Olink

Olink®
Part of Thermo Fisher Scientific

Multiple circulating inflammatory proteins are associated with pathological lesions and kidney function decline in IgA nephropathy

Inflammation Research, 2025

Kobayashi H., Murata Y., Akiya Y., Matsuoka T., Otsuka H., Tsunemi A., Nakamura Y., Azuma M., Abe M.

Disease areaApplication areaSample typeProducts
Immunological & Inflammatory Diseases
Nephrology
Patient Stratification
Serum
Olink Focus

Olink Focus

Abstract

Introduction
The clinical relevance of circulating inflammatory proteins in Immunoglobulin A nephropathy (IgAN) remains incompletely defined. We examined whether serum inflammatory proteins—particularly tumor necrosis factor (TNF) receptor–related markers—track with disease severity and progression in IgAN.

Methods
We enrolled Japanese subjects undergoing native kidney biopsy with newly diagnosed IgAN (n = 134); disease controls with membranous nephropathy (n = 24), minimal change disease (n = 45), or lupus nephritis (n = 23); and healthy controls (n = 88). We measured 10 serum inflammatory proteins before renal biopsy and evaluated their levels in different glomerulonephritis. Additionally, we assessed associations between these proteins and clinical outcomes, including kidney function and histological changes in IgAN.

Results
Inflammatory proteins, especially TNF-R1, TNF-R2, TNF-R3, TNF-R7, and TNF-R27, were elevated in patients with IgAN and were associated with the severity of tubulointerstitial lesions. Among disease controls, membranous nephropathy and lupus nephritis also showed elevated TNF-receptor–related proteins, whereas minimal change disease did not. TNF-R7 showed a significant early increase, suggesting possible involvement in IgAN pathogenesis. Multivariable analysis indicated these proteins could predict kidney function decline.

Conclusions
Specific circulating inflammatory proteins, particularly in the TNF receptor pathway, reflect disease activity and structural injury in IgAN and may help identify patients at higher risk of progression.

Read publication ↗