Objective: The erythropoietin receptor (EpoR) stimulates erythro- cyte proliferation after erythropoietin binding. EpoR belongs to the cytokine receptor superfamily and is also found on macrophages and endothelial cells, which play a role in systemic autoimmune diseases. As no data exist on EpoR in rheumatic disease, we studied soluble EpoR (sEpoR) in patients with Systemic Lupus Erythematosus (SLE) across clinical characteristics including anaemia, immunological biomarkers, disease activity and severity in SLE patients. Method: In a cross‐sectional study, we recorded clinical character- istics, medications, disease activity (SLEDAI‐2K) and organ damage (SDI) in 101 SLE patients. sEpoR, autoantibodies and cytokines were measured by ELISA while a Rheumatoid Arthritis (RA) cohort (n = 59) and healthy controls (HC) (n = 70) served as comparators. Data were analysed with nonparametric techniques. Result: There was no significant difference in sEpoR levels across the SLE, RA and HC groups. In both cohorts, sEpoR levels were simi- lar in anaemic (6% of SLE and 31% of RA) and non‐anaemic patients. sEpoR levels were unrelated to haemoglobin levels, SLEDAI‐2K or SDI scores, but in both cohorts correlated with acute phase reac- tants (CRP, Rs. 0.28, P = 0.007) and proinflammatory cytokines, par- ticularly IL‐6 and MIP‐1 (P < 0.001). Conclusion: sEpoR does not interfere with erythropoiesis, nor play a role in the pathogenesis of ACD in SLE or RA. Our data indicate that increased production of IL‐6 and MIP‐1 can stimulate alternative splicing of EpoR to sEpoR.