Korean Circ J.  2010 Oct;40(10):507-513. 10.4070/kcj.2010.40.10.507.

Hyponatremia and Syndrome of Inappropriate Antidiuretic Hormone Secretion in Kawasaki Disease

Affiliations
  • 1Department of Pediatrics, Ewha Womans University School of Medicine, Seoul, Korea. sohn@ewha.ac.kr

Abstract

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-1beta 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-1beta 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-1beta levels.
CONCLUSION
Hyponatremia occurs in KD patients with severe inflammation, while increased IL-6 and IL-1beta may activate ADH secretion, leading to SIADH and hyponatremia in KD.

Keyword

Hyponatremia; Inappropriate antidiuretic hormone syndrome; Kawasaki disease; Interleukins

MeSH Terms

C-Reactive Protein
Humans
Hyponatremia
Inappropriate ADH Syndrome
Incidence
Inflammation
Interleukin-6
Interleukins
Mucocutaneous Lymph Node Syndrome
Natriuretic Peptide, Brain
Neutrophils
Peptide Fragments
Plasma
Prospective Studies
Sodium
Triiodothyronine
C-Reactive Protein
Interleukin-6
Interleukins
Natriuretic Peptide, Brain
Peptide Fragments
Sodium
Triiodothyronine

Figure

  • Fig. 1 Changes in serum sodium (Na) level in 13 Kawasaki disease patients with hyponatremia (serum Na <135 mEq/L) before and after intravenous immunoglobulin (IVIG) infusion.

  • Fig. 2 Correlations between serum sodium (Na) and (A) C-reactive protein (CRP), (B) N-terminal pro-brain natriuretic peptide (NT-proBNP), and (C) triiodothyronine (T3) in 50 patients with acute Kawasaki disease.

  • Fig. 3 Comparison in serum levels of interleukin (IL)-6 and IL-1β between (A) Kawasaki disease (KD) patients and the control group (Control), (B) KD patients with (HypoNa) and without (Non-hypoNa) hyponatremia, and (C) hyponatremic KD patients with (SIADH) and without (Non-SIADH). SIADH: syndrome of inappropriate antidiuretic hormone secretion.

  • Fig. 4 Correlation of antidiuretic hormone (ADH) with serum levels of (A) interleukin (IL)-6 and (B) IL-1β in 7 Kawasaki disease patients with hyponatremia.


Cited by  1 articles

Kawasaki Disease with Acute Respiratory Distress Syndrome after Intravenous Immunoglobulin Infusion
Yu Hyeon Choi, Bong Jin Lee, June Dong Park, Seung Hyo Kim
Korean J Crit Care Med. 2014;29(4):336-340.    doi: 10.4266/kjccm.2014.29.4.336.


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