Moreover, dialysis cannot remove the body's toxins that cause osteodystrophy, and the drugs used to treat the condition carry serious side effects that threaten the lives of patients.
"Everyone knows that (patients on dialysis) cannot dispose normally of the typical toxins," Dr. Paolo Raggi, professor of medicine at Tulane University Medical School in New Orleans, told United Press International.
"What most people don't know is how dangerous the condition is to the human skeleton."
Raggi presented preliminary new research on osteodystrophy -- also known as osteomalacia -- at the annual meeting of the American Society of Nephrology. The research concerns possible dangers of the newest drugs used to treat the condition.
"We are beginning to think that calcium-based drugs may contribute to the heart and stroke problems (associated with kidney disease)," Raggi said.
"So we are looking at new alternatives since, obviously, we certainly don't want to hurt our patients while we try to treat them."
The calcium-based drugs are used to remove phosphorus in kidney disease patients. Phosphorus is one of the most dangerous toxins produced by the body, Raggi explained.
"In reaction to high phosphorus and the loss of vitamin D, the body reacts by secreting a lot of what we call parathyroid hormone. Parathyroid hormone goes to the bone and destroys it, chewing on the bone to get calcium out and take it to where the calcium is needed.
"Bones also need vitamin D. So loss of vitamin D and the activity of parathyroid hormone doubles up on the bones, causing progressive destruction."
Raggi said that virtually all patients on dialysis face some phosphate-induced form of bone disease and up to 45 percent of end-stage kidney failure patients have skeletons that have "shut down."
Although the bones do not decalcify, they can no longer repair the small fractures that arise routinely from daily activities. This is called "a-dynamic" bone, he said, where small fractures accumulate unhealed and lead to large fractures.
One of the most insidious aspects of osteodystrophy is that the bone changes it causes can begin many years before any symptoms appear in adults with kidney disease. It is called a "silent crippler" by physicians.
"Many more people are aware of the fact that calcium disorders can lead to heart attack or stroke in these patients than they are to the fact that bone disease is so pervasive and so threatening," John Davis, chief executive officer of the National Kidney Foundation, told UPI. "Dialysis is saving lives but alone it can't stop bone disease."
Bone and joint pain are early signs of renal osteodystrophy, which is very serious in children because their bones are still growing. The condition slows growth and causes deformities.
One such deformity occurs when the legs bend inward or outward. This deforming condition is often called "renal rickets." Another consequence is short stature.
Older patients and women who have gone through menopause are at greater risk for this disease because they already are vulnerable to osteoporosis.
Current treatment of osteodystrophy includes the maintenance of proper calcium and phosphorus levels in the blood, treatment with vitamin D and the phosphate-binding agents, reducing exposure to excess iron or aluminum and reducing aluminum toxicity.
Drugs on the U.S. market include the calcium-based phosphorus-binding agents and a polymer-based drug named sevelamer.
Lanthanum carbonate, a drug in the final stages of development, awaits action by the U.S. Food and Drug Administration.
"The most important thing is to get away from the use of aluminum-based phosphate binding drugs and to take a hard look at calcium-based agents," Raggi said. "So our real hope is in newer less-toxic agents."
The U.S. Centers for Medicare and Medicaid Services, formerly known as the Health Care Financing Administration, in Washington reports that more than 230,000 Americans are under treatment for end-stage renal disease. Men comprise 54 percent of the patients.
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