Lab result explainedInflammationLast updated November 11, 2026

ANCA test: p-ANCA, c-ANCA, MPO and PR3 antibodies and what a positive result means

Antineutrophil cytoplasmic antibody test (ANCA) · ANCA panel (immunofluorescence pattern with MPO and PR3 antibody immunoassays), ordered with urinalysis, creatinine, CBC and CRP · reported in Immunofluorescence titer (negative below 1:20 at most labs) with a pattern (c-ANCA, p-ANCA, atypical); antigen-specific MPO and PR3 results in units (AU/mL, IU/mL, U/mL) or an antibody index against the kit's own cut-off

Antineutrophil cytoplasmic antibodies (ANCA) are autoantibodies against proteins inside neutrophils, and the ANCA test is the main blood test for a group of small-vessel vasculitides now called ANCA-associated vasculitis: granulomatosis with polyangiitis (GPA, formerly Wegener's granulomatosis), microscopic polyangiitis (MPA) and eosinophilic granulomatosis with polyangiitis (EGPA, formerly Churg-Strauss syndrome). A normal result is negative: no fluorescence pattern at a 1:20 dilution and MPO and PR3 antibodies below the kit's cut-off. Most reports give two things: a staining pattern (c-ANCA, p-ANCA or atypical) and the specific target antigen, proteinase 3 (PR3) or myeloperoxidase (MPO).

The pattern and the antigen are read together. c-ANCA with PR3 antibodies points to GPA, where it is positive in 70 to 90 percent of active generalized disease; p-ANCA with MPO antibodies points to MPA (60 to 70 percent), to the vasculitic subset of EGPA (30 to 40 percent of EGPA overall) and to drug-induced vasculitis. A p-ANCA pattern without MPO antibodies, often labeled atypical ANCA, is common in ulcerative colitis, primary sclerosing cholangitis and autoimmune hepatitis and does not mean vasculitis. International guidance since 2017 recommends the PR3 and MPO immunoassays as the primary tests, with the fluorescence pattern as a supplement.

ANCA is ordered when symptoms suggest vasculitis: blood and protein in the urine with a rising creatinine, coughing blood or lung shadows, chronic bloody nasal crusting or sinus disease, a red painful eye, sudden foot or wrist drop, a purpuric rash, or unexplained fever and weight loss with a high CRP. In that setting a positive PR3 or MPO result has a specificity of about 98 percent and often leads straight to biopsy and treatment, because untreated ANCA vasculitis can destroy kidney function within weeks. Ordered for vague symptoms with a low prior likelihood, it produces more false positives than true ones.

ANCA at a glance

What it is: antibodies against neutrophil granule proteins; the key blood test for ANCA-associated vasculitis (GPA, MPA, EGPA) and some drug-induced vasculitis.
Normal: negative at a 1:20 dilution on immunofluorescence, with MPO and PR3 antibodies below the kit cut-off (kits differ; for example under 3.5 IU/mL or under 20 units).
c-ANCA with PR3: granulomatosis with polyangiitis (ears, nose, sinuses, lungs, kidneys). p-ANCA with MPO: microscopic polyangiitis, kidney-limited vasculitis, EGPA and drug-induced vasculitis.
p-ANCA or atypical ANCA without MPO or PR3: usually ulcerative colitis, primary sclerosing cholangitis, autoimmune hepatitis or rheumatoid arthritis, not vasculitis.
A negative ANCA does not exclude vasculitis (10 to 20 percent of GPA and up to 60 percent of EGPA are ANCA negative); a positive one does not prove it without matching symptoms, urine and tissue findings.
Next step: urinalysis with microscopy, creatinine, CBC, CRP, chest imaging and usually a biopsy; a positive result with kidney or lung involvement is treated as an emergency.

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What ANCA measures

Neutrophils store enzymes in granules to kill microbes. In ANCA vasculitis the immune system makes IgG antibodies against two of these enzymes, proteinase 3 and myeloperoxidase. When neutrophils are primed by infection or cytokines they display these proteins on their surface; ANCA binding activates the cells, which stick to small blood vessel walls, release enzymes and oxidants and form neutrophil extracellular traps, damaging capillaries in the kidney glomeruli, the lung alveoli and the skin. This is why the disease shows up as blood and protein in the urine, lung hemorrhage and purpura, and why the kidney lesion is typically 'pauci-immune' (few antibody deposits on biopsy) rather than immune-complex mediated.

