LabMed

Renal Osteodystrophy

At a Glance

Renal osteodystrophy is caused by phosphate retention in renal failure. Phosphate retention results in a secondary decrease in calcium activity ("ionized calcium") and a significant increase in parathyroid hormone (PTH) secretion. Low 1,25 dihydroxyvitamin D is also seen because of renal failure. All of these abnormalities cause very rapid bone degradation and bone formation with ineffective mineralization due to reduced calcium activity. "Rugger jersey spine" can be seen on x-ray. Often, there are no symptoms, although bone and joint pain may occur; however, the disease may be silent to the point of deformation or fracture.

What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?

Serum calcium, phosphorus, and PTH should be measured in patients with renal failure to assess for renal osteodystrophy.

Vitamin D activity (1,25 dihydroxyvitamin D) is also low, generally, because of the renal failure. The concentration varies depending on the degree of renal function. The level of 1,25 dihydroxyvitamin D is not appropriate for the PTH level. (Table 1)

Table 1.

Test Results Indicative of the Disorder
Serum phosphate Serum calcium ("ionized") Serum PTH
Increased Decreased Greatly increased

Are There Any Factors That Might Affect the Lab Results? In particular, does your patient take any medications - OTC drugs or Herbals - that might affect the lab results?

In less severe disease, dietary phosphate is a major contributing factor and a low phosphate diet alone may control the syndrome.

What Lab Results Are Absolutely Confirmatory?

It is usually not difficult to distinguish renal osteodystrophy from vitamin D disorders or other causes of osteomalacia due to the association with renal failure and high serum phosphate.

Bone biopsy may be useful in some cases, particularly when the disease is severe, and may cause secondary marrow failure because of occupancy of the marrow by differentiating bone ("osteitis fibrosa," which is neither inflammatory nor fibrous; these changes are completely reversed after renal transplant).

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