Hyponatremia in Kawasaki disease: What does it mean and how does it occur?

Abstract

Kawasaki disease (KD) is an acute febrile vasculitis that predominantly affects children ≤ 5 years of age. The cause of KD remains unknown, but it is thought that the immune system is activated by an infectious trigger in a genetically susceptible host. Because KD is systemic vasculitis, multiple organ involvement can develop, including hyponatremia. Hyponatremia is common in patients with KD, occurring in 29%–70% of patients. Although hyponatremia is usually mild and asymptomatic in nearly all patients with KD, profound hyponatremia contributes to the development of central nervous system dysfunction in some patients. KD patients with hyponatremia have clinical and laboratory findings that are consistent with severe inflammation, including higher C-reactive protein levels and an increased incidence of coronary artery lesions. While the pathogenesis underlying the development of hyponatremia in KD is incompletely understood, several possible mechanisms have been proposed, including hypovolemic hyponatremia, the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and ingestion of fluid that is hypo-osmolar relative to the fluid loss. Hypovolemic hyponatremia may be caused by gastrointestinal loss of fluid and sodium, and renal loss of fluid and sodium secondary to renal parenchymal injury and/or cytokine-induced renal tubular dysfunction. SIADH occurs in approximately 40% of KD patients with hyponatremia and may be a major cause of hyponatremia in KD. Although the pathogenesis underlying the development of SIADH in patients with KD is unclear, cerebral vasculitis or ADH secretion stimulated by cytokines, including interleukin (IL)-1β and IL-6, may contribute to the development of SIADH in patients with KD.