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• W2040358439 endingPage "304" @default.
• W2040358439 startingPage "267" @default.
• W2040358439 abstract "Recent developments in the study of azotaemic osteodystrophy are reviewed with especial reference to disordered vitamin D metabolism and to the genesis of secondary hyperparathyroidism. The kidney is exclusively responsible for synthesis of the effector metabolite of-vitamin D, 1,25-dihydroxycholecalciferol, and inadequate formation of this metabolite may account for the development of apparent vitamin D deficiency in advanced renal failure. The therapeutic effectiveness of vitamin D in renal failure may be attributable to 25-hydroxycholecalciferol. Dihydrotachysterol appears to be active in the absence of the kidneys and could prove to be the sterol of choice for correcting ‘vitamin D resistance’ in renal failure. It is now clear that secondary hyperparathyroidism develops early in renal disease, as an indirect consequence of the tendency to hyperphosphataemia produced by any reduction in glomerular filtration. This effect is potentiated later in renal failure by the effects of vitamin D deficiency on the bone; and ultimately by the effects of sustained hyperphosphataemia. Development of true secretory autonomy (‘tertiary hyperparathyroidism’) is probably rare in renal failure, and the occurrence of hypercalcaemia can be accounted for by a variety of alternative mechanisms. The problem of ‘dialytic bone disease’ is considered against the background of accumulated knowledge of azotaemic osteodystrophy developing in undialysed patients. Although the histopathological nature of the former is inadequately documented, the weight of available evidence suggests that the two conditions are not fundamentally different: in dialytic bone disease, a distinguishing feature may be a progressive reduction of bone mass. The dominant factor causing bone disease in dialysed patients appears to be continued hyperparathyroidism produced by the same factors as in the undialysed. Measures aimed at preventing or suppressing secondary hyperparathyroidism in the dialysed patient are demonstrably capable of preventing or improving bone disease. In addition to inadequate control of hyperphosphataemia, evidence is accumulating to suggest that a cryptically developing cumulative deficiency of calcium—attributable to dialysis against too low a concentration of calcium—may be the most important cause of hyperparathyroid bone disease in dialysed patients. Among extrinsic factors that may contribute to producing dialytic bone disease, a case can be made for induced fluorosis; but this cannot be finally accepted without further study of the effect of recalcifying regimens in patients exposed to fluoride, or observations on the effects of fluoride-free dialysis fluid." @default.
• W2040358439 created "2016-06-24" @default.
• W2040358439 creator A5010513991 @default.
• W2040358439 date "1972-03-01" @default.
• W2040358439 modified "2023-10-17" @default.
• W2040358439 title "Azotaemic renal osteodystrophy" @default.
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