Researchers examine CV risks related to chronic kidney disease treatments

Kestenbaum B. JAMA. 2011;305:1138-1139.

Palmer S. JAMA. 2011;305:1119-1127.

In a recent study, researchers were unable to find a correlation between serum levels of calcium and parathyroid hormone and the risk for CV mortality or all-cause death in patients with chronic kidney disease, although higher serum phosphorus in this population was linked with increased mortality risk.

This systematic review and meta-analysis included 47 cohort studies with a total of 327,644 patients. All studies measured the association between death and CV events and serum levels of phosphorus, parathyroid hormone or calcium, which are recommended in clinical practice guidelines for the management of mineral and bone disorders related to chronic kidney disease (CKD).

According to data, the risk for all-cause mortality increased with each 1-mg/dL increase in serum phosphorus (RR=1.18), but the likelihood of death remained largely unchanged with increased serum levels of parathyroid hormone (per 100-pg/mL increase, RR=1.01) and calcium (per 1-mg/dL increase, RR=1.08). Similarly, rates of CV mortality were only slightly affected with increased levels of serum phosphorus (RR=1.10), parathyroid hormone (RR=1.05) or calcium (RR=1.15).

These data, the researchers wrote, do not support the hypothesis that individuals with CKD should have treatment to achieve targeted levels of serum parathyroid hormone or calcium to reduce mortality or CV morbidity, “except at extreme levels in which hypocalcemia and hypercalcemia result in immediate, clinically apparent adverse events such as tetany and seizures,” they said. “Furthermore, treating high phosphorus levels is linked to a substantial pill burden that is associated with lower quality of life in individuals with CKD. While we do not conclude that normalizing serum levels of calcium or phosphorus or avoiding upper or lower extremes of serum level of parathyroid hormone is futile, high-quality evidence is required before specific treatment should be advocated strongly.”

However, extrapolating this research into clinical guidelines currently, wrote Bryan Kestenbaum, MD, with the University of Washington, Seattle, in an accompanying editorial, remains premature.

“Placebo-controlled clinical trials are the necessary next step to determine the risks and benefits of treatments that target mineral metabolism disturbances in patients with CKD as a means to improve their health,” he said.

Disclosure: Dr. Kestenbaum reported no relevant conflicts of interest.

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In a recent study, researchers were unable to find a correlation between serum levels of calcium and parathyroid hormone and the risk for CV mortality or all-cause death in patients with chronic kidney disease, although higher serum phosphorus in this population was linked with increased mortality risk.

This systematic review and meta-analysis included 47 cohort studies with a total of 327,644 patients. All studies measured the association between death and CV events and serum levels of phosphorus, parathyroid hormone or calcium, which are recommended in clinical practice guidelines for the management of mineral and bone disorders related to chronic kidney disease (CKD).

According to data, the risk for all-cause mortality increased with each 1-mg/dL increase in serum phosphorus (RR=1.18), but the likelihood of death remained largely unchanged with increased serum levels of parathyroid hormone (per 100-pg/mL increase, RR=1.01) and calcium (per 1-mg/dL increase, RR=1.08). Similarly, rates of CV mortality were only slightly affected with increased levels of serum phosphorus (RR=1.10), parathyroid hormone (RR=1.05) or calcium (RR=1.15).

These data, the researchers wrote, do not support the hypothesis that individuals with CKD should have treatment to achieve targeted levels of serum parathyroid hormone or calcium to reduce mortality or CV morbidity, “except at extreme levels in which hypocalcemia and hypercalcemia result in immediate, clinically apparent adverse events such as tetany and seizures,” they said. “Furthermore, treating high phosphorus levels is linked to a substantial pill burden that is associated with lower quality of life in individuals with CKD. While we do not conclude that normalizing serum levels of calcium or phosphorus or avoiding upper or lower extremes of serum level of parathyroid hormone is futile, high-quality evidence is required before specific treatment should be advocated strongly.”

However, extrapolating this research into clinical guidelines currently, wrote Bryan Kestenbaum, MD, with the University of Washington, Seattle, in an accompanying editorial, remains premature.

“Placebo-controlled clinical trials are the necessary next step to determine the risks and benefits of treatments that target mineral metabolism disturbances in patients with CKD as a means to improve their health,” he said.

Disclosure: Dr. Kestenbaum reported no relevant conflicts of interest.

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