Hemodialysis (HD) allows the removal of waste products (uremic toxins) and excess fluids from the blood of end-stage
renal disease (ESRD) patients. Waste products are normally removed by diffusion (concentration driven) while excess of
water accumulation in the body is removed by convection through ultra-filtration (pressure driven). Normally due to the
loss of the native kidney functions, an ESRD patient accumulates acid due to metabolism which causes patient’s blood
bicarbonate (HCO−
3 ) level to decrease below physiological range (28–30 molm−3). As a result, metabolic acidosis is present in
most ESRD patients receiving dialysis therapy. In fact, the cardiac function is affected by metabolic acidosis, and symptomatic
hypotension is a major risk factor contributing to high cardiovascular morbidity and mortality in ESRD patients [1–6]. Since
many ESRD patients are in a state of constant metabolic acidosis, HCO−
3 is now used as a buffer in the dialysis fluid (dialysate)
to correct metabolic acidosis in uremic patients. The HCO−
3 buffer consists of carbonic acid/bicarbonate ions and bicarbonate
ion/carbonate ions. The main goal of the buffer is to achieve acid–base correction of patients to the normal physiological
blood HCO−
3 range.