Affiliations: Department of Pediatrics, Niigata City General Hospital, Niigata City, Japan
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.
Keywords: Kawasaki disease, hypovolemic hyponatremia, renal salt wasting, syndrome of inappropriate secretion of antidiuretic hormone, cytokine, pathogenesis