirds of UK patients c-ANCA/anti-PR3 positive (Fujimoto 2011). Anti-MPO ANCA, which gives a p-ANCA pattern on indirect immunofluorescence, is the serological signature of the disease: in the French cohort, ANCA were found in 38 of 51 patients tested (74.5%), and enzyme-linked immunosorbent assay (ELISA) detected anti-MPO in 31 patients and anti-PR3 in 4 (Guillevin 1999).

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2. Pathogenesis and ANCA Immunology

MPA is the paradigmatic ANCA-associated vasculitis, and understanding its immunopathogenesis requires understanding how ANCA antibodies damage blood vessels at the molecular level.

ANCA Specificity in MPA

Mechanism of Vessel Injury

The current model of ANCA-mediated vascular damage involves the following sequence:

  1. Cytokine priming: Systemic infection or other stimuli trigger release of pro-inflammatory cytokines (IL-8, TNF-α). These cytokines prime neutrophils, causing MPO and PR3 — normally stored in azurophilic granules — to translocate to the neutrophil cell surface.
  2. ANCA binding: Circulating ANCA binds to the surface-expressed MPO or PR3. Fc receptors on the neutrophil simultaneously recognize the ANCA Fc region, causing cross-linking and inside-out signaling.
  3. Neutrophil-endothelial adhesion: Integrin activation (β2 integrins, LFA-1) anchors the primed neutrophil to the vascular endothelium.
  4. Degranulation and respiratory burst: Activated neutrophils release reactive oxygen species, proteases (elastase, cathepsin G), and MPO itself into the vessel wall microenvironment. This causes fibrinoid necrosis of the vessel wall — the hallmark of leukocytoclastic vasculitis.
  5. Pauci-immune injury: Because the injury is driven by activated neutrophils rather than immune complex deposition, the renal and vascular lesions show minimal IgG, IgM, IgA, or complement by immunofluorescence — the "pauci-immune" pattern that distinguishes AAV from immune complex-mediated vasculitides like lupus nephritis.

Complement Amplification and Avacopan

An amplification loop involves the complement system: complement activated during ANCA-driven neutrophil activation generates C5a → C5a binds C5aR on neutrophils → further priming and amplification of ANCA-mediated activation. This C5a–C5aR axis is the mechanistic rationale for avacopan, a selective C5aR antagonist approved by the US FDA in 2021 as an adjunctive treatment for MPA and GPA; its approval rested mainly on a trial whose published report was retracted in 2026 (see Avacopan below).

No Granuloma Formation

In sharp contrast to GPA, MPA does not involve significant T-cell granuloma formation. There is no orchestrated macrophage-T cell aggregate driving necrotizing granulomatous inflammation in the upper airways, lung parenchyma, or elsewhere. The inflammatory response in MPA is primarily a neutrophilic, antibody-mediated vascular injury — pure necrotizing vasculitis without the granulomatous superstructure that defines GPA pathology.

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3. Clinical Features: Renal Manifestations

Renal involvement is the most common and most consequential manifestation of MPA. Understanding the renal pathology in MPA requires understanding pauci-immune crescentic glomerulonephritis — the histological pattern that defines AAV-associated kidney disease.

Rapidly Progressive Glomerulonephritis (RPGN)

RPGN is the clinical syndrome of rapidly declining renal function — rising serum creatinine over days to weeks — combined with an active urinary sediment (hematuria, RBC casts, proteinuria). The time course ("rapidly progressive" over days to weeks, not months) distinguishes RPGN from slower forms of glomerular disease. RPGN is a renal emergency: without treatment it can progress to end-stage renal disease (ESRD) within weeks to months.

Pauci-Immune Crescentic Glomerulonephritis

Renal biopsy in MPA shows the following characteristic features:

Clinical Presentation of MPA Nephritis

Patients typically present with:

Severity and Outcomes

Renal outcomes in MPA are heavily dependent on the severity at presentation and speed of treatment:

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4. Clinical Features: Pulmonary and Systemic

Beyond the kidneys, MPA can damage the lungs, peripheral nerves, skin, and virtually any organ supplied by small vessels. The pulmonary manifestations are the most immediately life-threatening.

