Four hundred and eighty CAPD and 373 HD patients started regular dialysis treatment between 1981 and 1987 in 6 dialysis centers. The CAPD patients were 6 years older, on average, than the HD patients and had more complicating conditions (43.3% with 3 or more coexisting risk factors versus 28.9% with coexisting complications). The 7-year patient survival rate was not significantly different. Cox's proportional hazards regression showed that age, cardiovascular disease, cerebrovasculardisease, peripheral vasculardisease, diabetes, malignancy and multisystem disease had significant adverse effects on patient survival. After correcting for the influence of these factors, no significant differences in patient survival were seen. However, after 53.5 years of age, the increase in the risk of death was significantly higher in HD than in CAPD patients. Technique survival was significantly different in the 6 centers and was better for HD than for CAPD. There was no statistically significant difference between CAPD and HD technique survival when peritonitis was eliminated as a cause of failure. Based on this 7 year analysis, CAPD would appear to be an excellent alternative to HD.

Renal lesions of a new case of lecithin-cholesterol acyltransferase deficiency in an 18-year-old male are described. Large mesangial deposits and a sieve-like transformation of the peripheral basement membrane were the main glomerular lesions. Immunofluorescence identified C3 deposits in the mesangium. A heterogeneous pattern of ultrastructural findings was observed by electron microscopy. Thread-like structures with faint cross-striation and irregular tubular structures embedded in an amorphous material were found in mesangial and subepithelial sites. Mesangial areas and peripheral basement membranes showed irregular holes sometimes containing highly osmiophilic lamellar bodies. It is suggested that many mechanisms may be involved in the production of renal lesions induced by the lipoprotein abnormalities characteristic of the disease.

No abstract

Recently the possible storage of dextran-related material in patients undergoing regular haemodialysis has been suggested. We examined biopsy and autopsy specimens of 32 patients treated with regular haemodialysis for 61 +/- 34 months. All patients received dextran-40 as a plasma expander because of hypotension during haemodialysis. The same study was carried out in a control group of 11 haemodialysed patients who were given other plasma expanders. In the 11 patients who received larger doses of dextran-40 (0.38 g/kg body weight per week) we found particles in the cytoplasm of macrophages in various organs, which proved PAS positive and diastase resistant on light microscopy, and birefringent on polarisation. Electron microscopy revealed a fibrillar structure, but ionic analysis by electronic sampler on scanning electron microscopy excluded the presence of silicon. No intracellular inclusions were observed in the control group, nor in the patients given dextran-40 in doses lower than 0.08 g/kg body weight per week. As we also found a linear relationship between the number of particles and the dextran-40 doses given, we hypothesise that the material demonstrated in the macrophages is a structurally modified dextran.

Mixed-type cryoproteins, consisting of IgG and IgM, were demonstrated in the sera of four sisters. While the IgG component was polyclonal in every instance, in two of them the IgM component was found to be monoclonal with type κ light chains. Clinical diagnoses included the purpura-weakness-arthralgias syndrome, posthepatitis cirrhosis, congestive heart failure and mitral stenosis. The cryocrit differed in the four sisters, ranging from 3 to 16%; in addition, rheumatoid factor activity was consistently associated with both washed cryoprecipitates and their isolated IgM components. Endomembraneous deposits of IgG and IgM were revealed by immunofluorescent studies of the renal biopsy specimen from one patient. A genetic abnormality, possibly of the autosomal recessive type, is suggested in this instance of familial cryoglobulinemia.