We treated a patient with long-term hemodialysis who presented with polyarthritis, elevated CRP, and systemic inflammatory symptoms such as fever, in the context of dialysis-related amyloid deposition characteristic of the shoulder and femoral head. Although arthritis associated with dialysis-related amyloidosis is rarely reported, Ohashi et al. found inflammatory cell infiltrates, primarily CD68-positive macrophages, surrounding DRA deposits, with excessive TNF-α and IL-1β observed histologically within these macrophages [1]. They observed the tissue lesions in detail and inferred the following mechanism. When an amyloid region is formed, inflammatory cells, mainly macrophages, are mobilized as a foreign body response. These cells secrete inflammatory cytokines such as TNF-α and IL-1β, which not only damage intervertebral discs and cartilage in the vicinity of amyloid deposition, but also cause bone destruction through osteoclastic activity of macrophages, resulting in joint and bone lesions [1]. These mechanisms of joint and bone destruction are similar to those in RA. However, the factors that induce cytokine hypersecretion in RA joints are not fully understood.

While MRI has been increasingly used to detect DRA, Cheon et al. demonstrated that PET-CT can also be valuable, identifying hypermetabolic activity and osteolysis in the shoulder, wrist, and lumbar region in a hemodialysis patient with DRA, suggesting its utility in diagnosing DRA-related arthritis [9]. Given the established role of PET-CT in identifying inflammatory sites in RA, it may serve as a comparable indicator of arthritis activity in both DRA and RA [10,11,12]. In our case, PET-CT and histology confirmed both inflammation at the site of DRA and macrophage infiltration, highlighting the clinical and histological similarities between DRA-associated arthritis and RA with systemic inflammation.

Symptoms consistent with DRA-associated arthritis improved following tocilizumab administration. Regarding the mechanism of inflammation in amyloidosis, pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α are associated with the formation of amyloid plaques, and these cytokines are proposed to trigger inflammatory responses and promote tissue damage [11]. In our case, IL-6 and TNF-α were elevated as previous reports describe [13, 14]. Recent studies have demonstrated an upregulation of gene expression and activation of transcription factors within the IL-6/STAT3 pathway in anti-citrullinated peptide antibody (ACPA)-negative RA patients, in contrast to those who are ACPA-positive [12, 15, 16]. Therefore, tocilizumab, an anti-IL-6 receptor antibody, may be a beneficial option for managing inflammation in dialysis-related amyloidosis. To our knowledge, this is the first report of tocilizumab for DRA-associated arthritis. Given tocilizumab’s documented efficacy in seronegative RA complicated by AA amyloidosis, reducing serum amyloid A and improving clinical symptoms [17,18,19], and its successful use in familial Mediterranean fever-associated amyloidosis, we propose that tocilizumab may also be effective for arthritis associated with DRA and systemic inflammation [17, 20].

This case presentation has a notable limitation: we were unable to provide objective imaging evidence—such as follow-up musculoskeletal ultrasound or PET-CT—to confirm the resolution of synovitis after treatment. This is because tocilizumab therapy was continued at a different institution following the patient’s discharge and post-treatment imaging studies were not obtained. However, the patient was followed clinically and physical examinations were consistently documented. In this case, disease activity was assessed using CDAI, which is considered appropriate for evaluating inflammatory disease activity during IL-6 inhibitor therapy. A consensus statement on IL-6 receptor inhibition recommends the use of composite indices that exclude acute-phase reactants—such as the CDAI—for assessing disease activity in both rheumatoid arthritis and other inflammatory conditions [7]. Notably, the patient’s CDAI improved from 28 to 0 and transfusion-dependent anemia related to chronic inflammation resolved. Although the absence of imaging precludes definitive confirmation of arthritis remission, the improvement in symptoms suggests that tocilizumab may have been effective in alleviating clinical manifestations of arthritis.

In summary, we speculate that dialysis-related amyloidosis can present with arthritis involving cytokines, similar to RA, and tocilizumab may be effective for the resulting synovitis.