Two-operator glucose infusion test (GIT2) for vascular access recirculation measurement during hemodialysis.

Vascular access recirculation rate (AR) monitoring is fundamental to guarantee treatment adequacy and to detect access failure early. We have evaluated the GIT2 test to measure AR unaffected by cardio-pulmonary recirculation (CPR), based on a short glucose infusion in place of the bolus and on a two-operator sampling, differently from the classical glucose infusion test (GIT). The GIT2 test is based on four steps: 1) basal (B) glucose arterial sample; 2) 10% glucose infusion for 1 min, by infusion pump at 600 ml/hr; (or 20% at 300 ml/hr); 3) simultaneous sampling at arterial (A) and venous (V) ports, after 35-40 sec from starting the infusion, taking care to avoid blood pump stop during the test; 4) AR=100*((A-B)/(V-B)). In vitro tests by dialysis on a 40 L tank containing a urea solution, with AR volumetrically simulated at 0, 5, 10, 20%, and in vivo comparison of GIT, GIT2 with stop-flow (SF) urea method. Our results have shown in vitro an almost perfect correspondence of SF urea method and a better reliability of GIT2 than GIT. The methylene-blue test has shown that a single color bolus in V reaches the A port after variable time, depending on blood flow and AR, while the continuous infusion determines a steady gradient after about 30". In vivo tests (n=24) show good correspondence between GIT2 (4.37 +/- 3.36) and SF (4.51 +/- 3.62), while GIT data (1.01 +/- 0.51) are significantly underestimated. In conclusion, our preliminary results have evidenced a good reliability of the new test, the continuous infusion causing a steady gradient in V and A that more precisely reflects the AR rate.

Model-based analysis of potassium removal during hemodialysis.

Potassium ion (K(+)) kinetics in intra- and extracellular compartments during dialysis was studied by means of a double-pool computer model, which included potassium-dependent active transport (Na-K-ATPase pump) in 38 patients undergoing chronic hemodialysis. Each patient was treated for 2 weeks with a constant K(+) dialysate concentration (K(+)(CONST) therapy) and afterward for 2 weeks with a time-varying (profiled) K(+) dialysate concentration (K(+)(PROF) therapy). The two therapies induced different levels of K(+) plasma concentration (K(+)(CONST): 3.71 +/- 0.88 mmol/L vs. K(+)(PROF): 3.97 +/- 0.64 mmol/L, time-averaged values, P < 0.01). The computer model was tuned to accurately fit plasmatic K(+) measured in the course and 1 h after K(+)(CONST) and K(+)(PROF) therapies and was then used to simulate the kinetics of intra- and extracellular K(+). Model-based analysis showed that almost all the K(+) removal in the first 90 min of dialysis was derived from the extracellular compartment. The different K(+) time course in the dialysate and the consequently different Na-K pump activity resulted in a different sharing of removed potassium mass at the end of dialysis: 56% +/- 17% from the extracellular compartment in K(+)(PROF) versus 41% +/- 14% in K(+)(CONST). At the end of both therapies, the K(+) distribution was largely unbalanced, and, in the next 3 h, K(+) continued to flow in the extracellular space (about 24 mmol). After rebalancing, about 80% of the K(+) mass that was removed derived from the intracellular compartment. In conclusion, the Na-K pump plays a major role in K(+) apportionment between extracellular and intracellular compartments, and potassium dialysate concentration strongly influences pump activity.