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The assay of serum peptides of bone collagen formation and degradation could potentially provide an indirect estimate of the rate of bone turnover. In our study we have measured serum levels of the carboxy-terminal propeptide of type I procollagen (PICP) as a marker of bone formation and serum levels of the pyridinoline cross-linked telopeptide domain of type I collagen (ICTP) as a marker of bone resorption in 53 patients (47.7 +/- 10 years, M +/- SD) on haemodialysis (for 9.5 +/- 3.8 years) and affected by renal osteodystrophy. Besides PICP and ICTP, patients were also sampled for serum intact and C-terminal PTH, osteocalcin (BGP) and alkaline phosphatase (AP). A transiliac bone biopsy for histomorphometry was also performed in all. As expected both PTH assays, BGP and AP, were correlated reciprocally and to histomorphometric parameters. As for serum levels of PICP, they were on average increased (268.5 +/- 104.9 ng/ml, M +/- SD) compared to normals (range 66-176), but not correlated to classical humoral markers of hyperparathyroidism (PTH and AP), with the exception of BGP (with a rather low r value: 0.365, P0.01), nor to histomorphometric indices of bone resorption and formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Intact parathyroid hormone (iPTH) radioimmunoassay represents an important advancement in the measurement of serum PTH levels, permitting the evaluation of the actual rate of secretion of the parathyroid glands. The aim of the study was to compare the value of intact and C-terminal PTH measurements in predicting the osteodystrophic bone lesion in predialysis patients with chronic renal failure (CRF). We have studied 37 subjects with CRF who were receiving conservative treatment. In each subject a transiliac bone biopsy for histomorphometric examination was performed in addition to the assay of serum intact and C-terminal PTH, osteocalcin, and alkaline phosphatase. Serum C-terminal and intact PTH levels were closely correlated, both showing a high degree of correlation with serum osteocalcin. Similar degrees of correlation were observed between the two PTH assays and the histologic parameters osteoblastic surface (ObS/BS) and osteoclastic surface (OcS/BS). The evaluation of specificity and sensitivity of the two PTH assays in selecting patients with normal or pathologic histomorphometric parameters gave an equivalent number of false positive and negative cases. Based on discriminant analysis of histomorphometric parameters, intact PTH shows a higher discriminant power when compared with C-terminal PTH assay for the parameters OcS/BS and eroded surface (ES/BS), but without practical clinical value. In conclusion, in analogy to the short lived N-terminal PTH fragment assay, prediction of elementary hyperparathyroid bone lesions in predialysis CRF is not improved by the use of intact PTH as compared to the more traditional C-terminal assay.

Insulin-like growth factor-1 (IGF-1), produced by osteoblasts following parathormone (PTH) stimulation, is a local hormone with autocrine and paracrine functions on bone formation. To evaluate whether circulating IGF-1 is also important in stimulating bone formation, a study was carried out on 28 patients with slowly progressing nondialytic chronic renal failure. 9 patients were treated with 1,25(OH)2D3, while 19 did not receive vitamin D metabolites. In all patients a transiliac bone biopsy for histomorphometric studies was obtained, and the following determinations were made: immunoreactive PTH (iPTH), osteocalcin, alkaline phosphatase, IGF-1, serum calcium, phosphate and creatinine. Serum IGF-1 levels were similar in the two groups of patients, and higher than normal. iPTH and osteocalcin were positively correlated with serum creatinine, osteoblast surface and the eroded surface, but did not correlate with IGF-1. A negative (n.s.) relationship was found between dynamic bone parameters and circulating IGF-1, with the mineral apposition rate reaching a significant level (p less than 0.05). In conclusion, the circulating levels of IGF-1 are not correlated with bone formation parameters, thus apparently showing no role in bone turnover or dependency on bone production of the growth factor. The results may favor the hypothesis of a negative feedback control of circulating IGF-1 by suppressive signals originating from active bone metabolic units.