Diffuse Alveolar Hemorrhage (DAH)

In the French cohort, lung involvement was present in 24.7% of patients and alveolar hemorrhage in 11.8% (Guillevin 1999). DAH is caused by pulmonary capillaritis — the same neutrophilic, ANCA-mediated inflammatory mechanism that destroys glomerular capillaries, now targeting the alveolar-capillary interface. Neutrophilic inflammation and necrosis of pulmonary capillary walls allows red blood cells to flood the alveolar spaces, causing alveolar hemorrhage. This is distinct from cardiogenic pulmonary edema and from pneumonia.

Clinical presentation of DAH:

Pulmonary-Renal Syndrome

The simultaneous occurrence of DAH and crescentic glomerulonephritis is called pulmonary-renal syndrome, a medical emergency. In addition to MPA, it is also caused by GPA and anti-GBM (Goodpasture) disease. Distinguishing the cause rests on urgent ANCA testing (anti-MPO and anti-PR3) and anti-GBM antibody testing, because patients positive for both exist (see Anti-GBM Antibody Testing under Diagnosis).

Interstitial Lung Disease (ILD)

Pulmonary fibrosis is an uncommon manifestation of ANCA-associated vasculitis that occurs particularly in MPA. In a French multicentre series of 49 patients with pulmonary fibrosis and ANCA-associated vasculitis, 81.6% had MPA, ANCA were mostly anti-MPO (88%), a usual interstitial pneumonia (UIP) pattern (honeycombing, traction bronchiectasis, peripheral and basal predominance) was the main radiological pattern (43%), and the fibrosis was diagnosed before the vasculitis in 45% (Comarmond 2014). Pulmonary function tests (PFTs) and high-resolution CT (HRCT) are used at baseline to characterize lung involvement.

Peripheral Neuropathy: Mononeuritis Multiplex

Mononeuritis multiplex was present in 57.6% of the French cohort (Guillevin 1999) and is caused by ischemic infarction of individual named peripheral nerves via vasculitis of the vasa nervorum (the small vessels supplying nerve trunks). Characteristic features:

Skin: Palpable Purpura

Palpable purpura is the cutaneous hallmark of small-vessel vasculitis. Unlike flat (macular) petechiae from thrombocytopenia, palpable purpura is raised above the skin surface because the inflammatory infiltrate in dermal vessel walls physically elevates the overlying epidermis. Lower extremities predominate; skin involvement was present in 62.4% of the French cohort (Guillevin 1999). Skin biopsy shows leukocytoclastic vasculitis: neutrophilic infiltration of vessel walls, nuclear dust (karyorrhexis from neutrophil fragmentation), and fibrinoid necrosis. When skin biopsy shows leukocytoclastic vasculitis, ANCA testing is used to look for an ANCA-associated vasculitis as the systemic cause.

Constitutional Symptoms

Fever, night sweats, unintentional weight loss, and profound fatigue frequently precede organ-specific symptoms by weeks to months. These constitutional features reflect the systemic cytokine burden of active small-vessel inflammation. In the French cohort, weight loss was present in 72.9% and fever in 55.3% (Guillevin 1999). The symptoms are non-specific; together with signs of kidney or lung involvement, they are a common reason for ANCA testing and urinalysis.

Upper Airway Disease

Destructive upper-airway disease — sinusitis with bony erosion, nasal septal perforation, saddle-nose deformity, subglottic stenosis — is characteristic of GPA rather than MPA, and in the 2022 classification criteria sino-nasal symptoms or signs count against MPA (Suppiah 2022). A 2015 review notes, however, that ear, nose and throat involvement was reported in surprisingly high percentages of the MPA populations described (Greco 2015). When destructive upper-airway features are present, GPA is reconsidered as the diagnosis.

