And the exposure of mitochondria to calcium overload and oxidative stress causes reduced intramitochondrial ATP levels, necrotic cell death, and eventually myocardial fibrosis [78], whereas Sebastian et al. [79] have reported that, in CKD rats, intermittent administration of (1-34)PTH decreased vascular calcification, while the same dosage of (7-34)PTH had little effect in this regard. This evidence concerns the gene PTH and chronic kidney disease.