In an uncontrolled study, 22 dialysis patients (46 +/- 14 years, duration of dialysis 20 +/- 11 months) were treated with CaCO3 over a period of up to 3 years to lower their serum phosphate. The use of 4.5-9 g CaCO3 daily over a period of 9 months led to a reduction of mean serum phosphate from 2.51 to 1.51 mmol/l in 77% of patients, with a simultaneous increase in mean calcium concentration from 2.23 to 2.47 mmol/l, and an improved control of secondary hyperparathyroidism by reduction in mPTH from 1552 to 1032 pg/ml and in APH activity from 6.25 to 4.55 mumol/s/l. In long-term CaCO3 treatment of up to 3 years, however, a constant effective phosphate reduction could not be achieved. There was a progression (77%) of pre-existing microcalcification and a new appearance (42%) of microcalcification in vessels and soft-tissue areas of the hand. The percentage of patients with soft-tissue calcification increased from 43 to 67% during a treatment period of 3 years. We conclude that CaCO3 alone is not suitable on a long-term basis for phosphate reduction in dialysis patients.

It has recently been shown that beta 2-microglobulin isolated from amyloid deposits in dialysis patients is modified by advanced glycation (AGE). In this context it appeared of interest to examine in a cross-sectional multicentre study whether dialysis-related amyloidosis, as evaluated by X-ray assessment of cysts in the metacarpal bones, was different in diabetic patients on maintenance haemodialysis for more than 5 years time compared with matched non-diabetic controls. We evaluated the hand skeleton of 75 diabetic patients (9 type I, 66 type II; 35 male, 40 female; median age 64 years, range 31-86; median duration of dialysis 7 years, range 5-17). They were compared with 150 patients without diabetes mellitus who were matched for age, gender and duration of dialysis. Hand X-rays were centrally evaluated by one radiologist unaware of the underlying clinical diagnosis. The overall frequency of amyloid cysts was 9/75 (12%) in diabetic patients (95% confidence interval 4.6-19.3%) and 28/150 (19%) in matched controls (95% confidence interval 12.4-24.9%). The results indicate that diabetes mellitus does not confer an increased risk of dialysis-related amyloid cysts. The results are of interest with respect to the mechanism of amyloid formation.

Back pain and a cervicobrachial syndrome, as well as progressive sensory and motor deficits as far as symptoms of paraplegia, developed in two dialysis patients two and five years after the start of dialysis. One was a 60-year-old woman with pyelonephritis, the other a 55-year-old man with glomerulonephritis. There were typical radiological signs of destructive spondylarthropathy (narrowed intervertebral spaces and slippage of the vertebral bodies). The female patient required several operations (spondylothesis and orthothesis) and both patients received daily 10,000 IU vitamin D and 3-4 g calcium carbonate. In the woman the destructive process no longer progressed one year after onset of symptoms, but she still required many analgesics. She died three months later of circulatory failure. The man died four weeks after the onset of symptoms from purulent meningitis. At autopsy only renal fibrous ostitis was still demonstrable. Amyloidosis resulting from an increase in beta 2-microglobulin level were excluded by both histological and immunohistochemical examinations.

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