The Management of Renal Osteodystrophy

  • H. E. de Wardener
  • J. B. Eastwood
Part of the Advances in Experimental Medicine and Biology book series (AEMB)


Renal osteodystrophy is so transfixed by semantic confusion and traditional myths that I would like to start with a few definitions. We would define renal osteodystrophy as the presence in the bone of a patient with chronic renal failure, of histological evidence of hyperparathyroidism with or without co-existing evidence of osteomalacia. Hyperparathyroidism consists of erosions and tunnelling of bone trabeculae, osteocytic osteolysis and marrow fibrosis. Osteomalacia consists of a diminution in mineralisation of the osteoid lamella lying closest to the calcified bone as revealed by tetracycline labelling and toluidine blue stain. Both conditions are associated with an increase in osteoid volume which is greatest with osteomalacia. The evidence suggests that all the lesions of hyperparathyroidism described above are due to an increase in the circulating concentration of parathyroid hormone which acts directly on the bone stimulating both osteoclasts and osteoblasts. The aetiology of the osteomalacia is less certain but would appear to be due to a diminished circulating concentration of one or more Vitamin D metabolites, some of which are known to act directly on the bone1.


Chronic Renal Failure Calcium Carbonate Parathyroid Gland Plasma Calcium Renal Osteodystrophy 
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Copyright information

© Springer Science+Business Media New York 1977

Authors and Affiliations

  • H. E. de Wardener
    • 1
  • J. B. Eastwood
    • 1
  1. 1.Department of MedicineCharing Cross Hospital Medical SchoolLondonUK

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