Abstract
BACKGROUND AND OBJECTIVES: The pathogenesis of hyponatremia (serum sodium <135 mEq/L) in Kawasaki disease (KD) remains unclear. We investigated the clinical significance of hyponatremia, and the role of interleukin (IL)-6 and IL-1β in the development of hyponatremia and syndrome of inappropriate antidiuretic hormone secretion (SIADH) in KD. SUBJECTS AND METHODS: Fifty KD patients were prospectively enrolled and analyzed for clinical and laboratory variables according to the presence of hyponatremia or SIADH. RESULTS: Thirteen KD patients (26%) had hyponatremia and 6 of these had SIADH. In patients with hyponatremia, the percentage of neutrophils (% neutrophils), C-reactive protein (CRP), and N-terminal pro-brain natriuretic peptide (NT-proBNP) were higher than in those without hyponatremia, while serum triiodothyronine (T3) and albumin were lower. Patients with hyponatremia had a higher incidence of intravenous immunoglobulin-resistance but this was not statistically significant. No differences existed between patients with and without SIADH with regard to clinical or laboratory variables and the incidence of IVIG-resistance. Serum sodium inversely correlated with % neutrophils, CRP, and NT-proBNP, and positively correlated with T3 and albumin. Serum IL-6 and IL-1β levels increased in KD patients and were higher in patients with hyponatremia. Plasma antidiuretic hormone increased in patients with SIADH, which tended to positively correlate with IL-6 and IL-1β levels. CONCLUSION: Hyponatremia occurs in KD patients with severe inflammation, while increased IL-6 and IL-1β may activate ADH secretion, leading to SIADH and hyponatremia in KD.