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Patients on continuous ambulatory peritoneal dialysis (CAPD) were studied for three years. 29 of them who had been on CAPD for six months or more were compared with patients on intermittent peritoneal dialysis (IPD) and on haemodialysis (HD). CAPD patients had significantly higher levels of HDL-cholesterol than HD patients. Urea, potassium, phosphate, and urate levels were significantly lower, and haemoglobin levels significantly higher, than in the IPD and HD groups. 43 CAPD patients studied had a peritonitis rate of 2.22 episodes per patient-year. CAPD offers an alternative form of dialysis to those unsuitable for HD, but until peritonitis rates can be reduced CAPD cannot rival HD as a long-term treatment.

The supplementation of replacement solutions used during plasma exchange with calcium gluconate prevents hypocalcaemic symptoms.

An oral dose of 0.5 microgram of 1,25-dihydroxycholecalciferol (1,25-[OH]2D3) and 4 g of calcium carbonate was given daily to two dialysed patients and three undialysed patients in chronic renal failure with renal osteodystrophy. Treatment was given for 4-16 months. Intestinal calcium absorption became normal in all five patients. Plasma alkaline phosphatase, hydroxyproline, and immunoreactive parathyroid hormone were considerably reduced in all of the patients and in four of them these values were restored to normal. Bone histology was improved in all patients after treatment with 1,25-(OH)2D3. As well as a dramatic improvement in bone mineralisation, there was remodeling of trabecular architecture and a decrease in fibrosis in patients with initial parathyroid overactivity.

Four patients who had been on regular haemodialysis for periods of 3 1/2 to 7 years became hypophosphataemic with plasma-phosphate concentrations of 2.5 mg/dl or less before dialysis. None of them had been taking oral phosphate-binders for 2 years or more. Histologically all the patients had an excess of osteoid on bone biopsy. Intestinal absorption of phosphate and calcium was impaired, despite normal or high serum-25-hydroxycholecaliferol concentrations. Treatment with oral dihydrotachysterol resulted in corrections of the phosphate malabsorption and increases in plasma-phosphate concentration. The initial low plasma-phosphate values in these patients before dialysis probably reflected a state of phosphate depletion caused by the combination of malabsorption, loss during dialysis, and a low dietary intake.

It is hypothesised that chronic progressive kidney disease may be mediated by abnormalities of lipid metabolism. A series of self-perpetuating secondary events follows an initial glomerular injury. Increased glomerular basement membrane permeability leads to loss of lipoprotein lipase activators, resulting in hyperlipidaemia. Circulating low-density lipoprotein binds with glycosaminoglycans in the glomerular basement membrane and increases its permeability. Filtered lipoprotein accumulates in mesangial cells and stimulates them to proliferate and produce excess basement membrane material. The proximal tubular cells metabolise some of the filtered lipoprotein and the remainder are altered on passage down the nephron. Luminal apoprotein precipitates, initiating or aggravating tubulo-interstitial disease, if the intraluminal pH is close to the isoelectric point of the apoprotein. The hypothesis offers new approaches to the study of chronic progressive kidney disease by proposing a major pathogenetic role for lipid abnormalities.