Insulin-like growth factor 1 and 2 serum concentrations in dialysis patients with secondary hyperparathyroidism and adynamic bone disease.

BACKGROUND

Insulin-like growth factor-1 and -2 exert well characterized effects on bone metabolism via paracrine and endocrine pathways. However, the role of circulating levels of IGFs and their binding proteins (IGFBP) in renal bone disease is still controversial.

PATIENTS AND

METHODS

To investigate whether circulating IGFs play a role in the pathogenesis of different forms of renal bone disease, we performed a cross sectional study in 38 stable dialysis patients (32 hemodialysis, 6 peritoneal dialysis). Patients were selected for the type of bone disease according to biochemical bone markers and bone histology. 25 Patients had adynamic bone disease (ABD; defined by plasma iPTH < 1,5 fold the upper limit of normal). Thirteen patients had secondary hyperparathyroidism (sHPT; defined by plasma iPTH > 10 fold the upper limit of normal). Serological diagnosis was confirmed in a subgroup of patients by bone histology (12 patients with type IIa according to Delling, ABD; 9 patients with type IIIb according to Delling, sHPT). Patients with signs or symptoms of aluminum toxicity were excluded from the study.

RESULTS

Serum IGF-1 and -2 concentrations were comparable in both groups and were within the reported normal range for an age matched healthy control population. They did not correlate with biochemical markers (iPTH, bAP, osteocalcin) or histological manifestations of renal bone disease. Furthermore, semiquantitative analysis of IGFBP-2 and -3 carried out in patients with bone biopsies did not correlate with biochemical markers or histological indices of renal bone disease.

CONCLUSION

In conclusion, in contrast to previous reports, the present data do not confirm a correlation between serological or histological markers of renal osteodystrophy and circulating IGF-1 or -2 or IGFBP-2 and -3. This does not exclude that potential alterations of the local IGF system may play a role in the pathogenesis of uremic bone disease.