Parathyroid function, vitamin D and calcium metabolism in renal disease
| Autor: | R.G. Larkins |
|---|---|
| Rok vydání: | 1978 |
| Předmět: |
medicine.medical_specialty
Osteomalacia Hypercalcaemia business.industry Osteitis fibrosa cystica Parathyroid hormone medicine.disease Tertiary hyperparathyroidism Pathology and Forensic Medicine Ectopic calcification Endocrinology Internal medicine medicine Secondary hyperparathyroidism Hypocalcaemia business |
| Zdroj: | Pathology. 10:185-186 |
| ISSN: | 0031-3025 |
| DOI: | 10.1016/s0031-3025(16)38636-6 |
| Popis: | Knowledge of the pathogenesis of the osseous changes which so often contribute to the morbidity of chronic renal failure and long-term haemodialysis has been accelerated by the widespread application of assays for parathyroid hormone (PTH) and the unravelling of the metabolic pathways of vitamin D. PTH is secreted in response to low ionized Ca concentration. Ionized Ca tends to fall in the early stages of chronic renal failure, partly because of phosphate retention due to decreased glomerular filtration rate, and partly because of decreased absorption. Thus PTH secretion is increased. In addition, defective production of the most active metabolite of vitamin D, 1,25 dihydroxycholecalciferol(1,25(OH) 2 D 3 ) may directly increase PTH secretion. Failure of renal metabolism and excretion of PTH fragments exacerbates the tendency to increased PTH levels, although it should be remembered that immunological activity of PTH tends to overestimate biological activity in renal failure. Vitamin D is activated in the body by a two-step process involving 25-hydroxylation in the liver and 1-hydroxylation in the kidney to form 1.25(OH) 2 D 3 . Low levels of this metabolite lead to impaired calcium absorption, osteomalacia and secondary hyperparathyroidism. In individual patients either osteomalacia or hyperparathyroid bone disease (osteitis fibrosa cystica) may dominate the clinical, biochemical, radiological and histological pictures, although most patients show evidence of both. If secondary hyperparathyroidism is severe, serum Ca may be normal or elevated, the latter being termed tertiary hyperparathyroidism although this is misleading as the parathyroid tissue remains responsive to serum Ca concentration. Another problem associated with secondary hyperparathyroidisim is ectopic calcification, which is particularly troublesome if it involves the walls of arteries, when it can lead to ischaemic lesions, or the kidney when it may result in further impairment of renal function. The main treatment consists of prevention of hyperphosphataemia which indirectly causes parathyroid stimulation, judicious use of vitamin D or its metabolites in hypocalcaemia, osteomalacia, or osteitis fibrosa without hypercalcaemia, and subtotal parathyroidectomy where necessary for severe hypercalcaemia, ectopic calcification, or osteitis fibrosa with hypercalcaemia. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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