Electrolyte Composition


Sodium is the main cation of the extracellular fluid and, during dialysis, is removed from the body by both diffusion and convection. As dialysis evolved, there has been considerable interest in adjusting the sodium levels in the dialysis fluid largely to improve patient tolerance to the dialysis procedure. Sodium levels in the dialysis fluid may be considered as 'hyponatraemic' hypernatrae-mic' or 'isonatraemic' [6], with current technology, the levels no longer need to be constant throughout treatment [7].

In clinical practice the use of hyponatraemic dialysis fluid (sodium concentration 130-135 mmol/l) has declined and should be avoided as secondary to the loss of sodium by diffusion, there is a decrease in plasma osmolar-ity resulting in cellular over-hydration which contributes to disequilibrium syndrome (fatigue, 'washed-out' feeling, muscle cramps, headache, neurological symptoms), and intradialytic hypotension. For the majority of patients a hypernatraemic dialysis fluid (sodium concentration 140145 mmol/l) is used to avoid excessive sodium losses arising from ultrafiltration and to prevent cardiovascular in stability during treatment. The use of such sodium levels has drawbacks, namely that it can result in sodium gain, contribute to the development of hypertension, trigger thirst causing a high water intake in the interdialytic interval, which requires the use of high ultrafiltration rates during treatment resulting in hypotensive episodes. The hypotension induced may prevent dry body weight achievement and prompt the dialysis staff to administer hypertonic saline, thereby contributing to the progression of cardiac failure and/or pulmonary oedema.

Isonatraemic dialysis fluid requires the dialysis fluid sodium level to be matched to that of the sodium in plasma water, and the calculation of sodium balance using a mathematical model. Due to practical difficulties this approach has only seen experimental application.

The manipulation of the dialysis fluid sodium concentration or conductivity either alone or in combination with profiling of the fluid removal rate during treatment (to modulate vascular refilling) has been widely applied to improve blood volume preservation, and reduce hypoten-sive episodes during treatment. Whilst such an approach improves refill from both the intracellular and interstitial spaces to the intravascular compartment, the high dialysis fluid sodium levels used reduce dialytic removal of sodium and can result in a sodium overload [8].


The current dialysate calcium level has been arrived at over time in conjunction with the evolution of other aspects of calcium metabolism in this population. In the 1960s, the constituents of the dialysate were arbitrarily determined to best match normal serum levels. Because of impaired calcium absorption with resultant hypocal-caemia, it soon became apparent that higher levels of di-alysate calcium could be used to support the serum calcium level. Early studies of parathyroid hormone in the late 1960s showed that these higher dialysate calcium levels of 1.75 mmol/l (3.5 mEq/l) were also associated with lower parathyroid hormone levels.

At this time aluminium-containing compounds were the medication of choice to control phosphate levels, in preference to magnesium- or calcium-containing compounds. With the identification and synthesis of calcitri-ol, the problems of hypocalcaemia were ameliorated and the need for calcium loading via the dialysate lessened. The traditional high calcium dialysate continued to be widely used to maintain a high normal serum calcium using both dialysate and calcitriol in order to maximise parathyroid hormone suppression.

Today many dialysis patients dialyse with dialysis fluid containing 1.5 mmol/l calcium and some use levels of 1.75 mmol/l [9]. Recently, there has been a trend to lower dialysate calcium concentrations because of the frequent occurrence of hypercalcaemia with the use of calcium-containing phosphate binders. Accordingly the current K/DOQI guidelines recommend an absolute maximum elemental calcium load of 2,000 mg/day, including calcium-containing medication and a maximum dialysate calcium concentration of 1.25 mmol/l to avoid intradia-lytic calcium loading.

Calcium ions also play a pivotal role in the contractile process of both vascular smooth muscle cells and cardiac myocytes, and dialysis fluid calcium concentrations affect blood pressure [10]. Low dialysate calcium concentrations, however, expose the patient to the risks of negative calcium balance and increase in parathyroid hormone concentration, particularly if patients are non-compliant with the intake of calcium-containing phosphate binders [11, 12].

The choice of dialysis fluid calcium concentrations for patients undergoing haemodialysis remains a matter of considerable debate. Malberti and Ravani [13] concluded that a dialysis fluid calcium level of 1.5 mmol/l seems to be suitable for the majority of patients on haemodialysis or post-dilution on-line haemodiafiltration. However, Sigrist and McIntyre [14] took a more pragmatic approach and suggested that, even with a dialysis fluid level of 1.25 mmol/l, many patients were experiencing calcium overload contributing to the development of vascular calcification. They suggested that an upper dialysate concentration of 1.25 mmol/l may not be ideal for every patient and that dialysis fluid concentrations should be prescribed with reference to plasma calcium levels. With the availability of calcimimetics, which suppress the secretion of parathyroid hormone by sensitising the parathyroid calcium receptor to serum calcium, further adjustments in the dialysis fluid calcium levels are likely.


Potassium is the most abundant intracellular cation and a major determinant of intracellular osmolality. Hae-modialysis patients are subject to a disturbed potassium homeostasis and are frequently hyperkalaemic.

The removal of potassium during dialysis is via diffusion as the level in dialysis fluid is set lower than in the plasma water. The amount required to be removed during treatment varies between 50 and 100 mmol/l depending on patient dietary compliance, but for stable dialysis patients a dialysate potassium level of 2 mmol/l maintains the plasma levels at <6 mmol/l and avoids post-dialysis hypokalaemia.

Patients with cardiac disease and arrhythmias may require higher potassium levels in the dialysis fluid (33.5 mmol/l) and when using such concentrations, plasma levels should be frequently monitored during treatment as a fall in serum potassium is associated with an increased QT dispersion which is associated with severe ventricular arrhythmias and sudden cardiac death. Amelioration of such a dispersion may be helped by potassium profiling [15, 16].


Normal plasma concentrations of magnesium are between 0.8 and 1.2 mmol/l. In dialysis patients levels may be normal increased or even decreased. Low plasma levels have recently been identified as a possible risk factor for haemodialysis headache [17]. Commercially manufactured concentrates contain magnesium concentrations ranging from 0.25 to 0.75 mmol/l. Magnesium-free concentrate is also available. Normalisation of plasma levels can be achieved by the use of magnesium concentrations of 0.25-0.50 mmol/l. Further adjustment of the dialysis fluid levels may be necessary in patients treated with oral magnesium preparations such as OsvaRen (Fresenius Medical Care AG & Co), the recently approved phosphate-binding agent made from a combination of calcium acetate and magnesium carbonate. The use of zero concentrations should be avoided as their use is associated with severe muscle cramps.


The majority of the chloride in the body is found in the extracellular compartment where it is the main anion with normal plasma levels between 98 and 106 mmol/l. The chloride concentration of commercially produced dialysis fluids varies between 98 and 112 mmol/l and is governed by electrolytes such as sodium, potassium, calcium and magnesium levels in the dialysis fluid since they are present in the form of chloride salts.

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