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Parathyroid hormone and bone histology: response to hypocalcemia in osteitis fibrosa
Insights
In hemodialysis patients, a small drop in calcium triggers a significant parathyroid hormone (PTH) release. This PTH response is linked to bone disease, suggesting altered PTH regulation in these patients.
Area of Science:
- Nephrology
- Endocrinology
- Bone Metabolism
Background:
- Osteitis fibrosa is a common complication in hemodialysis patients.
- Parathyroid hormone (PTH) plays a crucial role in calcium homeostasis and bone remodeling.
- The PTH response to hypocalcemia in hemodialysis patients with osteitis fibrosa requires further elucidation.
Purpose of the Study:
- To investigate the parathyroid hormone (PTH) response to induced hypocalcemia in hemodialysis patients.
- To explore the relationship between PTH levels and bone histology in these patients.
Main Methods:
- Studied 18 hemodialysis patients with osteitis fibrosa and 26 hemodialysis patients.
- Induced hypocalcemia using a calcium-free dialysate during hemodialysis.
- Measured amino (N)-terminal and carboxy (C)-terminal PTH levels and plasma calcium.
Main Results:
- Both N-PTH and C-PTH reached maximum levels within 15 minutes of minimal plasma calcium decline.
- Elevated PTH levels persisted despite further calcium decrease, with some patients showing maximal response even with calcium above 9 mg/dl.
- Basal and stimulated PTH levels correlated with markers of bone resorption, osteoid, and fibrosis.
Conclusions:
- A minimal decrease in plasma calcium elicits a maximal PTH response.
- Some hemodialysis patients may exhibit an altered PTH set point.
- Basal PTH levels might indicate parathyroid gland mass.
- A correlation exists between PTH levels (basal and stimulated) and bone histology in hemodialysis patients.
Abstract:
The parathyroid hormone (PTH) response to hypocalcemia was studied in 18 hemodialysis patients with osteitis fibrosa, and the relationship with PTH and bone histology in 26 hemodialysis patients. Hypocalcemia was produced during hemodialysis by the use of a dialysate devoid of calcium. Both amino (N) (P less than 0.05) and carboxy (C) (P less than 0.005) terminal PTH attained maximum levels by 15 min despite only a minimal decline in plasma calcium. Throughout the remainder of the study, C and N-PTH levels remained elevated but did not increase despite a further decline in plasma calcium. Five patients increased both C and N-PTH to maximum or near maximum levels by the first sampling, although plasma calcium remained above 9 mg/dl. Basal C and N-PTH correlated with the maximum levels of each induced by hypocalcemia (P less than 0.005). Both basal N-PTH and the maximum change in C-PTH produced by hypocalcemia correlated with osteoblastic osteoid, active resorption, osteoclasts/mm2, and endosteal fibrosis (P less than 0.005). In conclusion, (1) a minimal decline in plasma calcium produces a maximum C and N-PTH response; (2) an altered PTH set point may be present in some hemodialysis patients; (3) the correlation between basal and maximally stimulated PTH levels suggests that basal PTH levels may reflect parathyroid gland mass; and (4) a correlation with basal and stimulated PTH and bone histology is present.