Association between urinary sodium and potassium excretion and blood pressure and inflammation in patients with rheumatoid arthritis

Hypertension is highly prevalent in patients with rheumatoid arthritis (RA). In other populations, high sodium (Na⁺) and low potassium (K⁺) intake are associated with an increased risk of hypertension, and in animal models, a high salt intake exacerbated arthritis. Patients with RA have many comorbidities associated with salt sensitivity, but their salt intake and its relationship to blood pressure and inflammation is unknown. Using the Kawasaki formula, Na⁺ and K⁺ urinary excretion (reflecting intake) was estimated in 166 patients with RA and 92 controls, frequency matched for age, sex, and race. Inflammatory markers and disease activity were measured in RA patients. We tested the associations between blood pressure and Na⁺ and K⁺ excretion. Estimated 24-h Na⁺ excretion was similarly high in both RA (median [IQR] 5.1 g, [3.9–6.6 g]) and controls (4.9 g, [4.0–6.5 g]), p = 0.9, despite higher rates of hypertension in RA (54 vs. 39%, p = 0.03). The Na⁺:K⁺ excretion ratio was significantly higher in RA (2.0 [1.6–2.4]) vs. 1.7 [1.5–2.1]), p = 0.02] compared to controls. In RA, a lower K⁺ excretion was inversely correlated with diastolic blood pressure (adjusted β = − 1.79, p = 0.04). There was no significant association between Na⁺ or K⁺ excretion and inflammatory markers. Despite a similar Na⁺ excretion, patients with RA had higher rates of hypertension than controls, a finding compatible with increased salt sensitivity. Patients with RA had a lower Na⁺:K⁺ excretion ratio than controls, and lower K⁺ excretion was associated with higher diastolic blood pressure in RA.