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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
Published on: February 8, 2019
Long-term outcomes and clinicopathological characteristics of propylthiouracil-induced ANCA-associated
Di Wu1, Ruifeng Zhang1, Xinyue Wang1
1National Clinical Research Centre for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Objectives:
This retrospective study aims to determine the clinical and histological features and outcomes of propylthiouracil (PTU)-induced anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis with primary ANCA-associated glomerulonephritis (AAGN).
Methods:
Twenty-five patients diagnosed with PTU-induced AAGN and 379 patients with primary AAGN, who underwent diagnostic renal biopsies at Jinling Hospital between January 2005 and December 2020, were included in the study. The clinical and histological features and long-term renal outcomes were analysed.
Results:
Patients with PTU-induced AAGN exhibited lower serum creatinine levels and higher MPO-ANCA titres compared with those with primary AAGN. Histopathological analysis identified crescentic and focal lesions as the predominant patterns in the PTU-induced group, which also exhibited a higher proportion of normal glomeruli and a lower percentage of global sclerosis. Although treatment regimens were comparable between groups, PTU-induced AAGN was associated with numerically lower, though statistically non-significant, rates of renal non-remission and relapse. During prolonged follow-up, serum MPO-ANCA positivity persisted existence in most PTU-induced AAGN patients. Kaplan-Meier survival analysis revealed a significantly higher renal survival rate in PTU-induced AAGN patients than those with primary AAGN (p=0.018).
Conclusions:
Patients with PTU-induced AAGN demonstrated distinct clinical features and more favourable renal outcomes despite persistent positivity of MPO-ANCA, indicating a less aggressive disease course compared to primary AAGN.

