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Unless closely monitored, renal bone disease (renal osteodystrophy) is a problem that will be experienced by most people suffering from end stage renal disease (ESRD). Renal bone disease is a complex issue and involves many more factors than can be listed in this limited space. Only the very basics are outlined here.

First, the kidneys are involved in the synthesis of vitamin D, which is the most essential factor regulating intestinal absorption of calcium in humans. When the kidneys fail and less vitamin D is created, the amount of calcium absorbed by the intestines is reduced. Calcium is most essential substance for bone maintenance and health. Next, calcium and phosphorus levels in the blood (which are normally regulated by the kidneys) are dependent upon each other. Therefore, when the kidneys fail and the phosphorus level in the blood goes up, the (free) calcium level in the blood decreases. In response to these two factors that lower serum calcium, the body then increases the parathyroid hormone (PTH) level in the blood.  PTH causes calcium to be released from the bones in order to increase the serum calcium level.  Left untreated, an ESRD patient will have bones that are depleted of calcium, brittle, and likely to fracture.

Treatment and prevention of renal bone disease usually include the use of phosphate binders and vitamin D analogs (to reduce PTH levels).  In the past, treatment frequently included the removal of the parathyroid glands.

Normal serum calcium is 8.5-10.8 mg/dL.

Normal serum phosphorus for dialysis patients is 3.5 to 5.5 mg/dl High phosphorus levels also cause itchy skin.

It is recommended that ESRD patients maintain a calcium phosphorous product that is below 70.