Two laboratory methods exist. Indirect immunofluorescence on ethanol-fixed neutrophils shows a granular cytoplasmic pattern (c-ANCA, nearly always PR3) or a perinuclear pattern (p-ANCA, usually MPO but also produced by antibodies to lactoferrin, elastase, cathepsin G and other proteins, and by antinuclear antibodies, which is why it needs confirmation). Antigen-specific immunoassays (ELISA, chemiluminescence or multiplex) measure PR3-ANCA and MPO-ANCA directly and report units against a cut-off. The 2017 international consensus recommends running the antigen-specific assays first because they are more specific and reproducible; many US labs still run both.

Units and cut-offs vary by kit, from under 3.5 IU/mL to under 20 units for negative, so the printed range matters more than the number. Titers broadly track disease burden at diagnosis but are an unreliable guide afterward: a meta-analysis found that a rising or persistently positive ANCA during remission only modestly raised the likelihood of relapse (positive likelihood ratio about 2.8), so treatment is not escalated on antibody levels alone. Dual positivity for both MPO and PR3, often at high titers, is a clue to levamisole-contaminated cocaine, hydralazine or propylthiouracil exposure.

Normal range for ANCA

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (Immunofluorescence titer (negative below 1:20 at most labs) with a pattern (c-ANCA, p-ANCA, atypical); antigen-specific MPO and PR3 results in units (AU/mL, IU/mL, U/mL) or an antibody index against the kit's own cut-off)	Notes
Negative	Immunofluorescence negative at 1:20; MPO and PR3 below the kit cut-off	Normal. Does not exclude vasculitis when the clinical picture is strong; biopsy still decides.
Immunofluorescence titer	Reported in doubling dilutions (1:20, 1:40, 1:80, 1:160 and above)	Higher titers at diagnosis go with more extensive disease, but titers are kit-dependent and not used alone for treatment decisions.
c-ANCA pattern	Granular cytoplasmic staining; almost always PR3-ANCA	Granulomatosis with polyangiitis in the right setting; rarely infection (endocarditis) or levamisole exposure.
p-ANCA pattern with MPO	Perinuclear staining confirmed by a positive MPO immunoassay	Microscopic polyangiitis, renal-limited vasculitis, EGPA, drug-induced vasculitis, and anti-GBM disease (20 to 30 percent are double positive).
p-ANCA or atypical ANCA without MPO or PR3	Perinuclear or atypical staining; antigen assays negative	Ulcerative colitis (50 to 70 percent), primary sclerosing cholangitis (up to 80 percent), autoimmune hepatitis, rheumatoid arthritis, lupus, cystic fibrosis. Not vasculitis.
PR3-ANCA positive	Above the kit cut-off (for example above 5 IU/mL or above 20 units; an equivocal band sits just over the line on many kits)	Specificity about 98 percent for GPA or MPA when ordered for vasculitis symptoms; PR3 positivity carries a higher relapse risk than MPO.
MPO-ANCA positive	Above the kit cut-off	MPA, EGPA, drug-induced disease; associated with more kidney scarring at presentation and with interstitial lung disease.
Dual MPO and PR3 positive	Both above the cut-off, often at high levels	Suggests levamisole-adulterated cocaine, hydralazine or propylthiouracil; expect to be asked about exposures.

Positive ANCA

A positive ANCA means antibodies against neutrophil proteins are present, and the type tells the story. PR3-ANCA with a c-ANCA pattern in someone with sinus, lung or kidney symptoms is granulomatosis with polyangiitis until proven otherwise; MPO-ANCA with a p-ANCA pattern in someone with blood and protein in the urine and a rising creatinine is microscopic polyangiitis or renal-limited vasculitis; MPO-ANCA in an adult with late-onset asthma, very high eosinophils and nerve or skin involvement is EGPA. In these settings the antibody is specific enough (about 98 percent) that treatment is often started while a biopsy is arranged, because glomerular damage and lung hemorrhage progress over days to weeks.

