The goal of dialysis for patients with chronic renal failure is to restore the composition of the body’s fluid environment toward normal. This is accomplished principally by formulating a dialysate whose constituent concentrations are set to approximate normal values in the body. Over time, by diffusional transfer along
favorable concentration gradients, the concentrations of solutes that were initially increased or decreased tend to be corrected. When an abnormal electrolyte concentration poses immediate danger, the dialysate concentration of that electrolyte can be set at a nonphysiologic level to achieve a more rapid correction. On a more chronic basis the composition of the dialysate can be individually adjusted in order to meet the specific needs of each patient.
Dialysate Composition for Hemodialysis
In the early days of hemodialysis, the dialysate sodium concentration was deliberately set low to avoid problems of chronic volume overload such as hypertension and heart failure. As volume removal became more rapid because of shorter dialysis times, symptomatic hypotension emerged as a common and often disabling problem during dialysis. It soon became apparent that changes in the serum sodium concentration—and more specifically changes in serum osmolality— were contributing to the development of this hemodynamic instability.
A decline in plasma osmolality during regular hemodialysis favors a fluid shift from the extracellular space to the intracellular space, thus exacerbating the volume-depleting effects of dialysis.
With the advent of high-clearance dialyzers and more efficient dialysis techniques, this decline in plasma osmolality becomes more apparent, as solute is removed more rapidly.
Use of dialysate of low sodium concentration would tend further to enhance the intracellular shift of fluid, as plasma tends to become even more hyposmolar consequent to the movement of sodium from
plasma to dialysate. The use of a higher sodium concentration dialysate (>140 mEq/L) has been among the most efficacious and best tolerated therapies for episodic hypotension.
The high sodium concentration prevents a marked decline in the plasma osmolality during dialysis, thus protecting the extracellular volume by minimizing osmotic fluid loss into the cells.
In the early 1960s acetate became the standard dialysate buffer for correcting uremic acidosis and offsetting the diffusive losses of bicarbonate during hemodialysis. Over the next several years reports began to accumulate that linked routine use of acetate with cardiovascular instability and hypotension during
dialysis. As a result, dialysate containing bicarbonate began to re-emerge as the principal dialysate buffer, especially as advances in biotechnology made bicarbonate dialysate less expensive and less cumbersome to use. For the most part, the bicarbonate concentration used consistently in most dialysis centers is 35 mmol/L. Emphasis is now being placed on individually adjusting the dialysate bicarbonate concentration so as to maintain the predialysis tCO2 concentration above 23 mmol/L.
Increasing evidence suggests that correction of chronic acidosis is of clinical benefit in terms of bone metabolism and nutrition.
Dialysis assumes a major role in the maintenance of a normal serum potassium concentration in patients with end-stage renal disease. Excess potassium is removed by using a dialysate with a lower potassium concentration, so that a gradient is achieved that favors movement of potassium. In general, one can expect
only up to 70 to 90 mEq of potassium to be removed during a typical dialysis session. As a result, one should not overestimate the effectiveness of dialysis in the treatment of severe hyperkalemia.
The total amount removed varies considerably and is affected by changes in acid-base status, in tonicity, in glucose and insulin concentration, and in catecholamine activity.
The concentration of calcium in the dialysate has implications for metabolic bone disease and hemodynamic stability. Like the other constituents of the dialysate, the calcium concentration should be tailored to the individual patient. Some data suggest that lowering the dialysate calcium concentration would exacerbate
hemodynamic instability during the dialysis procedure [21]. In this regard, the intradialysis drop in blood pressure noted in patients dialyzed against a low-calcium bath, while statistically significant, is minor in degree. Nevertheless, for patients who are prone to intradialysis hypotension avoiding low calcium dialysate concentration may be of benefit. On the other hand, the use of a lower calcium concentration in the
dialysate allows the use of increased doses of calcium-containing phosphate binders and lessens dependence on binders containing aluminum. In addition, use of 1,25-dihydroxyvitamin D can be liberalized to reduce circulating levels of parathyroid hormone and, thus, the risk of inducing hypercalcemia. With dialysate
calcium concentrations below 1.5 mmol/L, however, patients need close monitoring to ensure that negative calcium balance does not develop and that parathyroid hormone levels remain in an acceptable range.
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