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Azotemic renal osteodystrophy; clinical features and bone pathology
Endocrinologia Japonica
|June 1, 1979
Summary
Long-term hemodialysis in uremic patients can cause bone disease and calcification. Using 7.5 mg/dl dialysate calcium may prevent elevated alkaline phosphatase, a marker of bone turnover.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Uremic patients undergoing long-term hemodialysis often experience complications.
- Metabolic bone disease, including osteomalacia and osteitis fibrosa, is common in chronic renal failure.
- Calcification of soft tissues and vasculature is a significant concern.
Purpose of the Study:
- To investigate the long-term effects of hemodialysis on bone metabolism and mineral disturbances.
- To evaluate the impact of dialysate calcium levels on alkaline phosphatase and parathyroid hormone.
- To assess the efficacy of vitamin D analogs in managing renal osteodystrophy.
Main Methods:
- A 10-year observational study involving 543 uremic patients undergoing hemodialysis.
- Monitoring of metabolic calcium disturbances, alkaline phosphatase, and plasma immunoreactive parathyroid hormone (iPTH).
- Analysis of bone histology, including osteomalacic and osteitis fibrosa changes, with and without vitamin D analog administration.
Main Results:
- Hemodialysis was associated with metabolic calcium disturbances, soft tissue calcification, and fractures.
- Elevated alkaline phosphatase was observed with 5.0-6.0 mg/dl dialysate calcium but not with 7.5 mg/dl.
- Long-term hemodialysis led to mixed osteomalacia and osteitis fibrosa, which shifted to predominantly osteomalacia with vitamin D analog treatment.
Conclusions:
- Dialysate calcium levels significantly influence alkaline phosphatase in hemodialysis patients.
- Long-term hemodialysis can induce mixed renal osteodystrophy.
- Vitamin D analogs effectively alter bone histology towards osteomalacia with reduced osteoid thickness.