---
title: "Peripheral neuropathy in ANCA-associated vasculitis: clinical and electrodiagnostic context when a"
id: "frontiers-in-immunology-17-clinical-and-electrodiagnostic-features-of-nerve-conduction-study-classified"
canonical_url: "https://medichelpline.com/clinical-feed/frontiers-in-immunology-17-clinical-and-electrodiagnostic-features-of-nerve-conduction-study-classified"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "Frontiers in Immunology"
source_url: "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1807774"
published_at: "2026-07-30T00:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Peripheral neuropathy in ANCA-associated vasculitis: clinical and electrodiagnostic context when a
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/frontiers-in-immunology-17-clinical-and-electrodiagnostic-features-of-nerve-conduction-study-classified
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** Frontiers in Immunology
- **Source URL:** [Original Journal Publication](https://www.frontiersin.org/articles/10.3389/fimmu.2026.1807774)
- **Published At:** 2026-07-30T00:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The source article text was not present in the provided content; specific study methods, results, cohorts, and conclusions were not reported in the source material supplied. - The topic focuses on peripheral neuropathy in patients with **antineutrophil cytoplasmic antibody-associated vasculitis** (ANCA-associated vasculitis) and classification by **nerve conduction study** (NCS)/electrodiagnostic testing. - Peripheral neuropathy is a recognized manifestation of ANCA-associated vasculitis; electrodiagnostic studies such as NCS and electromyography help distinguish axonal versus demyelinating patterns and localize mononeuritis multiplex versus polyneuropathy. - Single-centre cohort studies on this topic typically describe clinical presentation, electrodiagnostic classification, temporal relationship to systemic disease activity, and associations with serologic or imaging findings; however, none of these specifics were available from the supplied source. - Important clinical features to evaluate include neuropathic pain, weakness, sensory loss distribution, progression (acute vs chronic), and presence of systemic vasculitis signs; electrophysiologic features commonly assessed include conduction velocity, amplitude, distal latency, and presence of conduction block. - Key implications of electrodiagnostic classification in clinical care are diagnostic confirmation, prognosis estimation, therapeutic decision-making, and baseline for monitoring treatment response; the supplied source did not report its findings on these outcomes. - The provided content lacked details on patient numbers, inclusion criteria, NCS protocols, diagnostic thresholds, statistical analyses, and reported limitations; these omissions prevent direct reporting of study results or evidence-based conclusions from this specific cohort.
## Clinical Analysis & Structured Key Points
Frontiers | Clinical and electrodiagnostic features of nerve conduction study-classified peripheral neuropathy in symptomatic patients with antineutrophil cytoplasmic antibody-associated vasculitis: a single-centre cohort study ORIGINAL RESEARCH article Front. Immunol. , 30 July 2026 Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1807774 Published in Frontiers in Immunology Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders 7 impact factor 11.3 citescore Editor & Reviewers Edited by Y S Yasuhiro Shimojima Reviewed by A M Andres Manuel De Leon S K Sebastian Klapa Outline Figures and Tables Figure 1 View in article Table 1 Baseline characteristics of AAV patients presenting clinical symptoms suggestive of VPN and having the results of NCS