Abstract
The first association between uraemia and bone disease was made by Lucas and reported in Lancet of 1883 [1]. However, it was not until nearly 40 years later that the major clinical and radiological manifestations of the skeletal changes were accurately defined [2, 3]. In 1943 the histopathology of osteitis fibrosa and osteomalacia was described [4], and in the same year the term ‘renal osteodystrophy’ was coined by Liu and Chu [5]. Subsequently the abnormalities of bone mass that occur in osteopenia and osteosclerosis were also described [6]. Following the research of Stanbury and Lumb [7, 8], there began a period of rapid advance in the understanding of the processes behind altered divalent ion metabolism, and the abnormalities of parathyroid hormone and vitamin D3 production that are seen in end-stage renal disease. Despite these advances, and the introduction of vitamin D3 replacement therapy, osteodystrophy remains a common complication of end-stage renal failure, and continues to pose diagnostic and therapeutic dilemmas for clinical nephrologists. It has become apparent that the spectrum of bone lesions seen in dialysis patients is changing, with hyperparathyroid disease becoming less common [9, 10], and furthermore, a different pattern of bone lesions is found in CAPD and haemodialysis patients [9–11]. In a histological study of 259 chronic dialysis patients in Canada the commonest bone lesion was found to be hyperparathyroid disease (50%) in haemodialysis patients, and adynamic bone (61%) in peritoneal dialysis patients [10]. In contrast, Malluche and Monier-Faugere (Kentucky, USA) reported that in a retrospective survey of 602 patients from 1982 to 1991 the mixed lesion was the commonest diagnosis [9], regardless of mode of dialysis (56% in CAPD and 49% in haemodialysis). The difference between these reports is noteworthy in itself, since both are large and reliable studies, but from centres many hundreds of miles apart. Whilst differing diagnostic criteria may account for some of the difference, it emphasizes the fact that, in dialysis patients, histomorphometric data represent the result of pathological processes, treatment regimes and environmental effects that have been on-going for many years.
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Hutchison, A.J. (2000). Calcium, phosphate and renal osteodystrophy. In: Gokal, R., Khanna, R., Krediet, R.T., Nolph, K.D. (eds) Textbook of Peritoneal Dialysis. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-3225-3_19
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