English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Open

Presents the pdf analysis as premium feature

PDF Analysis

Insights

Presents the summarisation as premium feature

Summarisation

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

It has already been established that in end-stage renal disease, hyperphosphatemia causes soft tissue calcification including vascular calcifications. It has also been supported that there is a connection between increased serum phosphate and morbidity in subjects, who suffer from renal disease. However, studies in these populations conferred mixed results. Several warnings are included in the role of serum phosphorus on cardiovascular disease in normal populations. Homeostasis of serum phosphate is obtained by the cooperation between regulatory hormones, cellular receptors and bone metabolic factors. There is the probability that one or more phosphate regulatory factors, rather than phosphate directly, may be responsible for observed associations with calcification and cardiovascular events in normal populations. Experimental studies have shown that the restriction of dietary phosphate prevents the progression of kidney dysfunction, although high dietary phosphate aggravates the renal function. In the current review, we discuss the role of serum phosphorus on progression of renal dysfunction and cardiovascular outcomes in chronic kidney disease patients and its involvement in important health risks in the general population.

Serum phosphate and chronic kidney and cardiovascular disease: Phosphorus potential implications in general population