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Bone disease in renal failure. Clinical and histomorphometric studies.

The purpose of the present investigation was to study various aspects of renal bone disease in patients treated at a centre with a low general incidence of symptomatic renal osteodystrophy. In a study of signs of progressive secondary hyperparathyroidism (HPT) in a random sample of patients with chronic renal disease, symptomatic bone disease occurred only in transplanted patients with osteonecroses of major joints. Biochemical and radiographic signs of severe progressive HPT were comparatively infrequent. Hypercalcaemia was the major indication for parathyroid surgery. Normocalcaemic patients on haemodialysis (HD) investigated with dynamic bone histomorphometry showed normal mean bone formation rates. Serum PTH was a major determinant of bone remodelling activity. Histochemical evidence of bone aluminium accumulation was found in the majority, and the trabecular surface extent of aluminium was directly related to indices of defective mineralization. Long-term continuous ambulatory peritoneal dialysis (CAPD) was associated with normocalcaemia and acceptable control of hyperphosphataemia. Serum PTH remained high and radiographic evidence of progressive HPT developed in some patients. Histomorphometrical findings, including signs of aluminium accumulation, were similar to those in HD, indicating that CAPD has no specific effect on renal bone disease. Low serum 25-hydroxycholecalciferol in CAPD could not be related to specific findings regarding histomorphometry. Chronic haemofiltration (HF) was associated with a high risk of calcium loss and hypocalcaemia. Despite decreasing serum calcium serum PTH decreased, and bone biopsy findings indicated decreased skeletal effects of PTH as a further cause of hypocalcaemia. Bone histomorphometry also showed the development of a progressive mineralization defect probably related to calcium deficiency, while trabecular bone aluminium decreased in all patients during HF.