performed within 3 months after AAV diagnosis (N = 97). View in article Table 2 Data regarding vasculitic peripheral neuropathy and NCS findings. View in article Table 3 Comparison of baseline variables of AAV patients having the results of NCS performed within 3 months after AAV diagnosis according to VPN (N = 97). View in article Table 4 Concordance or discordance of findings between NCS and nerve biopsy. View in article Table 5 Comparison of baseline variables between patients with histological evidence of vasculitis and those without (N = 12). View in article ORIGINAL RESEARCH article Front. Immunol. , 30 July 2026 Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1807774 Clinical and electrodiagnostic features of nerve conduction study-classified peripheral neuropathy in symptomatic patients with antineutrophil cytoplasmic antibody-associated vasculitis: a single-centre cohort study J W Jang Woo Ha 1 † O C Oh Chan Kwon 2 † Y P Yong-Beom Park 3,4 S L Sang-Won Lee 3,4 * 1. Division of Rheumatology, Department of Internal Medicine, Yongin Severance Hospital, Yonsei University College of Medicine, Yongin, Gyeonggi-do, Republic of Korea 2. Division of Rheumatology, Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea 3. Division of Rheumatology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea 4. Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Republic of Korea See more Article metrics View details Abstract Background: This study investigated the clinical and electrodiagnostic features of vasculitic peripheral neuropathy (VPN) in symptomatic patients with antineutrophil cytoplasmic antibody-associated vasculitis (AAV) who underwent nerve conduction studies (NCS) within 3 months after AAV diagnosis. Methods: Among 323 patients with AAV, 97 presenting with clinical symptoms suggestive of VPN and with the availability of results of NCS performed within 3 months after AAV diagnosis were included in this study. VPN was classified based on the case definition and guidelines proposed by the Brighton Collaboration Vasculitic Peripheral Neuropathy Working Group in 2017. Of the 97 patients, 12 underwent nerve biopsy. Results: At AAV diagnosis, the median age of the 97 patients was 63.0 years (57% women), consisting of 48 patients with microscopic polyangiitis (MPA), 20 with granulomatosis with polyangiitis (GPA), and 29 with eosinophilic granulomatosis with polyangiitis (EGPA). Among symptomatic AAV patients who underwent early NCS, 55 patients (56.7%) were classified as having electrodiagnostically supported VPN. The most common type of VPN was a mixed type (83.6%), and the most frequently affected nerve was the peroneal nerve (70.9%). The concordance rate between NCS and nerve biopsy findings was 75% based on histological evidence of vasculitis. Conclusion: In this selected cohort of symptomatic AAV patients who underwent NCS within 3 months after diagnosis, more than half were classified as having electrodiagnostically supported VPN. NCS may provide adjunctive objective information for characterizing peripheral nerve involvement in clinically suspected VPN. 1 Introduction Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a group of small vessel vasculitis clinically characterised by a link between circulating ANCA in the peripheral blood and histologically fibrinoid necrotising vasculitis ( 1 , 2 ). The types of vessels affected by AAV vary from capillaries alongside adjacent arterioles and venules to medium-sized arteries ( 1 ). AAV is generally categorised into three subtypes according to its clinical features: microscopic polyangiitis (MPA), granulomatosis with polyangiitis (GPA), and eosinophilic granulomatosis with polyangiitis (EGPA) ( 3 – 6 ). Meanwhile, based on the type of ANCA, it may be divided into