Dialysis dementia.

Dialysis dementia is a unique neurologic complication of renal failure associated with chronic dialysis. While many questions remain about the pathophysiology of the disease, aluminum toxicity is probably the major factor in the pathogenesis of the dementia. Reducing dialysate aluminum levels and minimizing oral aluminum intake has markedly decreased the incidence of the disease. Deferoxamine, a chelating agent, is effective if it is given early; however, chronic use may lead to serious complications, although they are rare.

Comparison between bioactivity and immunoreactivity of serum prolactin in uraemia.

The lactogenic potency of sera from 24 male uraemic patients on regular haemodialysis and 14 control subjects was measured by Nb2 node rat lymphoma cell bioassay, and was compared to serum prolactin levels measured by radioimmunoassay. Sera with immunoreactive growth hormone levels exceeding 5 ng/ml were excluded from comparisons. The uraemic patients had a higher serum immunoreactive prolactin (48.2 +/- 10.5 ng/ml) than controls (13.3 +/- 1.3 ng/ml (P less than 0.01). Similarly the lactogenic potency of uraemic serum was higher than that of the control sera (25.5 +/- 3.9 vs 12.6 +/- 1.4 ng/ml, P less than 0.02). The ratio of immunoreactive serum prolactin to the lactogenic potency of the serum was significantly higher in the uraemic group (1.80 +/- 0.14 vs 1.10 +/- 0.10, P less than 0.01) suggesting decreased bioactivity of prolactin in uraemic serum. To examine whether low molecular weight inhibitory molecules were responsible for this discrepancy, the lactogenic potency of 8 uraemic sera was studied before and after 4 h of dialysis against 1 litre of haemodialysis medium. Two of the eleven sera studied showed a significant increment in lactogenic potency after dialysis (47% and 57%). We conclude that there is a disparity between the bioactive and the immunoreactive serum prolactin concentrations in patients with chronic renal failure and that a dialysable factor may be partly responsible for this discrepancy in some cases.

Pharmacokinetics, protein binding, and predicted extravascular distribution of moxalactam in normal and renal failure subjects.

Ten normal subjects and ten patients with chronic renal failure requiring hemodialysis were given intravenous infusions of moxalactam ranging from 500 mg to 2 g. Serum and urine concentrations were measured for up to 12 h. Renal failure subjects were given doses both during and between hemodialysis treatments. Protein binding of moxalactam in both normal and uremic serum was determined by ultracentrifugation. The serum half-life in normal subjects was 2.1 and 2.3 h for the 1- and 2-g doses, respectively. The half-life of moxalactam in patients with renal failure was 13.9 h on the 500-mg dose and 13.3 h on the 1.0-g dose. During hemodialysis the serum half-life fell to 4.4 and 5.7 h, respectively. Moxalactam protein binding ranged from 52% in normal serum to 36% in renal failure patient serum. Unbound moxalactam appeared to distribute with the entire body water based on the serum pharmacokinetics and antibiotic serum protein binding determined in this study.