A p-ANCA pattern with negative MPO and PR3 assays is a different result and usually not vasculitis. This atypical ANCA is found in half or more of people with ulcerative colitis and primary sclerosing cholangitis, in autoimmune hepatitis, rheumatoid arthritis, lupus and after some infections. If your report shows p-ANCA positive but MPO negative and you have bowel or liver symptoms rather than kidney or lung ones, the finding is a marker of those conditions rather than a reason to suspect vasculitis.

A positive ANCA in someone with no compatible symptoms, a normal urinalysis and a normal CRP has a low predictive value and is not treated. Drugs (propylthiouracil, hydralazine, minocycline, levamisole-contaminated cocaine), infections (endocarditis, tuberculosis, hepatitis C, HIV) and other autoimmune diseases account for most such results. The right response is a careful review of exposures, a urine microscopy looking for red cell casts, and a repeat test, with the clinician alert to new symptoms.

Common causes

Granulomatosis with polyangiitis (GPA)
Vasculitis with granulomas affecting the nose, sinuses, ears, lungs and kidneys. PR3-ANCA is positive in 65 to 75 percent of all cases and up to 90 percent of active generalized disease; MPO-ANCA accounts for most of the rest, and 10 to 20 percent, mostly with disease limited to the upper airway, are ANCA negative.
Microscopic polyangiitis (MPA)
Small-vessel vasculitis without granulomas, typically presenting as rapidly progressive glomerulonephritis with or without lung hemorrhage. MPO-ANCA is positive in 60 to 70 percent and PR3-ANCA in 20 to 30 percent; renal-limited vasculitis is the same process confined to the kidney.
Eosinophilic granulomatosis with polyangiitis (EGPA)
Adult-onset asthma, eosinophils above 1,500 per microliter, sinus disease and vasculitis of nerves, skin, heart or kidneys. Only 30 to 40 percent are ANCA positive, almost all MPO; ANCA-positive patients have more kidney and nerve involvement, ANCA-negative patients more heart disease.
Drug-induced ANCA vasculitis
Propylthiouracil (and less often methimazole), hydralazine, minocycline, allopurinol and levamisole-adulterated cocaine induce ANCA, classically high-titer MPO or dual MPO and PR3, often with antinuclear, antiphospholipid or anti-elastase antibodies. Skin necrosis of the ears, nose and cheeks is characteristic of levamisole; stopping the drug is central to treatment.
Inflammatory bowel disease
Atypical p-ANCA without MPO or PR3 is found in 50 to 70 percent of ulcerative colitis and 10 to 25 percent of Crohn's disease, and is sometimes used with anti-Saccharomyces antibodies to help tell them apart. It is not vasculitis and does not predict it.
Autoimmune liver disease
Atypical ANCA is present in up to 80 percent of primary sclerosing cholangitis and 50 to 90 percent of type 1 autoimmune hepatitis. In someone with abnormal liver tests and a p-ANCA, these are more likely than vasculitis.
Infections
Infective endocarditis can produce a true PR3-ANCA with glomerulonephritis and mimic GPA, which is one reason blood cultures are taken before immunosuppression. Tuberculosis, HIV, hepatitis C and chronic bacterial infections produce low-level ANCA, usually MPO or atypical.
Anti-glomerular basement membrane (Goodpasture) disease
20 to 30 percent of people with anti-GBM antibodies also have MPO-ANCA. Double-positive patients behave like anti-GBM disease early (needing plasma exchange) and like ANCA vasculitis later (relapsing), so both tests are run in anyone with lung hemorrhage and kidney failure.
Other autoimmune diseases
Rheumatoid arthritis, lupus, Sjögren's syndrome and IgA vasculitis produce low-titer p-ANCA or MPO-ANCA in a minority of patients, usually without the clinical features of ANCA vasculitis; antinuclear antibodies can also create a perinuclear pattern that is mistaken for p-ANCA.