three subtypes: myeloperoxidase (MPO)-ANCA vasculitis, proteinase 3 (PR3)-ANCA vasculitis, and ANCA-negative vasculitis ( 7 ). Theoretically, AAV can involve and damage almost any organ, and the Birmingham vasculitis activity score version 3 (BVAS), five-factor score (FFS), and vasculitis damage index (VDI) forms were developed to assess AAV activity, prognosis, and extent of damage, and include nine items based on systemic manifestations according to each unique compartment ( 8 – 10 ). Among these various systemic manifestations of AAV, peripheral neuropathy (PN) caused by vasculitis (vasculitic peripheral neuropathy, VPN) has been reported in up to 50% of AAV patients ( 11 , 12 ). In real clinical practice, VPN is classified using objective clinical, electrodiagnostic, and/or histological evidence according to the Brighton Collaboration case definition, which was developed in the context of prior diagnostic frameworks, including the Peripheral Nerve Society guideline for vasculitic neuropathy ( 13 , 14 ). Nerve biopsy provides the most direct histological evidence of vasculitic involvement of peripheral nerves, but it is invasive and therefore cannot be routinely recommended for all AAV patients exhibiting clinical symptoms suggestive of VPN, such as multifocal or asymmetric pain, tingling sensation, numbness, and/or weakness in upper or lower extremities. Therefore, non-invasive nerve conduction studies (NCS) are performed more frequently and widely in real clinical practice ( 15 – 17 ). Clinical assessment, NCS, and appropriate imaging studies also help distinguish peripheral neuropathy from radiculopathy or other mimicking conditions. Nerve biopsy may be considered selectively when histological confirmation of vasculitic neuropathy is clinically necessary and feasible ( 18 , 19 ). Given that VPN is a severe life/organ-threatening cases of AAV that requires aggressive induction therapy with rituximab and/or cyclophosphamide ( 20 , 21 ), it should be classified earlier and more accurately in AAV patients. Furthermore, for the early classification of VPN, information on the frequency and clinical characteristics of VPN should be investigated and a consensus regarding the diagnostic methods for VPN classification should be established in AAV patients. However, data on early electrodiagnostic findings in symptomatic AAV patients with suspected VPN remain limited. Therefore, in the present study, we included AAV patients who presented with clinical symptoms suggestive of VPN and had NCS results available within 3 months after AAV diagnosis. We aimed to describe the proportion and clinical characteristics of electrodiagnostically supported VPN in this selected symptomatic cohort and to evaluate the potential adjunctive role of NCS in characterizing peripheral nerve involvement. 2 Methods 2.1 Patients We retrospectively reviewed the medical records of 323 patients enrolled in the Severance Hospital ANCA-associated Vasculitides cohort, a single-centre observational cohort of Korean patients with AAV. The inclusion criteria were as follows: 1) patients who were first classified as having AAV at this hospital and confirmed by rheumatologists; 2) patients who were classified based on the revised 2012 Chapel Hill Consensus Conference Nomenclature of Vasculitides ( 1 ); 3) patients who met the algorithm for AAV and polyarteritis nodosa proposed by the European Medicine Agency in 2007 (the EMA algorithm), and the classification criteria for MPA, GPA, and EGPA proposed by a joint group of the American College of Rheumatology and the European Alliance of Associations for Rheumatology in 2022 (the ACR/EULAR criteria) ( 2 – 6 ); 4) patients who had well-written medical records that included clinical, laboratory, radiological, and