Correlation of radial bone mineral content with total body calcium in chronic renal failure

Loss of bone mineral of the skeleton in renal disease can be measured directly by total body neutron activation analysis (TBNAA), and also by an absorptiometric technique applied to the appendicular skeleton (radius). In the present study the results of these two techniques are compared in 25 patients with renal insufficiency, 53 patients with end-stage renal failure on dialysis, and 24 normal control subjects. It is apparent that there is good correlation between total body calcium(TBCa) and bone mineral content (BMC) in all groups studied. The correlation in the normal contrast group was 0.944 as compared to 0.919 for the renal patients and 0.892 for patients with end-stage renal failure on dialysis. In order to measure the relative deficit in TBCa in individual patients from the absolute Ca measurement, it is necessary to normalize the data for sex, age, and skeletal size. For this purpose, an empirically derived relationship was used to predict the normal skeletal Ca in each subject, based on weight, height, sex, and age. The measured TBCa divided by the predicted TBCa is referred to as the calcium ratio. This ratio is useful in expressing the relative deficit of Ca in individual renal patients. In similar manner, BMC data were normalized, with the same relationship used to obtain BMC ratios. The normalization procedures allow both the TBCa and BMC measurements to be used to quantitate the Ca deficit in individual patients with renal insufficiency. However, the correlation coefficient relating changes in TBCa and BMC in individual patients on dialysis was very poor (0.25). It is clear that the BMC measurement alone cannot always predict the level of the total body Ca in individual patients with renal failure. In like manner, TBCa measurement alone does not define the distribution of total body Ca between the skeleton and soft tissue in these patients. However, taken together, the BMC measure along with that of TBCa does suggest possible alterations in the skeletal calcium distribution associated with renal disease.