Fig. 2

Schematic diagram illustrating the possible relationship of the hormonal factors associated with cardiac disorders in CKD. In CKD, both aldosterone and FGF23 are elevated, which directly and/or indirectly causes cardiac hypertrophy and heart failure. There is reported substantial interaction between aldosterone and FGF23, directly from aldosterone to FGF23 and indirectly from FGF23 to aldosterone through circulating volume status. Additionally, elevated FGF23 inhibits vitamin D activity and angiotensin converting enzyme 2 (ACE2) expression, both of which could result in augmentation in renin-angiotensin-aldosterone system. Aldosterone blockade by mineralocorticoid receptor antagonists and T-/N-type Ca channel blockers could mitigate cardiac hypertrophy. Phosphate binders not containing Ca reduce FGF23 and could potentially ameliorate cardiac hypertrophy, while those containing iron exert FGF23-lowering action not only through reducing serum phosphate but also through iron supplementation. NCC, sodium chloride cotransporter; ACE2, angiotensin converting enzyme 2; RAS, renin-angiotensin system; PTH, parathyroid hormone. The numbers in brackets denote the references cited in the text