histological information for classifying AAV according to both the EMA algorithm and ACR/EULAR criteria ( 2 – 5 ); 5) patients who had available ANCA results for perinuclear (P)-ANCA/cytoplasmic (C)-ANCA as well as MPO-ANCA/PR3-ANCA within 3 months before and after AAV diagnosis ( 22 ); 6) patients who had been follow-up for 3 months or more after AAV diagnosis; 7) patients who had no serious medical conditions mimicking AAV, such as malignancies and significant infectious diseases requiring hospitalisation ( 3 – 5 ); 8) patients who had been exposed to immunosuppressive drugs for AAV treatment within 4 weeks before AAV diagnosis; and 9) patients who presented clinical symptoms suggestive of VPN and had the results of NCS performed within 3 months after AAV diagnosis ( 19 – 21 ). Of the 323 AAV patients, 204 were excluded from this study because they had no NCS results. Of the 119 AAV patients with available NCS results, 22 were excluded from this study because they underwent NCS after 3 months or more following AAV diagnosis. Finally, 97 patients presenting with clinical symptoms suggestive of VPN and with the results of NCS performed within 3 months after AAV diagnosis were included in this study ( Figure 1 ). This study was approved by the Institutional Review Board (IRB) of Severance Hospital (Seoul, Korea, IRB No. 4-2020-1071) and conducted according to the Declaration of Helsinki. Due to the retrospective design of the study and the use of anonymised patient data, the requirement for written informed consent was waived. Figure 1 Inclusion and exclusion of patients with AAV. AAV, antineutrophil cytoplasmic antibody-associated vasculitis; NCS, nerve conduction studies; VPN, vasculitic peripheral neuropathy. 2.2 Clinical data at AAV diagnosis We collected variables recorded at the time of AAV as follows: 1) demographic data including age, sex, body mass index, and smoking history; 2) AAV-specific data including AAV subtype, ANCA type, indices for assessing activity and prognosis, and systemic involvement pattern; 3) laboratory data including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); and 4) comorbidities affecting the results of NCS performed within 3 months after AAV diagnosis and poor outcomes during follow-up, such as type 2 diabetes mellitus, hypertension, and dyslipidaemia ( 23 , 24 ). In terms of BVAS, because BVAS has an item containing a subitem of VPN, in cases where NCS was performed 1−3 months after diagnosis, the scores assigned to an item of nervous systemic manifestation were also added to the total BVAS at diagnosis retroactively ( 8 ). Conversely, because FFS has no neurological components, its retroactive application was unnecessary ( 9 ). MPO-ANCA and PR3-ANCA were measured using immunoassays, whereas P-ANCA and C-ANCA were evaluated using indirect immunofluorescence assays. The results of both assay methods were accepted as ANCA results according to the 2022 ACR/EULAR criteria for AAV ( 3 – 5 ). 2.3 Clinical features suggestive of VPN In this study, the clinical symptoms suggestive of VPN included pain, tingling sensation, numbness, and/or weakness in the upper or lower extremities. VPN was classified by adopting the following criteria, where 1) AND 2) should be satisfied: 1) evidence of PN: i) electrodiagnostic evidence of an axonal neuropathy (on NCS) or ii) clinical neurologic examination findings of PN; AND 2) clinical presentation of PN: i) sensory and/or motor, plus ii) multifocal/asymmetric pattern without nerve root abnormalities, plus iii) either further clinical features including predominant symptoms in lower extremities, pain, and typical progress pattern, or biopsy findings ( 13 ). We categorised VPN into three groups according to the primary accompanying neurological