Lactate or bicarbonate in dialysis fluid for daily home hemodialysis: advantages and disadvantages

Abstract

The availability since the beginning of the 20th century of hemodialysis monitors similar to the cyclers used for automated peritoneal dialysis (space-saving and easy-to-handle monitors using a low volume of dialysis fluid and suitable for daily dialysis) has led to renewed interest in home hemodialysis. As in peritoneal dialysis, these cyclers use either lactate - an anion whose metabolism leads to bicarbonate regeneration - or bicarbonate in the dialysate. The purpose of this article is to review the advantages and disadvantages of these two types of alkalinizing anion. Whichever type of anion is used, it is important to avoid over-alkalinization of the patient. Lactate dialysate, which is less expensive and easier to handle, seems to be suitable for most patients, but its use in patients with abnormal liver function should be discouraged.

Introduction

Under normal dietary conditions and as a result of nutrient metabolism, the body is continuously subjected to an acid load:

- volatile acid load due to carbon dioxide (CO₂), mainly from aerobic glucose metabolism: carbon dioxide is present in the body in dissolved form, behaving like a weak acid (partially dissociated acid). This acid is volatile, as it is eliminated by the lungs in the form of carbon dioxide.

- load in non-volatile acids (called fixed acids) which behave like strong acids (totally dissociated at the body’s pH). The load of fixed mineral acids (mainly sulfuric acid from amino acid metabolism, but also acids from the diet) is around 1 mEq per day per kg of body weight and is normally eliminated by the kidneys. The load of fixed organic acids (lactic acid, pyruvic acid, etc.) from carbohydrate and lipid metabolism is much higher but does not affect the acid-base balance because the corresponding anion (lactate, pyruvate, acetate, citrate, etc.) is metabolizable and alkalinizing: indeed, the metabolism of these anions (consuming oxygen), which takes place mainly in the liver and muscle, leads to the appearance of bicarbonate, which takes over the H+ ions provided by these acids.

As the kidneys of the dialysis patient no longer eliminate the load of fixed mineral acids, this leads to a drop in bicarbonate level (metabolic acidosis). Moreover, dialysis is responsible for the loss of alkalizing organic anions not present in the dialysate, which exacerbates metabolic acidosis and the drop in bicarbonates.

The dialysis session must be capable of restoring bicarbonatemia. The most logical approach would seem to be to provide the missing bicarbonate using a dialysis fluid with a higher bicarbonate concentration than the patient. As dialysis fluid must also contain divalent ions (calcium and magnesium), which have a strong tendency to precipitate as insoluble calcium and magnesium carbonates, it is necessary to acidify the dialysate to prevent this precipitation.

The method used in the early days of hemodialysis consisted of acidifying the dialysate by dissolving carbon dioxide contained in a cylinder. Since this method was very cumbersome to implement, Charles Mion, then working in Belding Scribner’s team in Seattle, proposed substituting the bicarbonate in the dialysate by acetate, an alkalinizing anion that does not precipitate calcium and magnesium salts[1]. Acetate was also chosen for the same reason during the development of continuous ambulatory peritoneal dialysis (CAPD) using bags of sterile dialysis fluid.

Progressive improvements in access to hemodialysis have made it possible to care for increasingly frail and elderly patients. However, the deleterious effects of acetate often make such treatment impossible. Technological advances have made it possible to manufacture a bicarbonate dialysate extemporaneously, without the need for a CO2 cylinder, and this type of dialysate became increasingly popular in the last two decades of the 20th century[2]. At the same time, acetate was found to be responsible for sclerosing peritonitis in patients treated with CAPD[3]and was replaced by lactate.

At the start of the 21st century, the benefits of short daily hemodialysis are becoming increasingly apparent, both in medical terms and in terms of quality of life. Its main (and perhaps only!) disadvantage is that, when performed in a center, it doubles the time and cost of transport, which are already very high. The development of simplified monitors to promote short daily home hemodialysis is therefore justified. This type of hemodialysis is carried out using low-flow dialysate[4], based on the example of peritoneal dialysis cyclers: space-saving, easy-to-handle monitors, suitable for daily dialysis and requiring only a small volume of dialysis fluid supplied in bags in which the alkalinizing ion is lactate or bicarbonate.

To my knowledge, there are as yet no published studies comparing the use of lactate and bicarbonate in short daily home hemodialysis. That’s why we’ll start with conventional hemodialysis. Although acetate dialysate is virtually no longer used, it will be mentioned in the preamble because acetate is a metabolizable alkalizing ion and, as such, shares properties with lactate. In chronic hemodialysis, there have been far more publications in the literature on acetate dialysate than on lactate dialysate.

Acetate buffered dialysate

The replacement of bicarbonate with acetate in the dialysate results in a significant loss of bicarbonate in the dialysate. A high acetate concentration (35 to 45 mmol/L) is therefore required to compensate for both bicarbonate consumption during the interdialytic period and bicarbonate and inorganic anions loss during the dialysis session. The result is a significant rise in acetatemia (normal: 0.01 to 0.3 mmol/L) during dialysis, which can reach over 4 mmol/L in some patients with particularly slow acetate metabolism[6].

The presence of acetate in the dialysate is responsible for several deleterious effects. The higher the acetate level, the greater the vasodilatation. This vasodilatation leads to a drop in blood pressure despite the increase in heart rate, resulting in hemodynamic instability. The presence of acetate in the dialysate is also responsible for abnormalities in lipid and carbohydrate[7]metabolism as well as stimulation of inflammation (production of TNF and IL1-β), explaining a mild febrile reaction[8][9].

In addition, the loss of dissolved CO₂in the dialysate, due to its absence in the dialysate, induces respiratory alkalosis, as evidenced by the decrease in PCO₂of around 4 mmHg during the session[7]. This respiratory alkalosis explains the maintenance or even slight increase in

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