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Significance of hyponatremia in Kawasaki disease

Kawasaki disease (KD) was first described by Japanese pediatrician Tomisaku Kawasaki in 1967. Since then, KD has been reported in all racial and ethnic groups, mostly in children; in most series, 85% of patients were younger than 5 years. Annual incidence per 100 000 children aged under 5 ranges from four in South America to 134 in Japan. In 1982, Laxer et al. reported, for the first time, that hyponatremia was frequently associated with KD. Since then, there have been reports that have examined the relationship between KD and hyponatremia, mainly in Japan. It is known that hyponatremia is observed in as many as 40–50% of patients in the acute stage of KD. About 4.4–15% of patients of KD have a serum sodium concentration lower than 130 mEq/L. In general, KD patients with hyponatremia have more severe conditions than those without hyponatremia. In particular, regarding the complication rate of coronary artery lesions, the odds ratio is as high as 4.78 in patients with KD who have hyponatremia as compared with those without. Watanabe et al. compared 51 patients with hyponatremia and 63 patients with orthonatremia. The results showed that there was no difference in the number of patients with age, gender, and diarrhea, but the number of patients with dehydration, fever, and coronary artery lesions was significantly higher in the hyponatremia group. The etiology of hyponatremia in Kawasaki disease is not yet clear. Hypotonic dehydration, antidiuretic hormone (ADH) inappropriate secretion syndrome, renal sodium loss due to impaired sodium reabsorption of renal tubules, and natriuresis due to brain natriuretic peptides (BNP) have been proposed as causes. Severe hyponatremia can lead to convulsion and death, so appropriate care is needed. In this issue of the Journal, Miura et al. showed that, in most Kawasaki disease patients, hypotonic dehydration was unlikely to be a cause of hyponatremia. And they report that hyponatremia in KD is euvolemic or hypervolemic and is associated with nonosmotic secretion of ADH and salt loss in the majority of patients. From their reports, it is considered that large amounts of fluid replacement are not necessary for correction of hyponatremia in KD. If hyponatremia is found in patients with Kawasaki disease, the urinary sodium and other electrolytes, osmotic pressure, and body fluid volume should be evaluated according to the basic hyponatremia diagnostic approach, and a correction method should be considered. However, caution is required because it has been reported that brain natriuretic peptide, which is a biomarker for evaluating fluid volume, is elevated in Kawasaki disease regardless of fluid volume. It should be noted that the sodium content of intravenous immunoglobulin (IVIG) that can be used for Kawasaki disease in Japan can range from trace to 154 mEq/ L. Kaneko et al. report that when children with hyponatremia caused by Kawasaki disease receive an IVIG containing little sodium, the improvement is delayed even if the hyponatremia does not worsen. Hyponatremia can cause brain edema and other factors, so patients with Kawasaki disease complicated by hyponatremia should consider using IVIG containing high concentration (154 mEq/L) of sodium.