FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2084161715> ?p ?o ?g. }

• W2084161715 endingPage "103" @default.
• W2084161715 startingPage "102" @default.
• W2084161715 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.
• W2084161715 created "2016-06-24" @default.
• W2084161715 creator A5090673540 @default.
• W2084161715 date "1961-08-01" @default.
• W2084161715 modified "2023-09-23" @default.
• W2084161715 title "346 Studies on the Intestinal Absorption of Steroid Hormones in the Rat" @default.
• W2084161715 doi "https://doi.org/10.1016/0006-2952(61)90528-7" @default.
• W2084161715 hasPublicationYear "1961" @default.
• W2084161715 type Work @default.
• W2084161715 sameAs 2084161715 @default.
• W2084161715 citedByCount "1" @default.
• W2084161715 crossrefType "journal-article" @default.
• W2084161715 hasAuthorship W2084161715A5090673540 @default.
• W2084161715 hasConcept C124490489 @default.
• W2084161715 hasConcept C126322002 @default.
• W2084161715 hasConcept C134018914 @default.
• W2084161715 hasConcept C2775945674 @default.
• W2084161715 hasConcept C2776096700 @default.
• W2084161715 hasConcept C2776169692 @default.
• W2084161715 hasConcept C2776541429 @default.
• W2084161715 hasConcept C2776699218 @default.
• W2084161715 hasConcept C2778653478 @default.
• W2084161715 hasConcept C2778838027 @default.
• W2084161715 hasConcept C2779674975 @default.
• W2084161715 hasConcept C2779740938 @default.
• W2084161715 hasConcept C2781208988 @default.
• W2084161715 hasConcept C519063684 @default.
• W2084161715 hasConcept C71924100 @default.
• W2084161715 hasConceptScore W2084161715C124490489 @default.
• W2084161715 hasConceptScore W2084161715C126322002 @default.
• W2084161715 hasConceptScore W2084161715C134018914 @default.
• W2084161715 hasConceptScore W2084161715C2775945674 @default.
• W2084161715 hasConceptScore W2084161715C2776096700 @default.
• W2084161715 hasConceptScore W2084161715C2776169692 @default.
• W2084161715 hasConceptScore W2084161715C2776541429 @default.
• W2084161715 hasConceptScore W2084161715C2776699218 @default.
• W2084161715 hasConceptScore W2084161715C2778653478 @default.
• W2084161715 hasConceptScore W2084161715C2778838027 @default.
• W2084161715 hasConceptScore W2084161715C2779674975 @default.
• W2084161715 hasConceptScore W2084161715C2779740938 @default.
• W2084161715 hasConceptScore W2084161715C2781208988 @default.
• W2084161715 hasConceptScore W2084161715C519063684 @default.
• W2084161715 hasConceptScore W2084161715C71924100 @default.
• W2084161715 hasIssue "1" @default.
• W2084161715 hasLocation W20841617151 @default.
• W2084161715 hasOpenAccess W2084161715 @default.
• W2084161715 hasPrimaryLocation W20841617151 @default.
• W2084161715 hasRelatedWork W2009183514 @default.
• W2084161715 hasRelatedWork W2040358439 @default.
• W2084161715 hasRelatedWork W2106848078 @default.
• W2084161715 hasRelatedWork W2128857229 @default.
• W2084161715 hasRelatedWork W2497394583 @default.
• W2084161715 hasRelatedWork W2603618718 @default.
• W2084161715 hasRelatedWork W2765830064 @default.
• W2084161715 hasRelatedWork W2948903201 @default.
• W2084161715 hasRelatedWork W4200432791 @default.
• W2084161715 hasRelatedWork W4255556714 @default.
• W2084161715 hasVolume "8" @default.
• W2084161715 isParatext "false" @default.
• W2084161715 isRetracted "false" @default.
• W2084161715 magId "2084161715" @default.
• W2084161715 workType "article" @default.