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