Symptoms that can go with it

Fever, night sweats, weight loss, fatigue and aching that have gone on for weeks
Persistent bloody or crusting nasal discharge, sinus pain, nosebleeds, hearing loss or a collapsed nasal bridge (GPA)
Coughing up blood, breathlessness or chest pain from lung involvement
Blood in the urine (sometimes visible, often only on a dipstick), foamy urine, swelling of the legs or a rising blood pressure from glomerulonephritis
A red, painful eye (scleritis), bulging eye or double vision
A purple, non-blanching rash on the lower legs, skin ulcers or black patches on the ears or cheeks (levamisole exposure)
Sudden numbness, burning pain or weakness in a foot or hand (mononeuritis multiplex)
New or worsening asthma with very high eosinophil counts and nerve or heart symptoms (EGPA)

Read it alongside

Urinalysis with microscopy — blood, protein and especially red cell casts in the urine indicate active glomerulonephritis and turn a positive ANCA into an emergency.
Creatinine and eGFR — kidney function can halve within weeks in ANCA vasculitis; the value at diagnosis is the strongest predictor of kidney survival.
Urine albumin-to-creatinine ratio or protein-to-creatinine ratio — quantifies glomerular leak and tracks response to treatment.
CRP and ESR — almost always high in active vasculitis; a positive ANCA with a normal CRP and normal urine is unlikely to be active disease.
CBC with differential — anemia from inflammation or lung bleeding, high platelets, high white cells, and eosinophils above 1,500 per microliter in EGPA.
Anti-GBM antibodies — ordered alongside ANCA in anyone with lung hemorrhage or rapidly worsening kidney function, because 20 to 30 percent are double positive.
ANA — a positive ANA can mimic p-ANCA on immunofluorescence and points toward lupus or drug-induced disease.
Complement C3 and C4 — usually normal in ANCA vasculitis; low levels suggest lupus, cryoglobulinemia or endocarditis instead.

What usually happens next

A positive PR3 or MPO result with any kidney, lung, nerve, eye or systemic symptoms leads to urgent referral to rheumatology or nephrology, same-day urine microscopy and creatinine, chest imaging and usually a kidney, nasal, lung or skin biopsy to confirm the diagnosis before or alongside starting treatment.
Blood cultures and an echocardiogram are often done first if there is fever or a murmur, because endocarditis can produce a true PR3-ANCA and must not be treated with immunosuppression.
An atypical ANCA (p-ANCA pattern, MPO and PR3 negative) with bowel or liver symptoms is redirected to a gastroenterology work-up rather than a vasculitis one.
If you take propylthiouracil, hydralazine, minocycline or use cocaine, say so: drug-induced ANCA vasculitis is managed first by stopping the exposure, and the antibodies fall over months afterward.
Once in remission, ANCA is usually rechecked every 3 to 6 months; a rise is a prompt for closer monitoring of urine and symptoms rather than for automatic treatment, since only a minority of rises are followed by relapse.

Diet, lifestyle and natural levers with evidence

What can move ANCA once the cause is known. Nothing here replaces finding the cause.

Nothing natural changes an ANCA result

Strong evidence

No diet, herb or supplement has been shown in human studies to lower MPO or PR3 antibody levels or to prevent or treat ANCA vasculitis, and the disease is life- and kidney-threatening, so immunosuppressive treatment (glucocorticoids with rituximab or cyclophosphamide, then maintenance therapy) is not optional. The levers below concern exposures that cause or trigger the antibodies and factors that affect relapse, not substitutes for treatment.

Stopping the drugs that induce ANCA

Strong evidence

Propylthiouracil induces ANCA in roughly 20 to 60 percent of long-term users (though only a few percent develop vasculitis), hydralazine and minocycline cause a smaller but well-documented share, and levamisole-adulterated cocaine is now a leading cause of dual MPO and PR3 positivity with skin necrosis. In each case, withdrawing the exposure is the first step: antibody titers fall over 6 to 12 months and mild disease often settles with that alone, while continued exposure drives relapse.

Never stop a prescribed thyroid or blood pressure drug on your own; the substitution must be arranged by your clinician.

