Fanconi's syndrome; treatment by massive dosage of calciferol and two-stage osteotomy.

نویسنده

  • M SINGER
چکیده

Rickets caused by deficiency of vitamin D has almost disappeared in Great Britain, and for this reason attention is being focused more and more on the group of conditions which in the past has been loosely termed ‘ ‘ resistant ‘ ‘ and ‘ ‘ renal ‘ ‘ rickets. Dent (1952) clarified the confusion that has surrounded the subject. He classified the etiolog ’ of the various rachitic and osteomalacic conditions into the following groups: I) vitamin D and calcium lack ; 2) the steatorrhoeas (coeliac, idiopathic, sprue) ; 3) bile salt deficiency : ? hepatic rickets ; 4) renal glomerular defect (polycystic kidney and other gross renal defects) ; 5) renal tubular defect ; ureterocolostomy. In renal glomerular rickets, which is in fact the classical ‘ ‘ renal rickets, ‘ ‘ both glomeruli and tubules are damaged or destroyed, leading to retention of urea, phosphates and other substances normally excreted in the urine. In renal tubular rickets there is an inherited or acquired defect of tubular reabsorption. Various functions may be lost, depending on the site and extent of the defect. For clinical purposes this group can be sub-divided into six types, according to the nature of the tubular reabsorption defect : 1) phosphates only (low blood phosphorus) ; 2) phosphate + glucose (glycosuria) ; 3) phosphate + glucose + amino-acids (amino-aciduria, including cystinuria); 4) phosphate +glucose + amino-acids, with faulty urine acidification (low CO2 combining

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Hypophosphataemic Osteomalacia in the Adult with Defective Renal Tubular Function. a Report of Four Cases, with Special Mention of the Effects of Massive Doses of Vitamin D (calciferol).

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عنوان ژورنال:
  • The Journal of bone and joint surgery. British volume

دوره 36-B 4  شماره 

صفحات  -

تاریخ انتشار 1954