Abstract
This article focuses on phosphate toxicity in kidney disease and namely in kidney failure. Twenty years ago, the first article documenting the link between hyperphosphatemia and mortality, was published.
Shortly after, the association between phosphate and cardiovascular complications in kidney failure was demonstrated. Phosphate itself plays an active role in vascular calcifications.
It induces phenotypic changes in vascular smooth muscle cells giving rise a matrix with consequent phosphate and calcium accumulation. The body is fighting again phosphate load.
Initially, these mechanisms are adaptive (PTH and FGF-23 elevation). In kidney failure, they become toxic.
Dietary measures, gastrointestinal phosphate binders and dialysis elimination are used for correction of hyperphosphatemia. Despite all observations, experimental and clinical studies with many discoveries, the relation between mineral and bone disorder and cardiovascular damage, remains still not fully solved.