Hyponatremia and Syndrome of Inappropriate Antidiuretic Hormone Secretion in Kawasaki Disease

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.