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FGF23 is purported to have direct (off-target) effects in the myocardium, as well as canonical effects on FGF receptor\/\u03b1-klotho receptor complexes in the kidney to activate the renin-angiotensin-aldosterone system, modulate soluble \u03b1-klotho levels, and increase sodium retention, to cause left ventricular hypertrophy (LVH). Conversely, FGF23 could be an innocent bystander produced in response to chronic inflammation or other processes associated with CKD that cause LVH and adverse cardiovascular outcomes. 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