Early Death in Dialysis Patients Linked to High Calcium, Phosphorus
Uncorrected serum calcium greater than 10.2 mg/dL is a new quality measure instituted by the Centers for Medicare and Medicaid Services (CMS) that will go into effect in 2016.
Dialysis patients who have high concentrations of serum calcium and phosphorus are at elevated risk of dying early, a new study finds. Whether controlling hypercalcemia and hyperphosphatemia would improve outcomes remains to be seen, however, and should be assessed by future studies.
The Centers for Medicare and Medicaid Services (CMS) recently finalized a rule that includes uncorrected serum calcium greater than 10.2 mg/dL as a quality measure within the Quality Incentive Program for end-stage renal disease starting in 2016. In the new study, researchers found that both uncorrected and corrected serum calcium levels of 10.2 mg/dL and above identified patients at increased risk of premature death.
The team led by Matthew B. Rivara, MD, of the Kidney Research Institute at the University of Washington in Seattle analyzed data from 119,010 hemodialysis patients and 10,066 peritoneal dialysis patients treated at DaVita, Inc., facilities from July 2001 to June 2006.
Both low and high levels of uncorrected calcium were associated with excess mortality, according to results published online in the Journal of the American Society of Nephrology. Adjustment for serum albumin lessened the association for low serum calcium (less than 8.5 mg/dL) and strengthened the association for high serum calcium of 10.2 mg/dL and above.
Serum phosphorus levels of 6.4 mg/dL and greater were also linked to increased mortality, the researchers found. The dialysis method did not appear to influence any of the results.
In dialysis patients, serum calcium can rise to high levels due to hyperparathyroidism, use of dialysate with calcium concentrations above 1.5 mmol/L, or use of medications such as calcium-containing phosphate binders. All of these are modifiable in clinical practice.
According to the investigators, high serum calcium could contribute to adverse clinical outcomes in many ways. It might promote vascular calcification, leading to atherosclerosis; alter smooth muscle tone, leading to hypertension; accelerate cell death; and impair white blood cells, promoting infection-related complications.
Hyperphosphatemia, likewise, may contribute to vascular calcification and/or infection via accelerated cell death and reductions in T lymphocytes.
Another possibility is that serum calcium is simply a marker for a “complex interplay” between phosphorus, parathyroid hormone, vitamin D and its metabolites, and fibroblast growth factor 23, according to the researchers. In that case, lowering serum calcium may not improve outcomes.