NT pro-BNP elevation in Kawasaki disease

What is it about?

Background: The aim of this study was to investigate the clinical significance and factors that affect N-terminal pro-brain natriuretic peptide (NT-proBNP) elevation in the acute phase of Kawasaki disease (KD) despite the absence of apparent cardiac complications. Methods: The laboratory and echocardiography results of 44 KD patients in the acute and subacute phases were reviewed. Results: With preserved cardiac function, median NT-proBNP was significantly elevated in the acute phase compared with the subacute phase (343 pg/mL, IQR, 162–1182 pg/mL vs 98 pg/mL, IQR, 61–205 pg/mL, respectively; P < 0.0001). The respective levels of tumor necrosis factor (TNF)-α, soluble TNF receptor (sTNFR)1, and sTNFR2 were also significantly elevated in the acute phase compared with the subacute phase: TNF-α, 3.3 pg/mL (IQR, 2.6–4.8 pg/mL) versus 2.4 pg/mL (IQR 1.9–4.0 pg/mL; P < 0.01), sTNFR1, 2741 pg/mL (IQR, 2080–3183 pg/mL) versus 976 pg/mL (IQR, 814–1247 pg/mL; P < 0.0001), sTNFR2, 5644 pg/mL (IQR, 4693–7520 pg/mL) versus 3169 pg/mL (IQR, 2132–3878 pg/mL; P < 0.0001). Log-transformed NT-proBNP was correlated with TNF-α (r = 0.29, P = 0.056), sTNFR1 (r = 0.60, P < 0.0001), and sTNFR2 (r = 0.65, P < 0.0001). TNF-α was correlated with sTNFR1 (r = 0.35, P = 0.02) and sTNFR2 (r = 0.51, P < 0.001). Conclusion: Tumor necrosis factor-α may cause NT-proBNP elevation in the acute phase of KD, and NT-proBNP level may be an indicator of TNF-α activity.

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Why is it important?

NT pro-BNP proBNP elevates in the acute phase of KD even when cardiac dysfunction is not proved by conventional echocardiogram, and NT-proBNP level significantly correlate with representative cytokines such as TNFR1 and TNFR2. These results suggest NT pro-BNP-pro can be a useful indicator for hypercytokinemia of Kawasaki disease.

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