Urinary potassium is a potential biomarker of disease activity in Ulcerative colitis and displays in vitro immunotolerant role

We evaluated the in-vitro effect of potassium on CD4(+) T cells and the role of urinary potassium as a potential biomarker of disease activity in patients with ulcerative colitis (UC). This prospective observational cohort study included healthy controls (n = 18) and UC patients [n = 30, median age: 40 (IQR: 28–46) years, 17 males)] with active disease(assessed by Mayo score) from September 2015–May 2016. Twenty-four hours urinary potassium along with fecal calprotectin (FCP) were estimated in UC patients (at baseline and follow-up after 3–6 months) and controls. In healthy volunteers, we also assessed the effect of potassium on CD4(+) T cells differentiated in the presence of Th17 polarizing condition. UC patients had significantly higher FCP (368.2 ± 443.04 vs 12.44 ± 27.51, p < 0.001) and significantly lower urinary potassium (26.6 ± 16.9 vs 46.89 ± 35.91, p = 0.01) levels than controls. At follow-up, a significant increase in urinary potassium among patients who had clinical response [n = 22, 21.4 (14.4–39.7) to 36.5 (20.5–61.6), p = 0.04] and remission [n = 12, 18.7 (9.1–34.3) to 36.5 (23.4–70.5), p = 0.05] was accompanied with a parallel decline in FCP. On in-vitro analysis, potassium under Th17 polarizing conditions significantly inhibited IL-17 and interferon-[Formula: see text] expression while favoring the induction of FoxP3(+) T cells. Therefore, urinary potassium levels are inversely associated with disease activity in UC with in-vitro data supporting an immune-tolerant role of potassium.