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5. MPA vs. GPA: Key Distinctions

MPA and GPA are frequently lumped together as "ANCA vasculitis," but they are distinct diseases with different histology, serology, organ tropism, and relapse biology. Understanding the differences is clinically essential.

Comparative Table

The ANCA-Phenotype Paradigm

A genome-wide association study of 1,233 UK patients with ANCA-associated vasculitis, replicated in 1,454 Northern European patients, found that GPA and MPA were genetically distinct and that the strongest genetic associations were with ANCA specificity rather than with the clinical syndrome: anti-PR3 ANCA with HLA-DP and the genes for α1-antitrypsin (SERPINA1) and proteinase 3 (PRTN3), and anti-MPO ANCA with HLA-DQ (Lyons et al. 2012, PubMed PMID: 22808956). A 2020 review states that genetic and other clinical findings suggest these syndromes may be better classified as PR3-ANCA and MPO-ANCA vasculitis (Kitching 2020). The 2022 ACR/EULAR classification criteria still combine clinical, histological and serological features.

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6. Diagnosis

Diagnosing MPA requires integrating clinical features, serological testing, urinalysis, and tissue biopsy. No single test is pathognomonic. Speed matters because organ injury can be fulminant.

ANCA Testing

ANCA are detected by indirect immunofluorescence (IIF), which shows the staining pattern, and by antigen-specific immunoassays such as ELISA for MPO and PR3. A 2017 international consensus states that high-quality MPO- and PR3-ANCA immunoassays can be used as the primary screening test for GPA and MPA, without the categorical need for IIF (Bossuyt 2017):

Renal Biopsy

Renal biopsy is the gold standard for diagnosing and characterizing renal involvement in suspected MPA. It confirms pauci-immune crescentic GN, quantifies the percentage of crescents (which predicts prognosis and informs treatment intensity), and excludes other causes of RPGN (immune complex GN, anti-GBM disease). Biopsy findings are also used in decisions about treatment intensity, including plasma exchange (see PEXIVAS below).

Urinalysis and Urine Microscopy

Fresh urine microscopy is a bedside test for active glomerulonephritis: RBC casts confirm it, and they are looked for in anyone with suspected AAV. Dysmorphic red blood cells (acanthocytes, "Mickey Mouse" cells) provide additional evidence of glomerular origin. Dipstick testing alone is inadequate — it misses casts.

Pulmonary Evaluation

Anti-GBM Antibody Testing

Anti-GBM antibody testing is part of the work-up of pulmonary-renal syndrome. Anti-GBM (Goodpasture) disease causes DAH + RPGN with linear IgG along the GBM on IF — distinct from pauci-immune. In a European cohort of 568 patients with ANCA-associated vasculitis, 41 with anti-GBM disease and 37 double-positive for ANCA and anti-GBM antibodies, the double-positive patients shared the older age and longer symptom duration of ANCA-associated vasculitis and the severe kidney disease and frequent lung hemorrhage of anti-GBM disease; about half of surviving ANCA-associated vasculitis and double-positive patients had recurrent disease over a median 4.8 years, while no single-positive anti-GBM patient relapsed. The authors describe a hybrid disease calling for aggressive early treatment of the anti-GBM disease and long-term follow-up with consideration of maintenance immunosuppression (McAdoo 2017).

2022 ACR/EULAR Classification Criteria for MPA

Suppiah et al. (Arthritis Rheumatol. 2022) published points-based ACR/EULAR classification criteria for MPA, derived in 149 cases and 408 comparators and validated in another 142 cases and 414 comparators. The items and weights are: p-ANCA or anti-MPO positivity (+6), pauci-immune glomerulonephritis (+3), lung fibrosis or interstitial lung disease (+3), sino-nasal symptoms or signs (−3), c-ANCA or anti-PR3 positivity (−1), and an eosinophil count of at least 1 × 109/L (−4). After mimics are excluded, a patient already diagnosed with small- or medium-vessel vasculitis is classified as MPA at 5 points or more; in validation the sensitivity was 91% and the specificity 94% (Suppiah 2022). The criteria are validated for clinical research, not as diagnostic criteria for individual patients.

