Haemodynamic Consequences of Changing Potassium Concentrations in Haemodialysis Fluids

INTRODUCTION:

Potassium is the most abundant cation in the body (35-40 mmol/kg in haemodialysis patients [1]), although only 2% of the pool is located extracellularly [2]. Whereas, on a short-term basis, serum potassium is regulated by the shift of potassium between the intracellular and the extracellular compartment by insulin, cathecolamines, acid-base balance, and osmolarity; kidneys are responsible for long-term potassium homeostasis [2]. Patients with end-stage renal disease are at high risk of hyperkalaemia [3-6], which may present itself as generalised weakness, paralysis, and cardiac arrhythmia [2]. Recovering potassium homeostasis is thus an important objective of dialysis. Still, considering that its location is mainly intracellular, which connects to the pharmacological concept of great distribution volume, its removal during a haemodialysis session is quantitatively modest (between 40 and 80 mmol corresponding to 1-2% of total body potassium) [1]. As a consequence, even if, in order to be suitable, potassium removal during dialysis should be equal to the amount accumulated during the inter-dialytic phase, in clinical practice the potassium concentration in the dialysate is usually adjusted with the suboptimal goal of avoiding pre-dialysis hyperkalaemia [7].

The importance of the body content and serum concentration of potassium to control blood pressure remains controversial. Epidemiological data suggest a role for potassium depletion as a co-factor in the development and severity of hypertension, while dietary potassium inversely correlates with blood pressure [8-10]. In animal models, an acute increase in serum potassium concentration produces vasodilatation mediated by the vascular endothelium; the opposite effect is observed if it decreases [11,12]. In haemodialysis, the extent of the difference between serum potassium and the potassium concentration in the dialysis fluid is directly correlated to an increase in blood pressure at the end of the dialysis session, producing what has been named "rebound hypertension" [1]. In this same study no significant changes in blood pressure were found during the dialysis.

In haemodialysis the nephrologists are faced with sudden changes in blood pressure and haemodynamic fragility phases that have a multi-factorial origin; ultrafiltration, decrease in osmolarity with imbalance and correction of metabolic acidosis play a predominant role [13-19]. Despite this, and thanks to some artifices, with particular reference to calcium concentration in the dialysate [15], dialysate temperature [20] and ultrafiltration and sodium concentration profiles [18,21-24], pressure stability is guaranteed as a general rule. Some electrolytes, particularly sodium and bicarbonate, can be modulated in profiles with the purpose of better respecting the gap in osmolarity or concentration that is established during the haemodialysis session, but their haemodynamic effect still remains controversial [20,22,24].

Serum potassium is an electrolyte whose concentration - in order to guarantee a negative balance - varies rapidly and significantly during dialysis, frequently resulting in going from pre-dialysis hyperpotassaemia to intra-dialysis hypopotassaemia. As mentioned above, in Dolson's study [1], differences in dialyses blood pressure were not found between the groups treated with dialysates containing 1, 2 or 3 mmol/l of potassium, but at the end of the dialyses those patients treated with the lower potassium concentrations showed what was called a "rebound hypertension".