Cardiovascular disease is extremely common in patients with
end-stage renal disease (
ESRD) and accounts for at least 50% of deaths among these patients.
Vascular calcifications (VC) have been recently implicated as a possible cause of this excess cardiovascular mortality. Medial calcification is a striking feature of
vascular disease in patients with
ESRD. The traditional view that VC is a degenerative and passive process has been seriously challenged, based on strong evidence suggesting that VC is an active and highly regulated process similar to bone formation. Different data support the notion that elevated levels of
phosphorus and/or other
uremic toxins may play an important role by transforming vascular smooth muscle cells into osteoblast-like cells, which can produce bone matrix
proteins. This nidus can then mineralize if the balance of pro-mineralizing factors outweighs inhibitory factors. The advent of newer noninvasive screening tests have generated great interest for screening patients with
ESRD for
vascular calcifications. Control of serum
phosphorus with
sevelamer, a recently developed non-
calcium, non-
aluminum phosphate binder, have attenuated or arrested progression of coronary artery and aortic calcifications compared to treatment with
calcium-based binders. Amino
bisphosphonates, have shown to completely inhibit soft tissue calcifications,
calciphylaxis and prevent death in animal models. The first generation
bisphosphonate,
etidronate, reduces the progression of coronary artery calcifications patients receiving long-term
hemodialysis and intravenous
pamidronate has produced a rapid improvement of
calciphylaxis. In conclusion, VC is a widespread phenomenon in patients with
ESRD with important cardiovascular consequences. A better understanding of the processes of VC is leading to
therapies to retard or improve this phenomenon and will probably have an important impact on patient mortality.