作者: E. Slatopolsky , K. Martin , K. Hruska
DOI: 10.1152/AJPRENAL.1980.239.1.F1
关键词:
摘要: Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels immunoreactive parathyroid hormone (i-PTH) in uremia may represent "uremic toxin" responsible for many abnormalities uremic state. Plasma i-PTH consists mixture intact hormone, single-chain polypeptide 84 amino acids, and smaller molecular weight hormonal fragments from both carboxy- amino-terminal portion PTH molecule. The arise metabolism by peripheral organs as well secretion glands. structural requirements known biological actions reside Carboxy-terminal fragments, biologically inactive at least terms adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on kidney their removal plasma, thus accumulate circulation unknown present time if other effects these carboxy-terminal contribute to some biochemical alterations observed uremia. most significant consequence increased development bone disease characterized osteitis fibrosa. In addition, it would appear plays an important role abnormal electroencephalographic patterns This be due potential increasing calcium content brain. Parathyroid also implicated pathogenetic factor uremia, i.e., neuropathy, carbohydrate intolerance, hyperlipidemia, alterations. Unfortunately, outstanding clinical research lacking this field conclusive experimental data are practically nonexistent. Further studies necessary one accept concept being toxin."