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7. Treatment

Treatment of MPA follows a two-phase structure: induction of remission (aggressive immunosuppression to halt active vasculitis and prevent organ loss) followed by maintenance of remission (prolonged lower-intensity immunosuppression to prevent relapse). The evidence base for MPA treatment is largely shared with GPA through landmark randomized controlled trials. The doses below are those used in the trials named, not instructions; decisions about treatment belong with a clinician.

Induction — Rituximab

Rituximab (anti-CD20, depletes B cells) plus high-dose glucocorticoids is one of the two main induction regimens:

Induction — Cyclophosphamide

Cyclophosphamide (IV pulse or oral) plus high-dose glucocorticoids is the other main induction regimen (Hellmich 2024). Situations in which it is commonly used include:

High-Dose Glucocorticoids

Intravenous methylprednisolone pulses are commonly given at presentation in DAH or severe RPGN, followed by oral prednisone with a planned taper. The 2022 EULAR update recommends tapering to a target of 5 mg prednisolone equivalent per day within 4–5 months (Hellmich 2024), and in PEXIVAS a reduced-dose oral glucocorticoid regimen was non-inferior to a standard-dose regimen for death or end-stage kidney disease, with fewer serious infections at 1 year (Walsh 2020). Prolonged high-dose steroid exposure causes substantial morbidity, which is the rationale for steroid-sparing strategies such as rituximab and, where it remains approved, avacopan (see below).

Avacopan (C5aR Antagonist)

Avacopan, an oral selective complement 5a receptor (C5aR) antagonist, was approved by the US FDA in October 2021 as an adjunctive treatment for adults with severe active ANCA-associated vasculitis (GPA and MPA), in combination with standard therapy including glucocorticoids; the US label states that it does not eliminate glucocorticoid use, and the label dose is 30 mg orally twice daily. The approval rested mainly on the ADVOCATE trial (Jayne et al., NEJM 2021, PubMed PMID: 33596356), whose published report was retracted by the journal on 29 June 2026 (retraction notice PMID 42377355). The European Medicines Agency opened a review in January 2026 over the integrity of the ADVOCATE data and concluded in June 2026 that the trial was conducted in breach of good clinical practice and that the study data provided at the time of assessment were “incorrect and misleading” and could no longer be relied upon to show the medicine’s effectiveness; the EU marketing authorisation was revoked by European Commission decision on 4 August 2026 (EMA announcement, 26 June 2026). In the United States, the FDA’s Drugs@FDA record still listed the 2021 approval with prescription marketing status as of October 2026; whether the FDA has taken any action since the retraction could not be confirmed. The EMA’s review also states that avacopan is associated with an increased risk of drug-induced liver injury and vanishing bile duct syndrome, including fatal cases, particularly in the first three months of treatment (EMA referral record). The 2022 EULAR update, published before the retraction, had stated that avacopan may be considered as part of a strategy to reduce glucocorticoid exposure (Hellmich 2024).

Plasma Exchange — PEXIVAS Results

The PEXIVAS trial (Walsh et al. 2020, PubMed PMID: 32053298) randomized patients with severe ANCA-associated vasculitis (eGFR <50 mL/min/1.73 m² or diffuse pulmonary hemorrhage) to plasma exchange (seven exchanges within 14 days) or none. Death from any cause or end-stage kidney disease (ESKD) occurred in 100 of 352 patients (28.4%) with plasma exchange and 109 of 352 (31.0%) without it (hazard ratio 0.86, not statistically significant): plasma exchange did not reduce death or ESKD. The 2022 EULAR update states that plasma exchange may be considered in patients with rapidly progressive glomerulonephritis (Hellmich 2024). For patients double-positive for ANCA and anti-GBM antibodies, the authors of a European cohort describe aggressive early treatment of the anti-GBM disease (McAdoo 2017).