Reducing silica dust and smoke exposure

Moderate evidence

Occupational exposure to crystalline silica (quarrying, sandblasting, construction, farming dusty soils) is associated with about 2.5 to 3 times the risk of developing ANCA vasculitis in a meta-analysis of case-control studies, and heavy exposure is linked to MPO-ANCA disease in particular. Smoking has been associated with a higher risk of ANCA vasculitis in a large case-control study. Respiratory protection at work and stopping smoking are reasonable measures for anyone with a positive ANCA, although neither has been tested as a way of changing the antibody.

Nasal Staphylococcus aureus carriage and infection prevention

Moderate evidence

In GPA, chronic nasal carriage of Staphylococcus aureus was associated with a several-fold higher relapse rate, and in a randomized trial of 81 patients in remission, 24 months of trimethoprim-sulfamethoxazole reduced relapses by about 60 percent compared with placebo. The drug is a prescription decision, but the lever it reveals is real: infections prime neutrophils and precede many relapses, so prompt treatment of sinus infections, vaccination against influenza and pneumococcus, and attention to nasal hygiene are standard advice.

When to see a clinician promptly

Emergency: coughing up blood or sudden breathlessness in anyone with a positive ANCA, which may be alveolar hemorrhage.
Emergency: a fall in urine output, new swelling of the legs or face, visibly bloody or cola-colored urine, or a creatinine that has risen on a repeat test, which may be rapidly progressive glomerulonephritis; kidney function can be lost within days to weeks.
A red, painful eye, bulging eye, double vision or sudden loss of vision, which can be scleritis, orbital disease or optic nerve involvement and threatens sight.
Sudden foot drop, wrist drop or burning numbness in a limb (mononeuritis multiplex), which signals nerve infarction and needs treatment within days to limit permanent damage.
Persistent bloody nasal crusting, nosebleeds, new hearing loss or sinus pain with fever, weight loss or a purpuric rash.
Any new fever, cough or infection symptoms while on immunosuppressive treatment, since infection is the leading cause of death in the first year of therapy.

Frequently asked questions

What is the normal range for an ANCA test?

Negative. On immunofluorescence that means no c-ANCA or p-ANCA staining at a 1:20 serum dilution (some labs use 1:10 or 1:40), and on the antigen-specific assays it means MPO and PR3 antibodies below the kit's cut-off, which varies from about 3.5 IU/mL to 20 units depending on the manufacturer. Many kits have an equivocal band just above the cut-off that is repeated rather than called positive. There is no 'low' ANCA of concern.

What does p-ANCA positive mean?

A perinuclear staining pattern was seen on immunofluorescence. On its own it is non-specific; what matters is the MPO result that accompanies it. p-ANCA with a positive MPO antibody points to microscopic polyangiitis, EGPA, renal-limited vasculitis or drug-induced vasculitis. p-ANCA with negative MPO and PR3 (atypical ANCA) is seen in ulcerative colitis, primary sclerosing cholangitis, autoimmune hepatitis, rheumatoid arthritis and lupus and does not indicate vasculitis. Your symptoms and a urinalysis decide which interpretation applies.

Does c-ANCA positive mean I have Wegener's granulomatosis?

Usually, if PR3 antibodies are also positive and you have compatible symptoms (sinus, nose, ear, lung or kidney disease). c-ANCA with PR3 is about 98 percent specific for granulomatosis with polyangiitis or microscopic polyangiitis in that setting. Without symptoms, or with a c-ANCA pattern but a negative PR3 assay, the result is much less reliable, and infective endocarditis and levamisole-contaminated cocaine can produce a true PR3-ANCA. A biopsy is usually obtained to confirm the diagnosis before long-term immunosuppression.

Why is my ANCA positive if I have ulcerative colitis?

Because 50 to 70 percent of people with ulcerative colitis make an atypical ANCA, an antibody against neutrophil proteins other than MPO and PR3 that gives a p-ANCA-like pattern on immunofluorescence. It is a marker of the bowel disease, is also seen in primary sclerosing cholangitis, and has nothing to do with vasculitis. If your MPO and PR3 assays are negative and your urine and kidney function are normal, no vasculitis work-up is needed.

