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A new experimental model for secondary hyperparathyroidism

Publication Date
  • American Association Of Endocrine Surgeons


Abstract We have developed an animal model to study the pathogenesis of secondary hyperparathyroidism by inducing stable uremia in Sprague-Dawley rats by selective microligation of terminal branches of the left renal artery, followed by right nephrectomy. After 4 weeks the animals were killed, the parathyroid glands were removed and weighed, and blood samples were obtained. Of 30 rats, uremia developed in 22 (73%; uremic group) and eight (27%) died or did not become uremic. A sham-operated group of 15 rats served as control (control group). Creatinine levels were 1.8 ± 0.5 mg/dl in the uremic group versus 0.5 ± 0.1 mg/dl in the control group (p < 0.0001). Parathyroid glands were hyperplastic in all rats with uremia and were heavier than parathyroid glands of control animals (70.3 ± 26 vs 19.1 ± 8 μm; p < 0.0001). In the group with uremia, parathyroid hormone levels were increased over those of the control group (112.6 ± 13 vs 28.9 ± 6.2 pg/ml; p < 0.0001), whereas osteocalcin levels were similar (36.6 ± 11 vs 37.5 ± 1 ng/ml). Serum calcium, phosphate, and alkaline phosphatase levels were similar in both groups. Our model can be used to test hypotheses concerning the treatment of secondary hyperparathyroidism and the relative pathogenesic relevance of vitamin D deficiency and phosphate retention.

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