Chronic renal disease, secondary parathyroid hyperplasia, decalcification of bone and metastatic calcification

Herbert, Freda K.; Miller, Henry; Richardson, G. O.

doi:10.1002/path.1700530202

Cited by 57 publications

(13 citation statements)

References 25 publications

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“…We have previously (Ellis and Peart, 1972) It is well established that there is secondary parathyroid hyperplasia in chronic renal failure (Pappenheimer and Wilens, 1935;Gilmour and Martin, 1937;Castleman and Mallory, 1937;Herbert, Miller, and Richardson, 1941;Gilmour, 1947;Roth and Marshall, 1969 (Ellis and Knight, 1969). Like others (Gilmour, 1947;Christie, 1967) we have observed increased numbers of oxyphil cells in the parathyroid glands of some patients with chronic renal failure particularly those with Gilmour type IV nodular hyperplasia where aggregates of these cells form nodules easily visible to the naked eye.…”

Section: Discussionmentioning

confidence: 99%

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

1973

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SYNOPSISThe histopathology of bone is described in 60 patients with chronic renal failure due to a variety of renal diseases. Changes of azotaemic renal osteodystrophy included osteitis fibrosa, osteomalacia, and osteosclerosis. Quantitative histology using a point-counting technique revealed a significant increase in total bone, mineralized bone, and osteoid in comparison with a control group of 68 individuals. Osteitis fibrosa due to secondary hyperparathyroidism occurred in 93 %, osteomalacia in 40%, and osteosclerosis in 30% of patients. Woven bone formation was a characteristic feature and was related to the severity of osteitis fibrosa. There were significant correlations between the weights of parathyroid glands and the number of osteoclasts, amounts of woven bone, and marrow fibrosis in the ilium. Hyperparathyroidism caused degradation of mineralized bone but the loss was balanced or exceeded by the aggradation of woven mineralized bone. Woven bone formation together with excess osteoid gave rise to osteosclerosis. The histological findings indicate that hyperparathyroidism and osteitis fibrosa usually occur early in chronic renal failure and that osteomalacia develops subsequently.Chronic renal failure may be accompanied by bone disease (Stanbury, 1957(Stanbury, , 1972 and the changes, which include osteitis fibrosa due to secondary hyperparathyroidism, osteomalacia and osteosclerosis, may conveniently be termed renal osteodystrophy (Liu and Chu, 1943). Although it is recognized that the clinical effects of such changes may be severe in childhood (Claireaux, 1953;Haust, Landing, Holmstrand, Currarino, and Smith, 1964) 20 December 1972. in this study it appeared that there were histological differences between the bone changes in dialysed and non-dialysed patients. The latter tended to show osteitis fibrosa, osteomalacia, and a normal or raised total bone mass with normal or elevated amounts of mineralized bone. In contrast, in the bones of dialysed patients there was a loss of mineralized lamellar bone and total bone after about one or two years on dialysis. In others, following more prolonged dialysis, the total bone mass was elevated due to excess osteoid formation whilst the amount of mineralized bone remained low. The bones of dialysed patients in general also showed less severe changes of osteitis fibrosa (Ellis and Peart, 1971).To determine whether or not these differences were real it became necessary to quantitate the amounts of mineralized bone and osteoid present and the severity of the osteitis fibrosa. Critical quantitative histological studies of the mineralized and non-mineralized bone in renal failure were lacking until Garner and Ball (1966) reported their findings in 42 controls and in 18 selected cases of azotaemic renal osteodystrophy using a pointcounting technique to study undecalcified sections of iliac crest. As a basis for our quantitative observations in renal failure we have similarly studied the 83

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Section: Discussionmentioning

confidence: 99%

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

1973

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“…In still fewer instances bone lesions similar in every respect to the osteitis fibrosa of primary hyperparathyroidism have been present. Such cases have been reported by Hubbard and Wentworth (1920-1), Albright et al (1937), and Herbert et al (1941). The renal lesion has varied from case to case.…”

Section: Birminghanmmentioning

confidence: 69%

“…Barr (1932) stated that it was difficult to find cases of metastatic calcification in which a renal element could be excluded. Herbert et al (1941) collected 19 cases of metastatic calcification from thp literature, and 16 of these were-associated with gross renal disease. In 11 of these 16 there was evidence of parathyroid hyperplasia, and in only one case was parathyroid hyperplasia definitely excluded.…”

Section: Birminghanmmentioning

confidence: 99%

Chronic Renal Disease with Secondary Hyperparathyroidism

Richards¹

1951

BMJ

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“…Chronic renal failure is almost always associated with metastatic calcification of some degree. The aetiology of this widespread metastatic calcification is undoubtedly multifactoral, but it has always been considered that a high calcium-phosphorus product in the peripheral blood is the most important factor (Logan, 1940;Berlyne and Shaw, 1967;Herbert, Miller and Richardson, 1941). The plasma phosphate level in uraemia may vary over a much wider range than the plasma calcium, and consequently hyperphosphataemia is probably the most important single factor leading to metastatic calcification in these patients (Parfitt 1969).…”

Section: Discussionmentioning

confidence: 99%

Tumoral calcinosis: a manifestation of extreme metastatic calcification occurring with 1, alpha-hydroxycholecalciferol therapy

Walker

Davison²,

McLachlan

1977

Postgraduate Medical Journal

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SummaryTwo cases are reviewed, both of which developed tumoral calcinosis whilst receiving 1, a-hydroxycholecalciferol therapy. Tumoral calcinosis is an extreme form of peri-articular calcification, and its occurrence in patients with chronic renal failure is unusual. These peri-articular masses developed around the shoulders in both patients, and the action of 1, ahydroxycholecalciferol as a possible factor promoting this form of metastatic calcification is discussed.

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Chronic renal disease, secondary parathyroid hyperplasia, decalcification of bone and metastatic calcification

Cited by 57 publications

References 25 publications

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

Azotaemic renal osteodystrophy: a quantitative study on iliac bone

Chronic Renal Disease with Secondary Hyperparathyroidism

Tumoral calcinosis: a manifestation of extreme metastatic calcification occurring with 1, alpha-hydroxycholecalciferol therapy

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