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Nonosmotic secretion of arginine vasopressin and salt loss in hyponatremia in Kawasaki disease
Author(s) -
Miura Kenichiro,
Harita Yutaka,
Takahashi Naoto,
Tsurumi Haruko,
Yasudo Hiroki,
Isojima Tsuyoshi,
Hirata Yoichiro,
Inuzuka Ryo,
Takizawa Keiichi,
Toyofuku Etsushi,
Nishimoto Hajime,
Takamizawa Masaru,
Ando Taro,
Sugawa Masahiro,
Yanagisawa Atsuhiro,
Inatomi Jun,
Nogimori Yoshitsugu,
Kinumaki Akiko,
Namai Yoshiyuki,
Hattori Motoshi,
Oka Akira
Publication year - 2020
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/ped.14036
Subject(s) - hyponatremia , medicine , vasopressin , hypovolemia , gastroenterology , endocrinology , hypervolemia , hypernatremia , blood volume , sodium , chemistry , organic chemistry
Background The precise mechanism of hyponatremia in Kawasaki disease (KD) remains elusive because assessment of volume status based on serial changes in body weight is lacking in previous reports. Methods Seventeen patients who were diagnosed with KD and hyponatremia (serum sodium levels <135 mmol/L) were analyzed. Volume status was assessed based on serial changes in body weight. Plasma arginine vasopressin (ADH), urine electrolytes, and serum cytokine levels were measured on diagnosis of hyponatremia. An increase in body weight by >3% was defined as hypervolemia and a decrease in body weight by >3% was defined as hypovolemia. Results The volume status was hypervolemic in three patients (18%), euvolemic in 14 (82%), and hypovolemic in none (0%). Five (29%) patients were diagnosed with “syndrome of inappropriate secretion of antidiuretic hormone” (SIADH) and no patients were diagnosed with hypotonic dehydration. The contribution of decreased total exchangeable cations (salt loss) to hyponatremia (5.9% [interquartile range, 4.3%, 6.7%]) was significantly larger than that of increased total body water (−0.7% [−1.8%, 3.1%]) ( P  = 0.004). Serum interleukin‐6 levels were elevated in all of the nine patients who were evaluated. Among the 12 (71%) patients who did not meet the criteria of SIADH and hypotonic dehydration, plasma ADH levels were inappropriately high in ten patients. These patients were also characterized by euvolemic or hypervolemic hyponatremia and salt loss, which might be compatible with a diagnosis of SIADH. Conclusions Our study shows that hyponatremia in KD is euvolemic or hypervolemic and is associated with nonosmotic secretion of ADH and salt loss in the majority of patients.

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