There are several considerations in this patient that could account for her symptoms. The initial consideration is that she had hyperparathyroid bone disease, as a result of secondary hyperparathyroidism. In this regard, measurements of intact PTH had ranged within 300-400 pg/mL, which is clearly above the normal interval for these PTH assays, in which the upper limit of normal would be approximately 65 pg/mL. While at first glance this may indicate severe hyperparathyroidism, it is important to note that in the setting of advanced chronic kidney disease, there is known to be skeletal resistance to the actions of PTH, and higher than normal concentrations of PTH appear to be required to maintain bone turnover. In recent times, clinical practice guidelines have been introduced for the control of the abnormalities of mineral metabolism in patients with chronic kidney disease, and it is recommended that intact PTH should ideally be maintained between 150 and 300 pg/mL in order to maintain normal bone turnover. Thus, in the patient under consideration, PTH concentrations are only marginally increased above the desired therapeutic range. Although measurement of intact PTH is useful to assess the effects of hyperparathyroidism on bone, there is a considerable range of concentrations that may be seen and this patient's PTH concentration is in a "gray zone" where prediction of the effects of PTH on bone may be difficult. Other biochemical determinations may be helpful in conjunction with the PTH assay. In this particular patient, the elevated alkaline phosphatase suggests evidence of increased osteoblast activity, which could potentially be due to the effects of excess PTH on bone. However, most patients with hyperparathyroid bone disease sufficient to cause symptoms have higher concentrations of intact PTH, the elevated alkaline phosphatase raises that concern in this patient. An additional consideration is that this patient had osteoporosis accounting for her back pain from microfactures. She was postmenopausal and had been treated with cor-ticosteroids in the past, both of which can be significant contributors to decreased bone density and osteoporosis. Osteoporosis, however, rarely results in pain in the lower limbs associated with proximal muscle weakness, as was seen in this patient.
In recent times there have been refinements in the assay for PTH as a result of the observation that so-called "intact" PTH assays are now known to also measure aminoterm-inally truncated PTH fragments, such as PTH 7-84. This has led to assays that are specific for the full-length 84-amino-acid PTH molecule. Examples of commercially available assays of this type are the Bio-Intact PTH assay (Nichols Diagnostics Institute) and the Whole PTH assay (Scantibodies Clinical Laboratories). It is hoped that these assays will have improved clinical performance and allow for better reproducibility between assays from various manufacturers.
An additional consideration is that this patient had an osteomalacic lesion of bone, due to defective bone mineralization. Most symptomatic osteomalacia in the setting of chronic kidney disease has been the result of accumulation of aluminum in bone in the era where aluminum-based phosphate binders were utilized to try to prevent hyperphosphatemia. This patient had never received aluminum-containing compounds, and accordingly, this is an unlikely possibility.
However, the patient had a long history of proteinuria, which is associated with significant loss of vitamin D-binding protein in the urine, and was likely vitamin D-deficient. Therefore, the possibility exists that she had vitamin D deficiency-induced impaired mineralization in bone.
Accordingly, on clinical grounds, it is not possible to make a specific diagnosis of bone disease in this patient, and accordingly, a decision was made to perform bone biopsy following double tetracycline labeling to allow for the measurement of dynamic parameters of bone mineralization. She therefore received two short courses of tetracycline for 2 days, each at 14-day intervals, and had a transiliac bone biopsy performed 5 days after the second course. The bone core was analyzed for histomorphometry and revealed the presence of severe osteitis fibrosa cystica with evidence of markedly increased bone resorption, some delayed mineralization, and markedly decreased trabecular bone. The diagnosis, therefore, was osteitis fibrosis cystica.
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