Flanigan Michael J
Nephrology Division, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA.
ASAIO J. 2005 Nov-Dec;51(6):xxxii-xxxv. doi: 10.1097/01.mat.0000187397.85551.0b.
Salt and water are the major components of extracellular fluid, and each patient on dialysis has a unique serum sodium activity that is defended to ensure homeostasis. Dialysate use that does not restore extracellular composition to its equilibrium value results in disequilibrium and affects dialysis discomfort, blood pressure, thirst, and weight gain. When dialysate sodium activity exceeds the dialyzable plasma sodium activity, sodium diffuses from the dialysate into the patient. This results in hypertonicity, cellular dehydration, plasma volume expansion, and hypertension. A dialysate sodium activity below the patient's dialyzable plasma sodium reverses this process. Neither of these situations is desirable. Rather, dialysis should restore homeostasis by reconstituting the extracellular fluid to its desired salt and water content. Because each patient has a unique serum sodium activity, this goal can only be realized by using individualized dialysate sodium prescriptions. Further, because a patient's dialyzable sodium is dynamic and determined by serum chemistry plus dialyzer membrane behavior, the dialysate sodium needed to achieve isonatemic dialysis can only be defined by measuring the dialyzable serum sodium activity during dialysis. Achieving balanced salt and water removal to preserve homeostasis and intracellular tonicity requires automated sensors and feed-back control of dialysate conductivity.