In chronic kidney disease, parathyroid hormone (PTH), like all proteins, can undergo post-translational modifications, including oxidation. This can lead to structural and functional changes of the hormone. It has been hypothesized that currently used PTH measurement methods do not adequately reflect PTH-related bone and cardiovascular abnormalities in chronic kidney disease owing to the presence of oxidized, biologically inactive PTH in the circulation. Ursem et al. now report a strong correlation between serum non-oxidized and total PTH, and comparable associations with histomorphometric and circulating bone turnover markers, pleading against this hypothesis.
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