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)

The influence of dialyzer geometry on blood coagulation and biocompatibility.

The influence of dialyzer geometry on blood coagulation, heparin requirement and complement activation was studied in fourteen chronic hemodialysis patients. Each patient was dialyzed with two different cuprophan dialyzers, hollow fiber GF 120M and parallel plate Lundia IC5N. Both dialyzers had a wall thickness of 11 microns, surface area of 1.2 m2 and both were sterilized with ethylene oxide. Heparin doses were individually titrated. The mean heparin dose was 6089 +/- 988 U. Platelet count decreased from 218 x 10(9)/l to 193 x 10(9)/l and from 235 x 10(9)/l to 197 x 10(9)/l respectively (hollow fiber/plate dialyzer, ns). The number of leucocytes decreased at 15 min after start of dialysis by 56% and 61% (hollow fiber/plate dialyzer, ns). The heparin requirement, measured as prolongation of whole blood activated coagulation time after identical doses of heparin, were the same in hollow fiber and plate dialysis sessions. The arterial fibrinopeptide A concentrations increased during dialysis from 5.4 to 7.1 nmol/l and 8.5 to 9.6 nmol/l respectively (hollow fiber/plate dialyzer, ns). The residual blood volume in the hollow fiber dialyzers was 1.3 +/- 1.1 ml and in the plate dialyzers 1.5 +/- 0.9 ml (ns). C3a activation, indicated by a marked arterio-venous difference, was observed at 15 min after start of dialysis with hollow fiber as well as plate dialyzers. The arterio-venous difference was less pronounced at the end of dialysis. There were no differences in C3a activation between hollow fiber and plate dialyzers at any timepoint. It is concluded that dialyzer geometry does not significantly influence platelet count, blood coagulation, heparin requirement or complement activation.

Leukocyte overshoot: a new sign of bioincompatibility in fast hemodialysis.

A high blood flow of 400 ml/min induces leukocytosis after 2 hr of dialysis with leukocyte concentrations of 110-150% of predialysis values. The leukocytosis occurs with both low and high biocompatible membranes, such as Cuprophan, Hemophan, and Polyamide. Cuprophan induces the most profound leukopenia, and also induces the most pronounced leukocytosis. For treatments with a given membrane there was, however, no correlation between leukopenia and leukocytosis. Leukopenia was independent of blood flow, while leukocytosis was strongly influenced by this factor. These observations indicate that different factors cause leukopenia and leukocytosis. Although a larger area induced more leukopenia, the effect was small. Membrane area had no effect on leukocytosis. There were no acute clinical side effects during dialysis that could be related to the leukocyte overshoot. The cause and chronic clinical consequences of leukocyte overshoot are unknown.