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Mack, S.* ; Coassin, S.* ; Vaucher, J.* ; Kronenberg, F.* ; Lamina, C.* ; Rueedi, R.* ; Yousri, N.A.* ; Seppälä, I.* ; ApoA-IV-GWAS Constortium (Gieger, C.) ; Schönherr, S.* ; Forer, L.* ; Erhart, G.* ; Kollerits, B.* ; Marques-Vidal, P.* ; ApoA-IV-GWAS Constortium (Müller-Nurasyid, M.) ; Waeber, G.* ; Bergmann, S.* ; Dähnhardt, D.* ; Stöckl, A.* ; Kiechl, S.* ; Raitakari, O.T.* ; Kähönen, M.* ; Willeit, J.* ; Kedenko, L.* ; Paulweber, B.* ; ApoA-IV-GWAS Constortium (Peters, A.) ; ApoA-IV-GWAS Constortium (Meitinger, T.) ; ApoA-IV-GWAS Constortium (Strauch, K.) ; Lehtimäki, T.* ; Hunt, S.C.* ; Vollenweider, P.*

Evaluating the causal relation of ApoA-IV with disease-related traits - A bidirectional two-sample mendelian randomization study.

Sci. Rep. 7:8734 (2017)

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Apolipoprotein A-IV (apoA-IV) has been observed to be associated with lipids, kidney function, adiposity- and diabetes-related parameters. To assess the causal relationship of apoA-IV with these phenotypes, we conducted bidirectional Mendelian randomization (MR) analyses using publicly available summary-level datasets from GWAS consortia on apoA-IV concentrations (n = 13,813), kidney function (estimated glomerular filtration rate (eGFR), n = 133,413), lipid traits (HDL cholesterol, LDL cholesterol, triglycerides, n = 188,577), adiposity-related traits (body-mass-index (n = 322,206), waist-hip-ratio (n = 210,088)) and fasting glucose (n = 133,010). Main analyses consisted in inverse-variance weighted and multivariable MR, whereas MR-Egger regression and weighted median estimation were used as sensitivity analyses. We found that eGFR is likely to be causal on apoA-IV concentrations (53 SNPs; causal effect estimate per 1-SD increase in eGFR = -0.39; 95% CI = [-0.54, -0.24]; p-value = 2.4e-07). Triglyceride concentrations were also causally associated with apoA-IV concentrations (40 SNPs; causal effect estimate per 1-SD increase in triglycerides = -0.06; 95% CI = [-0.08, -0.04] ; p-value = 4.8e-07), independently of HDL-C and LDL-C concentrations (causal effect estimate from multivariable MR = -0.06; 95% CI = [-0.10, -0.02]; p-value = 0.0014). Evaluating the inverse direction of causality revealed a possible causal association of apoA-IV on HDL-cholesterol (2 SNPs; causal effect estimate per one percent increase in apoA-IV = -0.40; 95% CI = [-0.60, -0.21] ; p-value = 5.5e-05).

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