Prevalence and clinical consequences of elevated Ca x P product in hemodialysis patients

Control of serum phosphorus (P) levels is a central goal of managing patien ts with chronic renal failure (CRF). Hyperphosphatemia develops invariably with kidney failure, and inadequate control of serum P leads to an elevated calcium-phosphorus (Ca x P) product, Further contributing to an elevated C a x P product is the fact that hemodialysis patients are generally in a net positive calcium balance-dietary intake of calcium, ingestion of calcium-b ased phosphate binders, calcium absorption from dialysate, and abnormalitie s in bone buffering and turnover all contribute to the calcium burden in he modialysis patients. In addition, treatment with calcitriol to manage secon dary hyperparathyroidism increases intestinal absorption of both calcium an d P. These abnormalities in divalent ion metabolism can result in a number of harmful conditions in CRF patients, including vascular calcification, ca rdiovascular disease, calciphylaxis, and death. We are now beginning to rea lize that our current therapeutic approaches to CRF management may not only be ineffective in controlling P and Ca x P product, but may actually contr ibute to serious calcific and cardiovascular hazards in these patients. Ele vated P and Ca x P product an both significant predictors of cardiovascular mortality in hemodialysis patients. These effects are observed at P and Ca x P product levels that were considered safe until recently. Based on curr ent national studies, we now recommend that serum P levels and Ca x P produ ct of patients with CRF be maintained between 3.0 - 5.0 mg/dl and less than 55 mg(2)/dl(2), respectively. Achieving these more rigorous treatment goal s will require a shift in our therapeutic management strategies to incorpor ate aggressive use of calcium-free phosphate binders and, when necessary, u se of less calcemic vitamin D analogs.