Objective To evaluate the effect of 1.1% amino acid dialysate (A AD) (Nutrineal, Baxter, Castlebar, Ireland) on lipid metabolism in hyperlipidemic patients on continuous ambulatory peritoneal dialysis (CAPD). Design Patients were alternately assigned to receive AAD in the first (group A), or the second (group B), 6 months of a prospective cross-over study. Setting University teaching hospital. Patients Eighteen stable CAPD patients with a serum cholesterol 5.5 mmol/L or greater. Interventions One post prandial exchange of AAD during a 24-hour period for 6 months. Main Outcome Measures A significant change in serum lipid levels. Results Patients in group A (n = 10) received a single daily exchange of AAD in place of their post prandial dextrose exchange for the first 6 months, and then crossed over to the dextrose phase. Patients in group B (n = 8) continued their usual dextrose dialysis for the first 6 months and then crossed over to receive AAD in the latter 6 months. Measurements of serum lipids and lipoproteins along with other biochemical parameters were made at regular intervals. Although a downward trend in mean serum total cholesterol was seen on AAD in group A, no significant change in total cholesterol, low-density lipoprotein cholesterol, or high-density lipoprotein cholesterol was observed in any group. Mean serum triglycerides fell on AAD in both groups, but were not statistically significant. Serum lipoprotein(a) [Lp(a)] and apolipoprotein B were elevated in both groups but did not change on AAD or with time. No change was observed in serum apoprotein A1 levels. Serum Lp(a) was not correlated to dialysate protein excretion. No change in mean serum albumin was observed, in either group, on AAD. KT/V urea, total weekly creatinine clearance, net ultrafiltration, and dialysate protein excretion remained unchanged on AAD. Conclusions The use of A AD, although clinically safe and without side effects, had no effect on the dyslipidem ia in our group of CAPD patients.
SummaryTwo patients with long-standing nephrotic syndrome are described in whom urinary iron losses may have contributed towards an iron deficiency state. Seven other nephrotic patients were also studied. Increased urinary iron excretion was found in six out of nine patients and increased urinary copper excretion in all eight patients in whom it was measured. Trace metal losses in the urine in nephrotics may be important clinically.
Plasma glucose concentrations obtained from blood collected into tubes containing glyceraldehyde, sodium fluoride and potassium oxalate will more closely reflect those of the patient at venepuncture.
Four hundred and six white caucasian patients with diabetes mellitus (243 male, mean age 54 +/- 16 (SD) years) were screened for haemochromatosis. Four patients had a fasting transferrin saturation > 62% and all were HLA A3 positive. Two were probable homozygotes for haemochromatosis and two heterozygotes. Homozygote haemochromatosis prevalence in this diabetic population was therefore 2/406 (0.0049) which is identical to that reported in the general population. These findings do not support a genetic relationship between the two conditions.
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