Vascular calcification in dialysis patients.
Renal osteodystrophy, vascular disease and mortality are believed to be linked in patients with chronic kidney disease (CKD), although to date most of the evidence is based only on statistical associations. The precise pathophysiology of vascular calcification in end stagerenal disease (ESRD) is unknown, but risk factors include age, hypertension, time on dialysis, and, most significantly, abnormalities in calcium and phosphate metabolism. Prospective studies are required before 'cause and effect' can be established with certainty, but it is an active metabolic process with inhibitors and promoters. Clinical management of hyperphosphataemia is being made easier by the introduction of potent non-calcium based oral phosphate binders such as lanthanum carbonate. Short and long term studies have demonstrated its efficacy and safety. Vitamin D analogues have been a disappointment as far as control of serum parathyroid hormone (PTH) levels, but evidence is emerging that vitamin D has other important metabolic effects apart from this, and may confer survival advantages to patients with CKD. Calcimimetics such as cinacalcet enable much more effective and precise control of PTH levels, but at the price of major financial burden. Whilst it is unreasonable to expect that any one of these recent pharmacological developments will be a panacea, they provide researchers with the tools to begin to examine the complex interplay between calcium, phosphate, vitamin D and PTH such that further progress is fortunately inevitable.
Hutchison
J A
JA
Manchester Institute of Nephrology and Transplantation, The Royal Infirmary, United Kingdom. Alastair.Hutchison@CMMC.nhs.uk
D002114:Calcinosis / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D006801:Humans; D054559:Hyperphosphatemia / Q000209:etiology / Q000517:prevention & control; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism / Q000628:therapy; D006435:Renal Dialysis; D014652:Vascular Diseases / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control