Qi Q, Monier-Faugere MC, Gent Z, Malluche HH
Predictive value of serum parathyroid hormone levels for bone turnover in patients on chronic maintenance hemodialysis

Am J Kidney Dis (Oct) 26:622-631 1995

This article described the correlation of PTH values with a relatively unfamiliar (to nephrologists) measure of bone turnover, activation frequency. This measurement requires assessment of both bone formation and bone resorption for its calculation. Seventy-nine patients were studied. Half were biopsied for study purposes only, whereas half were biopsied for a variety of clinical concerns, some of which were not clearly specified. Twenty percent had two biopsies.

The results suggested that a single serum PTH level discriminated poorly between high, normal and low bone turnover states, whether activation frequency or the more familiar bone formation rate was used. High bone turnover could be seen with PTH levels of 80 to 1800 pg/ml, normal bone turnover between levels of 15 and 440, and low bone turnover between 0 and 600. PTH levels above 450 pg/ml were almost always associated with high bone turnover, although how many of the data points represent duplicate biopsy results is unknown. PTH values between 80 and 450 pg/ml could be any condition, while values below 80 were nearly equally divided between normal and low turnover states. The authors conclude that PTH levels between 65 and 450 pg/ml do not discriminate between the various bone lesions and that such patients should have a bone biopsy to distinguish their bone disease.

Comment: With regard to adynamic bone disease, what has been recommended by previous investigators is a goal PTH of 1.5 to 5.0 times the upper limits of normal (100 to 300 pg/ml). Some studies have shown good (but not perfect) discrimination of low from normal bone turnover at a PTH of 100 and normal from high turnover at a PTH of 300. The conclusions by Qi et al, purporting to show that PTH values between 65 and 450 are of no value whatsoever in predicting bone turnover (formation) rates are not entirely convincing, as this study suffers from a number of methodologic difficulties. One has to do with use of activation frequency as a measure of bone turnover. This measure includes both bone formation and resorption. The latter can not be accurately quantitated (in contrast to bone formation) so it is at best an estimate. Activation frequency has been used mostly in osteoporosis studies; this paper is the first large scale use in renal osteodystrophy. Activation frequency has not been validated in any longitudinal, reproducible way in renal patients and many people question its use in osteoporosis as well. Interestingly, the bone formation rate and activation frequency data look essentially identical, raising some questions about the additional value of the newer methodology.

While 79 patients were studied, the actual size of the patient population they were recruited from is not given. The population was not well characterized, with half being presumably asymptomatic and half being evaluated for problems which are not clearly specified. The fact that 20% had two biopsies with both biopsies included in the report is likely to increase the amount of data, but does not provide a real diversity of bone lesions. The patients were also on a variety of treatments with respect to calcitriol, aluminum, calcium, etc. In a study from the southern US an important bit of demographic data, race, was not included. Since normal blacks appear to have a lower bone formation than whites, and bone formation is an important result of this study, it is surprising not to see it here. Only one PTH level was determined. Most clinicians would not base an important clinical decision on a single laboratory value; at least 3 PTH determinations per patient would have been preferable. (Sherrard)

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