types—sensory, motor, and mixed (sensory + motor)—and collected data regarding VPN types. Additionally, we reviewed the sites affected by VPN which were divided into seven main nerves: the median, ulnar, peroneal, posterior tibial, saphenous, sural, and plantar nerves. Because this was a retrospective study, NCS was performed as part of routine clinical practice rather than according to a prospectively standardized research protocol. NCS findings were reviewed from medical records. Clinical records were also reviewed to exclude evident alternative explanations for peripheral neuropathy, including nerve root compression, entrapment neuropathy, diabetic neuropathy, infection, malignancy, treatment-related neuropathy, or other mimicking conditions. The routine NCS protocol used at our institution has been described previously ( 25 ). 2.4 Histological description Like the clinical information regarding VPN on NCS, data on the histological findings of nerve tissues were retrospectively collected from medical records. A critical clue for deciding the concordance or discordance of findings between NCS and nerve biopsy was based on the presence or absence of the terms ‘histological evidence of vasculitis’ after ‘axonopathy’. 2.5 Clinical data during follow-up Medications administered to patients from the time of AAV diagnosis to the last visit were recorded. All-cause mortality (ACM), end-stage kidney disease (ESKD), cerebrovascular accident (CVA), and acute coronary syndrome (ACS) were investigated as poor AAV outcomes after diagnosis and during follow-up. For patients with each poor outcome, the follow-up duration based on each poor outcome was determined as the period from AAV diagnosis to each poor outcome occurrence. Meanwhile, for patients without each poor outcome, it was defined as the period from AAV diagnosis to the last visit. 2.6 Statistical analysis All statistical analyses were performed using SPSS version 26 (IBM Corporation, Armonk, NY, USA) for Windows (Microsoft Corporation, Redmond, WA, USA). Continuous and categorical variables were expressed as a median (25–75 percentile), and a number (percentage). Significant differences between the two categorical variables were analysed using the chi-square and Fisher’s exact tests, whereas the continuous variables using the Mann-Whitney U test. A hazard ratio (HR) for each poor AAV outcome was obtained using Cox proportional hazard analyses. To address the potential confounding effect of diabetes mellitus on peripheral neuropathy and NCS findings, clinical and electrodiagnostic features were additionally compared between patients with and without type 2 diabetes mellitus. Statistical significance was set as P <0.05. 3 Results 3.1 Baseline characteristics At the time of AAV diagnosis, patients were 63.0 (51.0─70.0) years old at median, and the percentage of men and women were 43% and 57%, respectively. Of the 97 patients, 48 patients were diagnosed with MPA, 20 patients with GPA, and 29 patients with EGPA. MPO-ANCA (or P-ANCA) and PR3-ANCA (or C-ANCA) were detected in 77 and 10 patients, respectively. The median BVAS and FFS were 12.0, and 1.0, respectively, and when investigated based on the items of BVAS, the most observed systemic manifestation was pulmonary (79.4%), followed by nervous systemic (67.0%), and renal (47.4%) manifestations. Among the laboratory results, the median ESR and CRP were 72.5 mm/h, and 16.2 mg/L, respectively. Other laboratory results and comorbidities are presented in Table 1 . Table 1 Variables AAV (N = 97) MPA (N = 48) GPA (N = 20) EGPA (N = 29) MPO-AAV (N = 75) PR3-AAV (N = 8) Demographic data Age (years) 63.0 (51.0─70.0) 67.5 (60.5–74.0) 58.0 (42.0–69.5) 52.0 (41.5–65.5) 66.0 (56.0–72.0) 52.5 (36.3–62.0) Male sex [N, (%)] 42 (43.3) 22 (45.8) 8 (40.0) 12 (41.4) 33 (44.0) 3 (37.5) Female sex [N, (%)] 55 (56.7) 26 (54.2) 12 (60.0) 17 (58.6) 42 (56.0) 5 (62.5) BMI (kg/m 2 ) 22.5 (20.2─24.2) 22.5 (20.8–23.7) 22.9 (20.4–25.7) 22.0 (19.4–25.3) 22.6 (20.8–24.1) 22.2 (20.1–25.4) Ex-smoker [N, (%)] 4 (4.1) 1 (2.1) 1 (5.0) 2 (6.9) 3 (4.0) 0 (0.0) AAV subtype [N, (%)] MPA 48 (49.5) 48 (100.0) 0 (0.0) 0 (0.0) 48 (64.0) 0 (0.0) GPA 20 (20.6) 0 (0.0) 20 (100.0) 0 (0.0) 11 (14.7) 7 (87.5) EGPA 29 (29.9) 0 (0.0) 0 (0.0) 29 (100.0) 16 (21.3) 1 (12.5) ANCA type and positivity [N, (%)] MPO-ANCA (or P-ANCA) positivity 77 (79.4) 48 (100.0) 13 (65.0) 16 (55.2) 75 (100.0) 0 (0.0) PR3-ANCA (or C-ANCA) positivity 10 (10.3) 0 (0.0) 9 (45.0) 1 (3.4) 0 (0.0) 8 (100.0) Both ANCA positivity 2 (2.1) 0 (0.0) 2 (10.0) 0 (0.0) 0 (0.0) 0 (0.0) ANCA negativity 12 (12.4) 0 (0.0) 0 (0.0) 12 (41.4) 0 (0.0) 0 (0.0) AAV-specific indices BVAS 12.0 (7.5─19.0) 15.0 (8.3–19.0) 9.5 (7.3–15.0) 11.0 (7.0–18.5) 14.0 (8.0–19.0) 10.5 (7.3–19.3) FFS 1.0 (0─2.0) 2.0 (1.0–2.0) 1.0 (0.0–2.0) 0.0 (0.0–1.0) 2.0 (1.0–2.0) 0.5 (0.0–1.0) Systemic manifestations based on BVAS General 43 (44.3) 27 (56.3) 7 (35.0) 9 (31.0) 36 (48.0) 3 (37.5) Cutaneous 14 (14.4) 6 (12.5) 1 (5.0) 7 (24.1) 10 (13.3) 1 (12.5) Mucous and ocular 6 (6.2) 2 (4.2) 2 (10.0) 2 (6.9) 3 (4.0) 2 (25.0) Otorhinolaryngological 44 (45.4) 10 (20.8) 10 (50.0) 24 (82.8) 26 (34.7) 6 (75.0) Pulmonological 77 (79.4) 37 (77.1) 14 (70.0) 26 (89.7) 61 (81.3) 6 (75.0) Cardiovascular 10 (10.3) 4 (8.3) 1 (5.0) 5 (17.2) 7 (9.3) 1 (12.5) Gastrointestinal 3 (3.1) 1 (2.1) 0 (0.0) 2 (6.9) 2 (2.7) 0 (0.0) Renal 46 (47.4) 35 (72.9) 8 (40.0) 3 (10.3) 43 (57.3) 2 (25.0) Nervous systemic 65 (67.0) 29 (60.4) 15 (75.0) 21 (72.4) 50 (66.7) 5 (62.5) Laboratory results White blood cell count (/mm 3 ) 10,080.0 (7,095.0─13,720.0) 10,265.0 (6,497.5–15,097.5) 9,705.0 (6,927.5–12,857.5) 9,540.0 (7,280.0–13,775.0) 10,080.0 (6,830.0–13,640.0) 10,875.0 (8,315.0–13,637.5) Haemoglobin (g/dL) 11.8 (9.9─13.3) 10.5 (9.0–12.3) 11.7 (9.8–12.5) 13.6 (12.4–14.6) 11.3 (9.5–12.8) 11.5 (9.5–13.1) Platelet count (× 1000/mm 3 ) 308.0 (232.0─396.5) 332.5 (236.0–392.0) 309.0 (230.8–431.3) 265.0 (211.0–405.0) 292.0 (228.5–383.0) 400.0 (284.0–454.3) Blood urea nitrogen (mg/dL) 16.3 (12.4─24.7) 19.4 (14.9–33.4) 15.4 (11.8–26.3) 14.3 (9.6–18.1) 17.3 (13.3–27.8) 14.6 (11.6–25.1) Serum creatinine (mg/dL) 0.7 (0.6─1.0) 0.8 (0.6–1.5) 0.7 (0.6–1.1) 0.7 (0.6–0.8) 0.7 (0.6–1.2) 0.7 (0.5–1.0) Serum total protein (g/dL) 6.8 (6.1─7.3) 6.8 (6.1–7.2) 6.7 (5.9–7.3) 6.8 (6.2–7.5) 6.8 (6.1–7.2) 6.5 (6.0–7.2) Serum albumin (g/dL) 3.7 (3.2─4.2) 3.3 (3.1–3.8) 3.8 (3.2–4.3) 3.8 (3.5–4.3) 3.6 (3.1–4.1) 3.7 (3.2–4.3) ESR (mm/hr) 72.5 (26.0─118.8) 96.0 (55.0–120.0) 66.0 (24.0–95.0) 32.0 (11.0–74.3) 77.0 (36.5–120.0) 60.5 (12.5–100.3) CRP (mg/L) 16.2 (1.9─76.5) 37.7 (3.5–117.6) 26.3 (1.0–65.3) 5.8 (0.9–18.0) 18.4 (1.9–79.2) 28.6 (6.6–79.1) Albuminuria [N, (%)] 25 (52.1) 4 (20.0) 6 (20.7) 30 (40.0) 2 (25.0) Haematuria [N, (%)] 18 (37.5) 4 (20.0) 6 (20.7) 24 (32.0) 3 (37.5) Comorbidities [N, (%)] Type 2 diabetes mellitus 16 (16.5) 11 (22.9) 5 (25.0) 0 (0.0) 15 (20.0) 1 (12.5) Hypertension 28 (28.9) 16 (33.3) 7 (35.0) 5 (17.2) 23 (30.7) 1 (12.5) Dyslipidaemia 11 (11.3) 6 (12.5) 4 (20.0) 1 (3.4) 10 (13.3) 1 (12.5) Baseline characteristics of AAV patients presenting clinical symptoms suggestive of VPN and having the results of NCS performed within 3 months after AAV diagnosis (N = 97). Values are expressed as a median (25–75 percentile) or N (%). AAV, ANCA-associated vasculitis; ANCA, antineutrophil cytoplasmic antibody; NCS, nerve conduction studies; BMI, body mass index; MPA, microscopic polyangiitis; GPA, granulomatosis with polyangiitis; EGPA, eosinophilic granulomatosis with poly
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