Maintenance Therapy

After successful induction, maintenance immunosuppression is used to prevent relapse:

Dialysis and Renal Replacement Therapy

Acute renal replacement therapy (hemodialysis or CRRT) is used for oliguric RPGN with uremia, hyperkalemia, or fluid overload, alongside immunosuppression rather than in place of it. Renal recovery (dialysis independence) remains possible even after weeks on dialysis with ongoing immunosuppression.

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8. Prognosis and Monitoring

Immunosuppressive treatment has improved survival in ANCA-associated vasculitis, though with considerable morbidity from glucocorticoids and other immunosuppressive drugs (Kitching 2020). The disease remains serious, with relapse, permanent renal impairment, and deaths from treatment complications.

Remission and Relapse

Renal Outcomes

Mortality

Anti-MPO ANCA and Interstitial Lung Disease

Patients with anti-MPO-associated pulmonary fibrosis are followed with PFTs (spirometry and DLCO) and HRCT. In the French series of 49 patients with pulmonary fibrosis and ANCA-associated vasculitis, 18 (37%) died over a median 48 months, 11 of them from respiratory insufficiency; 3-year survival was 64% with glucocorticoids alone and 94% with glucocorticoids plus cyclophosphamide or rituximab, and the authors describe pulmonary fibrosis as a rare manifestation with a very poor prognosis (Comarmond 2014).

Monitoring Commonly Described

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Key Research Papers

The following peer-reviewed publications represent key milestones in understanding and treating Microscopic Polyangiitis.

