Accordingly, in the present sample, FGF-23 was not statistically different between groups with or without hypovitaminosis D, nor correlated with 25(OH)D or 1,25(OH)2D. Since both groups had been equally exposed to the use of ACEi (61 vs. 59%), the latter could have acted as a confounder, negatively regulating FGF-23 levels and disrupting the cross-talk between vitamin D and RAS (24). Here, FGF23 is linked to rickets.