Worsening CKD Tied to Mineral Levels

Chronic kidney disease progression linked to abnormal mineral metabolism

/ Author:  / Reviewed by: Robert Carlson, M.D

(RxWiki News) It's not always easy for doctors to spot which patients with chronic kidney disease are at risk for kidney failure. Now, researchers have found a new way to help in this effort.

Problems with mineral metabolism (too much or too little mineral levels in the blood) could be a sign of faster kidney decline. That is, kidney disease patients with abnormal levels of minerals in the blood may have a higher risk of kidney failure.

In a recent study of African Americans with kidney disease, mineral levels rose over time among all patients. However, patients who had larger increases in mineral levels also had faster declines in kidney function.

"See your doctor regularly to keep track of kidney disease."

While it can be hard to tell which kidney disease patients will go on to develop kidney failure, doctors do know that African American patients tend to progress to kidney failure more quickly than whites. It is also known that problems with mineral metabolism - which happens when failing kidneys cannot maintain the right mineral levels in the blood - are more severe among African Americans with kidney disease.

For their study, Julia Scialla, MD, of the University of Miami Miller School of Medicine, and colleagues wanted to see if measuring blood mineral levels could help spot which patients were at risk of kidney failure - a condition that requires either dialysis or a transplant.

"We were hoping to determine whether abnormal blood levels of calcium and phosphate, and the hormones that regulate them - fibroblast growth factor 23 (FGF23), vitamin D, and parathyroid hormone - are risk factors for kidney disease progression in African Americans," said co-author Myles Wolf, MD, also of the University of Miami Miller School of Medicine.

In addition, the researchers wanted to see if there was a relationship between blood mineral levels at the beginning of the study and the risk of kidney failure or death.

Both calcium and phosphate are minerals filtered out of the blood by the kidneys. FGF23, vitamin D and parathyroid hormone are hormones that control levels of calcium and phosphate.

Dr. Scialla and colleagues found:

  • Levels of phosphate, FGF23 and parathyroid hormone increased throughout the study. Patients with the greatest increases in these mineral and hormone levels also had faster rates of kidney function decline.
  • Patients who started the study with the highest levels of FGF23 had more than two times the risk of kidney failure or death, regardless of how well their kidneys worked. Patients with higher levels of parathyroid hormone and phosphate also had an increased risk of death, but not as high as those with high levels of FGF23.
  • A total of 95 percent of patients had low vitamin D, but these low levels were not linked to kidney failure or death.

These findings suggest that mineral levels in the blood may help doctors track kidney function and spot patients at risk of kidney failure. Measuring blood mineral levels could be another tool for assessing kidney function beyond what doctors already use.

"Also, it might be possible to slow kidney disease progression in African Americans using treatments that normalize mineral levels and the hormones that regulate them," said Dr. Scialla.

She added that more research is needed to see if such treatments would work.

The first part of the study - in which researchers measured mineral levels over an average of 4 years - included 420 African American patients with chronic kidney disease. In the second part, researchers looked for the potential link between blood mineral levels and the risk of kidney failure or death in 809 participants.

Study co-author Tamara Isakova, MD, disclosed ties to Shire and Genzyme. Dr. Wolf disclosed ties to Abbott, Amgen, Diasorin, Genzyme, Kai, Luitpold, Mitsubishi and Shire. The study was published December 14 in the Journal of the American Society of Nephrology.

Reviewed by: 
Review Date: 
December 20, 2012
Last Updated:
February 6, 2013