Patient related factors leading to slow urea transfer in the body during dialysis.

We studied the trans compartmental speed of urea transfer by comparing concentration changes of blood urea nitrogen to mass changes of urea during 80 dialyses in six patients. The speed of urea transfer was studied as a dependent factor of 15 patient characteristics: age; gender; fluid overload; and pre and post values of and change in pulse and temperature, calcitonin gene related peptide, and mean arterial blood pressure. Concentration changes in blood urea nitrogen were measured as pre and post dialysis urea concentration, the total urea in the body was measured by pre dialysis urea and tritium total body water determinations, and the actual mass of urea removed by collecting all dialysate. As a mean, concentration of blood urea nitrogen fell 54% but the mass urea removed was only 40% for a mean ratio of 1.41. Nine factors were associated with the speed of urea transfer. Patients with fast transfer had more normal fluid balance, a normal pulse rate, body temperature, calcitonin gene related peptide values, and blood pressure both before and after dialysis. The patients with a slower transfer of urea had a lower blood pressure before and after dialysis and a more labile pulse rate and body temperature. Patients with unpredictable urea transfer were the most edematous and had the most labile blood pressure. It is important to know which patients have slow urea transfer. Such patients should not be treated by fast dialysis, and those with the slowest rates may do particularly well on continuous ambulatory peritoneal dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumin metabolism and gastrointestinal loss of protein in chronic renal failure.

The catabolism of albumin labelled with 125I has been studied in 10 patients with advanced renal failure and in 5 with nephrotic syndrome. In 10 patients the gastrointestinal protein loss was studied simultaneously by determing the faecal excretion during 7 days of 51Cr after i.v. administration of 51Cr-labelled chromic chloride. The results were related to a control group in which 12 subjects were studied with respect to albumin catabolism and 17 with respect to the gastrointestinal protein losses. The results showed that: 1) In the two patient groups the means for serum albumin concnetration and the intravascular albumin pool, expressed as g or g/kg b.wt., were significantly decreased compared with those of the control group. 2) The two patient groups had an increased extravascular albumin pool as well as an elevated ration between extra- and intravascular pools. 3) The mean albumin catabolic rate was not increased in the renal insufficiency group, expressed as a percentage of the intravascular pool/24 h or as g/24 h. In the patients with nephrotic syndrome, however, it was significantly increased. 4) The renal insufficiency group had a mean cumulative 51Cr excretion during 7 days of 1.6+/- 0.80% of the given dose, the control group 0.63+/- 0.30%. This difference is highly significant. The patients with nephrotic syndrome did not differ from the control group.

Protein binding of salicylate in uremic and normal plasma.

Protein binding of salicylate was studied by equilibrium dialysis at 37 degrees C in plasma from uremic patients and healthy subjects. The protein binding was considerably lower in the uremic plasma at all salicylate concentrations studied (14 to 1,400 mug/ml). Scatchard plots of the data were computer-analyzed assuming binding to the classes of binding sites. According to this analysis, the binding to the class of primary binding sites was considerably decreased in the uremic plasma. In addition to the effect of the uremic state, the binding was considerably decreased at high therapeutic plasma levels and at low albumin levels. The combined effect of two or three of these factors may lead to unexpectedly high unbound fractions of salicylate, which should be considered in the monitoring of plasma salicylate levels in patients.