Can ANCA be positive without vasculitis?

Yes. Besides inflammatory bowel and autoimmune liver disease, low-level or atypical ANCA occurs with endocarditis, tuberculosis, HIV, hepatitis C, rheumatoid arthritis, lupus and with drugs such as propylthiouracil, hydralazine, minocycline and levamisole-adulterated cocaine. A positive ANCA with no symptoms, a normal urinalysis and a normal CRP is not treated; it is explained by looking for these causes and repeated after a few months.

Can I have vasculitis with a negative ANCA?

Yes. About 10 to 20 percent of granulomatosis with polyangiitis (especially disease limited to the nose and sinuses), around 10 percent of microscopic polyangiitis and 60 percent or more of EGPA are ANCA negative, and many other vasculitides (giant cell arteritis, Takayasu, polyarteritis nodosa, IgA vasculitis, cryoglobulinemia) are not ANCA-associated at all. When the clinical picture is strong, a negative ANCA leads to biopsy and imaging rather than reassurance.

Should my ANCA level be used to monitor treatment?

Only loosely. ANCA levels usually fall with successful treatment and a rise can precede relapse, but a meta-analysis found that a rising or persistently positive ANCA during remission only modestly increased the chance of relapse, and many patients with a rising titer never flare. Guidelines therefore advise against changing treatment on the antibody alone; a rise is a signal to check urine, kidney function, CRP and symptoms more closely. PR3-ANCA positivity does carry a higher relapse risk than MPO over the long term.

How long does an ANCA test take and do I need to prepare?

No fasting or preparation is needed; it is a standard serum sample. Immunoassay results are often available within a few days and immunofluorescence within one to two weeks, depending on whether the lab sends it out. If vasculitis is suspected clinically, clinicians do not wait for the result before arranging urgent urine microscopy, kidney function tests and imaging, and in severe cases treatment is started on the clinical picture while the ANCA and biopsy are pending.

References

ANCA (antineutrophil cytoplasmic antibodies) test. MedlinePlus, US National Library of Medicine (2023)
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. Nature Reviews Rheumatology (2017)
Jennette JC, Falk RJ, Bacon PA, et al.. 2012 revised International Chapel Hill Consensus Conference nomenclature of vasculitides. Arthritis & Rheumatism (2013)
Kitching AR, Anders HJ, Basu N, et al.. ANCA-associated vasculitis. Nature Reviews Disease Primers (2020)
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 & Rheumatology (2021)
Tomasson G, Grayson PC, Mahr AD, LaValley M, Merkel PA. Value of ANCA measurements during remission to predict a relapse of ANCA-associated vasculitis — a meta-analysis. Rheumatology (Oxford) (2012)
Hagen EC, Daha MR, Hermans J, et al.. Diagnostic value of standardized assays for anti-neutrophil cytoplasmic antibodies in idiopathic systemic vasculitis. EC/BCR Project for ANCA Assay Standardization. Kidney International (1998)
Stegeman CA, Cohen Tervaert JW, de Jong PE, Kallenberg CG. Trimethoprim-sulfamethoxazole (co-trimoxazole) for the prevention of relapses of Wegener's granulomatosis. New England Journal of Medicine (1996)
Gómez-Puerta JA, Gedmintas L, Costenbader KH. The association between silica exposure and development of ANCA-associated vasculitis: systematic review and meta-analysis. Autoimmunity Reviews (2013)
Choi HK, Merkel PA, Walker AM, Niles JL. Drug-associated antineutrophil cytoplasmic antibody-positive vasculitis: prevalence among patients with high titers of antimyeloperoxidase antibodies. Arthritis & Rheumatism (2000)
McGrath MM, Isakova T, Rennke HG, Mottola AM, Laliberte KA, Niles JL. Contaminated cocaine and antineutrophil cytoplasmic antibody-associated disease. Clinical Journal of the American Society of Nephrology (2011)
Granulomatosis with polyangiitis (GPA). Merck Manual Professional Version (2024)

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