  1. Stone JH, et al. Rituximab versus cyclophosphamide for ANCA-associated vasculitis. N Engl J Med. 2010;363(3):221–232. — PubMed PMID: 20647199 (RAVE trial)
  2. Jones RB, et al. Rituximab versus cyclophosphamide in ANCA-associated renal vasculitis. N Engl J Med. 2010;363(3):211–220. — PubMed PMID: 20647198 (RITUXVAS trial)
  3. Jayne DRW, et al. Avacopan for the treatment of ANCA-associated vasculitis. N Engl J Med. 2021;384(7):599–609. (ADVOCATE trial). — PubMed PMID: 33596356 — Retracted (retraction notice: PubMed PMID: 42377355)
  4. Walsh M, et al. Plasma exchange and glucocorticoids in severe ANCA-associated vasculitis. N Engl J Med. 2020;382(7):622–631. — PubMed PMID: 32053298 (PEXIVAS trial)
  5. Jayne D, et al. A randomized trial of maintenance therapy for vasculitis associated with antineutrophil cytoplasmic autoantibodies. N Engl J Med. 2003;349(1):36–44. — PubMed PMID: 12840090 (CYCAZAREM)
  6. Guillevin L, et al. Rituximab versus azathioprine for maintenance in ANCA-associated vasculitis. N Engl J Med. 2014;371(19):1771–1780. — PubMed PMID: 25372085 (MAINRITSAN)
  7. Greco A, et al. Microscopic polyangiitis: advances in diagnostic and therapeutic approaches. Autoimmun Rev. 2015;14(9):837–844. — PubMed PMID: 25992801
  8. Seo P, Stone JH. The antineutrophil cytoplasmic antibody-associated vasculitides. Am J Med. 2004;117(1):39–50. — PubMed PMID: 15210387
  9. Suppiah R, Robson JC, Grayson PC, et al. 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology classification criteria for microscopic polyangiitis. Arthritis Rheumatol. 2022;74(3):400–406. — PubMed PMID: 35106973 (first author corrected; this entry previously listed Grayson PC, the third author, as first author)
  10. Guillevin L, et al. Microscopic polyangiitis: clinical and laboratory findings in eighty-five patients. Arthritis Rheum. 1999;42(3):421–430. — PubMed PMID: 10088763
  11. Lyons PA, et al. Genetically distinct subsets within ANCA-associated vasculitis. N Engl J Med. 2012;367(3):214–223. — PubMed PMID: 22808956
  12. Jennette JC, et al. 2012 revised International Chapel Hill Consensus Conference Nomenclature of Vasculitides. Arthritis Rheum. 2013;65(1):1–11. — PubMed PMID: 23045170
  13. de Groot K, Harper L, Jayne DR, et al. Pulse versus daily oral cyclophosphamide for induction of remission in antineutrophil cytoplasmic antibody-associated vasculitis: a randomized trial. Ann Intern Med. 2009;150(10):670–680. — PubMed PMID: 19451574 (CYCLOPS trial)
  14. Hiemstra TF, Walsh M, Mahr A, et al. Mycophenolate mofetil vs azathioprine for remission maintenance in antineutrophil cytoplasmic antibody-associated vasculitis: a randomized controlled trial. JAMA. 2010;304(21):2381–2388. — PubMed PMID: 21060104 (IMPROVE trial)
  15. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Rheumatol. 2021;73(8):1366–1383. — PubMed PMID: 34235894
  16. Hellmich B, Sanchez-Alamo B, Schirmer JH, et al. EULAR recommendations for the management of ANCA-associated vasculitis: 2022 update. Ann Rheum Dis. 2024;83(1):30–47. — PubMed PMID: 36927642
  17. Kitching AR, Anders HJ, Basu N, et al. ANCA-associated vasculitis. Nat Rev Dis Primers. 2020;6(1):71. — PubMed PMID: 32855422
  18. Redondo-Rodriguez R, Mena-Vázquez N, Cabezas-Lucena AM, et al. Systematic review and metaanalysis of worldwide incidence and prevalence of antineutrophil cytoplasmic antibody (ANCA) associated vasculitis. J Clin Med. 2022;11(9):2573. — PubMed PMID: 35566698
  19. Fujimoto S, Watts RA, Kobayashi S, et al. Comparison of the epidemiology of anti-neutrophil cytoplasmic antibody-associated vasculitis between Japan and the U.K. Rheumatology (Oxford). 2011;50(10):1916–1920. — PubMed PMID: 21798892
  20. He P, Hu JP, Tian XJ, et al. Prevalence and risk factors of relapse in patients with ANCA-associated vasculitis receiving cyclophosphamide induction: a systematic review and meta-analysis of large observational studies. Rheumatology (Oxford). 2021;60(3):1067–1079. — PubMed PMID: 33677596
  21. Flossmann O, Berden A, de Groot K, et al. Long-term patient survival in ANCA-associated vasculitis. Ann Rheum Dis. 2011;70(3):488–494. — PubMed PMID: 21109517
  22. Comarmond C, Crestani B, Tazi A, et al. Pulmonary fibrosis in antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis: a series of 49 patients and review of the literature. Medicine (Baltimore). 2014;93(24):340–349. — PubMed PMID: 25500703
  23. McAdoo SP, Tanna A, Hrušková Z, et al. Patients double-seropositive for ANCA and anti-GBM antibodies have varied renal survival, frequency of relapse, and outcomes compared to single-seropositive patients. Kidney Int. 2017;92(3):693–702. — PubMed PMID: 28506760
  24. Bossuyt X, Cohen Tervaert JW, Arimura Y, et al. Position paper: Revised 2017 international consensus on testing of ANCAs in granulomatosis with polyangiitis and microscopic polyangiitis. Nat Rev Rheumatol. 2017;13(11):683–692. — PubMed PMID: 28905856

PubMed Topic Searches

  1. PubMed: Microscopic polyangiitis treatment
  2. PubMed: ANCA vasculitis rituximab maintenance
  3. PubMed: Pauci-immune crescentic glomerulonephritis
  4. PubMed: Anti-MPO ANCA interstitial lung disease
  5. PubMed: Avacopan ANCA vasculitis ADVOCATE trial

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10. Connections

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