Cytogenetic analyses reveal "atypical cells" in the peritoneal dialysis effluent.

Cytogenetic analyses were performed on dividing cells from the peritoneal effluent of 26 patients undergoing chronic peritoneal dialysis (CPD). Numerical and structural abnormalities of karyotype served as the diagnostic criteria for "atypical cells." The following cytogenetic abnormalities were observed in 7 patients: hyperdiploidy (in 6 patients), hypodiploidy (in 2 patients), and marker chromosomes (in 2 patients). In 3 patients more than one chromosome abnormality was present. Dividing cells with normal mitoses were observed in 11 patients, while in the remaining 8 patients no dividing cells could be found. There were no differences in age, sex, duration of dialysis, and peritonitis incidence between patients with pathological mitoses and those without it. The question whether this unexpected finding is a consequence of immunosuppressed uremic status, dialysis procedure, or some other factor remains to be elucidated.

[The effect of hyperprolactinemia on biohumoral parameters of bone metabolism in women of reproductive age on chronic hemodialysis]. / Uticaj hiperprolaktinemije na biohumoralne parametre metabolizma kosti kod zena reprodukcionog doba na hronicnoj hemodijalizi.

The study was carried out on a group of 20 women in reproductive age on chronic haemodialysis and on a control group of 11 healthy women. The women on a regular haemodialysis were divided into two subgroups: normoprolactinaemic and hyperprolactinaemic. The following parameters of bone metabolic changes were studied: serum calcium, phosphorus, alkaline phosphatase, pharathormon, osteocalcin, calcitonin, and also LH, FSH, prolactin and estradiol. The values of serum Ca, P, AP, PTH, CTC, OS and of LH and FSH were significantly higher in women on haemodialysis. The hyperprolactinaemic women on haemodialysis had lower values of bone metabolic parameters than normoprolactinaemic women. Hyperprolactinaemia did not significantly contribute to acceleration of bone metabolic changes which were already very accelerated due of secondary hyperparathyroidism.