Correcting metabolic acidosis leads to an increase in dietary protein intake in patients with established chronic kidney disease

Abstract

Background: Metabolic acidosis is a feature of chronic kidney disease (CKD) due to the reduced capacity of the kidney to synthesize ammonia and excrete hydrogen ions. It is identified by low plasma bicarbonate levels on routine blood testing. The literature suggests that correction of metabolic acidosis using sodium bicarbonate tablets can reduce protein degradation, reduce amino acid oxidation, reduce inflammation and increase albumin synthesis (Brady & Hasbargen, 1998). The evidence of the benefits and the risks of correcting metabolic acidosis are limited with no randomized controlled trials (RCTs) in pre-dialysis patients (Roderick et al., 2007). Metabolic acidosis has been associated with protein-energy malnutrition and it has been questioned if acidosis plays a part in reducing appetite leading to a reduction in energy and protein intake. The aim of the project was to determine the effects of the correction of chronic metabolic acidosis on energy and protein and kilocalorie intake in patients with established CKD. Method: The project was an observational, prospective study involving seven pre-dialysis subjects recruited from nephrology review clinics. Participants were invited to take part in the project on identification of acidosis with a bicarbonate level of <22 mM during a 6 months recruitment period. A power calculation was not deemed necessary for this initial pilot study. No medical conditions were excluded from the project. Three participants failed to return their diaries and were withdrawn from the project. Sodium bicarbonate tablets were given to correct acidosis at the clinic. A 5 day food diary was issued at the first nephrology review along with five questions on appetite. Participants self reported their appetite status using a scale of 1–4 (very good, good, fair and poor respectively). A further diary was given at their subsequent review appointment. Blood biochemistry, anthropometric measurements, blood pressures and diary analysis were completed at each review. Energy and protein intakes were assessed using DietPlan6; dietary analysis software package. Any difference between the energy and protein intake means were determined using SPSS statistical software package and scores for appetite were assessed. Difference in energy and protein intake was assessed using t-tests, statistical significant assessed at P < 0.05. Ethical approval was obtained from the Lancashire and Cumbria Ethical Committee. Results: Results of the paired t-test statistical testing for the variables using 95% confidence. Variable Mean Difference SD Difference t Significance 2-tailed *No changes seen in appetite scores. Weight (Kg) 1.48 1.93 1.88 0.119 eGFR (mls per min per sa) -0.86 2.91 -0.78 0.466 Dialystolic BP (mmHg) 9.71 11.03 2.09 0.081 Systolic BP (mmHg) -4.29 12.58 -0.90 0.402 Energy (kilocalories) 175 236 1.96 0.098 Protein (g) 7.3 7.07 2.73 0.034 Discussion: The project supports earlier studies which suggest that bicarbonate supplementation can increase protein intake, which in turn can have beneficial effects on the nutritional status of people with CKD. The study looked at a very small group of individuals therefore strong conclusions cannot be made due to the limiting amount of data retrieved. Plasma bicarbonate levels increased in all seven participants indicating compliance with the medication. Using a scoring system for appetite changes is difficult to detect small changes and no treatment blinding was possible in this project. Further research on the health effects of chronic metabolic acidosis are needed to determine the level of bicarbonate needed for optimal health. Conclusion: The results of the project suggest that correcting metabolic acidosis can improve dietary protein intake and nutritional parameters in CKD without causing any detrimental effects to health.