Pathophysiology and therapies of CKD-associated secondary hyperparathyroidism

This review article discusses the increasingly complex pathophysiology of secondary hyperparathyroidism (SHP) in chronic kidney disease (CKD), moving beyond traditional factors to include FGF23, klotho, the phosphate pool, and intestinal dysbiosis. These new insights are leading to a better understanding of CKD-related mineral and bone disorder (CKD-MBD) and paving the way for novel therapies, such as targeting specific phosphate transporters or modifying the gut microbiota, which aim beyond managing elevated PTH levels. This review is supported by a grant from CSL Vifor; authors also declared individual COIs related to various pharmaceutical companies.

The authors declared various conflicts of interest, including being board members, receiving honoraria, consulting fees, and travel support from pharmaceutical companies. It is mentioned that the paper was published as part of a supplement financially supported by an educational grant from CSL Vifor.

This review article provides a thorough overview of a complex topic. It covers the classical understanding of secondary hyperparathyroidism (SHP) and delves into newer research areas, offering potential therapeutic avenues. While not presenting original research, its comprehensive approach and focus on emerging aspects like phosphate pool, FGF23, intestinal dysbiosis and their roles in SHP are valuable for guiding future research and clinical practice. The declared conflicts of interest are duly noted and don't appear to unduly bias the content.