Vitamin D regulation of renin expression is independent of calcium metabolism, and calcitriol markedly suppresses renin transcription by a vitamin D receptor—mediated mechanism in cell cultures [19]. Ferder et al. suggested a possible feedback link between vitamin D and the reninangiotensin system (RAS), considering that vitamin D and
angiotensin II receptors are distributed in the same tissues, changes in RAA activity and activation of the vitamin D receptors seem inversely related, and vitamin D deficiency could be explained by the cellular inflammatory response activity induced by the RAA system [25]. Therapy should combine RAS blockade and VDR stimulation [25].