# The Association Between Serum Immunoglobulin G Titers Against Porphyromonas gingivalis and Chronic Kidney Disease in Patients With Rheumatoid Arthritis and Periodontitis: A Retrospective Cohort Study

**Authors:** Tetsuo Kobayashi, Satoshi Ito, Noriko Sugita, Akira Murasawa, Hajime Ishikawa, Koichi Tabeta

PMC · DOI: 10.1002/cre2.70271 · 2026-01-29

## TL;DR

This study found that higher levels of antibodies against a specific mouth bacteria are linked to chronic kidney disease in patients with rheumatoid arthritis and gum disease.

## Contribution

The study is the first to show a link between anti-Porphyromonas gingivalis IgG titers and chronic kidney disease in RA patients with periodontitis.

## Key findings

- Higher anti-Porphyromonas gingivalis IgG titers were significantly associated with lower eGFR in RA patients with periodontitis.
- CKD patients had significantly higher anti-Porphyromonas gingivalis IgG titers compared to non-CKD patients after adjusting for multiple factors.
- No significant association was found between anti-PPAD IgG titers and CKD.

## Abstract

Chronic kidney disease (CKD) is relatively common in patients with rheumatoid arthritis (RA). Periodontitis and periodontopathic Porphyromonas gingivalis are risk factors for CKD. However, the association of serum immunity to P. gingivalis and its peptidylarginine deiminase (PPAD), as well as periodontitis severity, with CKD in relation to RA has not been elucidated. The present study evaluated whether or not serum immunoglobulin G (IgG) titers against P. gingivalis and PPAD and periodontitis severity are associated with CKD in patients with RA and periodontitis.

Demographic, comorbidity, rheumatologic, and periodontal data were collected from 127 patients with RA and periodontitis in a retrospective cohort study. CKD was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 and/or proteinuria of ≥ 3 months’ duration. Serum IgG titers against P. gingivalis and PPAD were determined using an electrochemiluminescence immunoassay.

Twenty patients showed an eGFR < 60 mL/min/1.73 m2, while no patients had proteinuria. The 20 CKD patients were significantly older (p = 0.002), had higher percentages of former smokers (p = 0.01), had more sites with probing depth and clinical attachment level ≥ 4 mm (p = 0.03 and p = 0.02), and had higher levels of serum creatinine and eGFR (p < 0.001 for both) and anti‐P. gingivalis IgG titers (p = 0.04) than the 107 non‐CKD patients. A significant association was observed between anti‐P. gingivalis IgG titers and eGFR (p < 0.001 for both) by bivariate and multivariate analyses and between anti‐P. gingivalis IgG titers and CKD (p < 0.001) using a multiple logistic regression analysis after adjusting for age, gender, smoking status, comorbidity, RA condition, and RA‐related drugs.

These results suggest that serum IgG titers against P. gingivalis, but not against PPAD, are associated with CKD in patients with RA and periodontitis.

## Linked entities

- **Proteins:** IGG (Immunoglobulin G level)
- **Diseases:** chronic kidney disease (MONDO:0005300), rheumatoid arthritis (MONDO:0008383), periodontitis (MONDO:0005076)
- **Species:** Porphyromonas gingivalis (taxon 837)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL6R (interleukin 6 receptor) [NCBI Gene 3570] {aka CD126, HIES5, IL-1Ra, IL-6R, IL-6R-1, IL-6RA}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** myocardial infarction (MESH:D009203), CKD (MESH:D051436), transient ischemic attack (MESH:D002546), amyloidosis (MESH:D000686), Kidney Disease (MESH:D007674), CAL (MESH:D019962), dyslipidemia (MESH:D050171), Rheumatic (MESH:D012216), pneumonia (MESH:D011014), autoimmune inflammatory (MESH:D007249), DM (MESH:D003920), CVD (MESH:D002318), inflammatory periodontal disease (MESH:D010510), NETs (MESH:C536657), Proteinuria (MESH:D011507), RA (MESH:D001172), oral (MESH:D020820), PD (MESH:D007222), BOP (MESH:D006470), infection (MESH:D007239), Periodontitis (MESH:D010518), stroke (MESH:D020521), blood abnormalities (MESH:D006402), HT (MESH:D006973), bacterial infections (MESH:D001424), RF (MESH:D001171)
- **Chemicals:** methotrexate (MESH:D008727), IFX (MESH:D007069), bucillamine (MESH:C026535), Gd (MESH:D005682), infliximab (MESH:D000069285), triglyceride (MESH:D014280), tocilizumab (MESH:C502936), CZP (MESH:D000068582), tofacitinib (MESH:C479163), adalimumab (MESH:D000068879), iguratimod (MESH:C519076), sulfasalazine (MESH:D012460), golimumab (MESH:C529000), CCP (MESH:C487763), creatinine (MESH:D003404), TCZ (-), galactose (MESH:D005690), mizoribine (MESH:C010052), ABT (MESH:C002502), CPZ (MESH:D002746), tacrolimus (MESH:D016559), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606], Porphyromonas gingivalis (species) [taxon 837]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12853967/full.md

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Source: https://tomesphere.com/paper/PMC12853967