PURPOSE OF REVIEW: Calciprotein particles (CPPs) are colloidal nanoparticles composed of solid-phase calcium phosphate and serum proteins (mainly fetuin-A) that form as part of a defense system preventing ectopic mineral crystal growth. Recent studies have repositioned CPPs from passive byproducts of mineral imbalance to biologically active particles implicated in chronic kidney disease (CKD). RECENT FINDINGS: Experimental studies have shown that CPP uptake by vascular endothelial cells and monocytes induces mitochondrial and lysosomal dysfunction, oxidative stress, and inflammasome activation. In clinical studies, circulating CPP levels and T50, an index of calcification propensity, are consistently associated with vascular calcification, cardiovascular events, and all-cause mortality across CKD stages. Interventional studies further indicate that modulation or removal of CPPs alters vascular and inflammatory phenotypes in vivo. SUMMARY: Accumulating mechanistic and clinical evidence supports the concept that CPPs are plausible pathogenic mediators of CKD-associated complications. Targeting CPP formation, maturation, or clearance therefore represents a promising therapeutic strategy. Whether such approaches will translate into sustained clinical benefit remains an important question for ongoing and future trials.
Makoto Kuro-o (Tue,) studied this question.