# From Pulmonary Tuberculosis to Antineutrophil Cytoplasmic Antibody (ANCA) Seroconversion: A Case of Rapidly Progressive Glomerulonephritis

**Authors:** Omar A AlShammari, Ibrahim Abuqurayn, Iffat kiran, Abdullah Almansour, Mohammad Almarzoqi, Bander Alazmi, Shifa Bilal Delvi, Abdulrahim Comert, Nada Abotouk, Raghad Bokhari, Basim A Amatouq, Abdulrahman A Almane

PMC · DOI: 10.7759/cureus.103961 · Cureus · 2026-02-20

## TL;DR

A patient with tuberculosis developed a rare kidney disease linked to ANCA antibodies months after starting treatment.

## Contribution

This case highlights the rare occurrence of delayed ANCA seroconversion and kidney disease during anti-tuberculosis therapy.

## Key findings

- A 49-year-old man with tuberculosis developed ANCA-associated glomerulonephritis months after starting treatment.
- Renal biopsy confirmed pauci-immune crescentic glomerulonephritis despite initial negative autoimmune serology.
- Immunosuppressive therapy was initiated alongside continued anti-tuberculosis treatment, but dialysis was still required.

## Abstract

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a small-vessel inflammatory disorder that can lead to rapidly progressive glomerulonephritis. Although tuberculosis has been linked to ANCA positivity, the development of biopsy-confirmed immune-mediated kidney disease during anti-tuberculosis therapy is rare. Herein, we describe a rare presentation of delayed ANCA seroconversion associated with rapidly progressive glomerulonephritis in a patient undergoing pulmonary tuberculosis treatment. We report the clinical course, laboratory findings, histopathology, and management of the case. A 49-year-old man with pulmonary tuberculosis initially presented with mild renal impairment and negative autoimmune serology and was treated with standard anti-tuberculosis therapy. Several months later, he developed recurrent hemoptysis accompanied by rapidly worsening kidney function and active urinary sediment. Repeat serological evaluation demonstrated a new cytoplasmic staining pattern on indirect immunofluorescence for antineutrophil cytoplasmic antibodies, consistent with proteinase 3 antibody positivity on antigen-specific immunoassay. Renal biopsy revealed pauci-immune crescentic glomerulonephritis, confirming ANCA-associated rapidly progressive glomerulonephritis. Following a multidisciplinary discussion, immunosuppressive therapy was initiated, and anti-tuberculosis treatment was continued. Despite the therapy, the patient remained dialysis dependent. In summary, delayed ANCA seroconversion may occur during anti-tuberculosis therapy and may be associated with severe immune-mediated renal disease. Kidney biopsy is essential when unexplained kidney deterioration develops during treatment. In selected patients with severe organ involvement, immunosuppressive therapy may be required despite active infection, following careful multidisciplinary evaluation.

## Linked entities

- **Diseases:** pulmonary tuberculosis (MONDO:0006052), rapidly progressive glomerulonephritis (MONDO:0017236)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, PRTN3 (proteinase 3) [NCBI Gene 5657] {aka ACPA, AGP7, C-ANCA, CANCA, MBN, MBT}, MPO (myeloperoxidase) [NCBI Gene 4353], IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}
- **Diseases:** hematuria (MESH:D006417), asthmatic (MESH:D013224), hyperkalemia (MESH:D006947), pulmonary involvement (MESH:C566343), inflammation (MESH:D007249), vasculitis (MESH:D014657), GBM (MESH:D019867), eosinophilia (MESH:D004802), renal pathologies (MESH:D002114), ANA (MESH:D056648), oliguria (MESH:D009846), dyspnea (MESH:D004417), kidney failure (MESH:D051437), hemoptysis (MESH:D006469), acute kidney injury (MESH:D058186), anti (MESH:D006679), fatigue (MESH:D005221), pulmonary hemorrhage (MESH:D006470), autoimmune (MESH:D001327), acute pyelonephritis (MESH:D011704), proteinuria (MESH:D011507), fever (MESH:D005334), fibrinoid necrosis (MESH:D038261), small-vessel inflammatory disorder (MESH:D059345), EGPA (MESH:D014890), MPA (MESH:D055953), acute tubular injury (MESH:D001930), Glomerulonephritis (MESH:D005921), metabolic acidosis (MESH:D000138), renal involvement (MESH:C565423), weight loss (MESH:D015431), cough (MESH:D003371), MPGN (MESH:D015432), ESRD (MESH:D007676), infection (MESH:D007239), Pulmonary Tuberculosis (MESH:D014397), RPGN (MESH:C538458), loss of appetite (MESH:D001068), Tuberculosis (MESH:D014376), granuloma (MESH:D006099), abnormal renal function (MESH:D007674), bacterial infection (MESH:D001424), Infectious (MESH:D003141), necrosis (MESH:D009336), TB (MESH:D014390)
- **Chemicals:** isoniazid (MESH:D007538), allopurinol (MESH:D000493), pyrazinamide (MESH:D011718), aminoguanidine (MESH:C004479), propylthiouracil (MESH:D011441), methylprednisolone (MESH:D008775), sofosbuvir (MESH:D000069474), methimazole (MESH:D008713), penicillamine (MESH:D010396), haematoxylin (MESH:D006416), sulfasalazine (MESH:D012460), RIPE (-), rifampicin (MESH:D012293), rituximab (MESH:D000069283), hydralazine (MESH:D006830), ethambutol (MESH:D004977), minocycline (MESH:D008911), oxygen radicals (MESH:D017382), creatinine (MESH:D003404)
- **Species:** hepatitis C virus [taxon 11103], Homo sapiens (human, species) [taxon 9606], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Staphylococcus aureus (species) [taxon 1280], human gammaherpesvirus 4 (Epstein Barr virus, no rank) [taxon 10376], Protoparvovirus (genus) [taxon 1506574], Cytomegalovirus (genus) [taxon 10358]

## Full text

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## Figures

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## References

15 references — full list in the complete paper: https://tomesphere.com/paper/PMC12922458/full.md

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Source: https://tomesphere.com/paper/PMC12922458