Metabolic acidosis is a typical concern in renal populations, including renal transplant recipients (RTRs). The role of nutrition on metabolic acidosis has often been studied in different populations with renal insufficiency, but data specifically addressing nutrition and metabolic acidosis in RTR populations have been lacking.

Thus, a group of researchers from the Netherlands recently published an observational study on this topic (Clin J Am Soc Nephrol 2012; published online ahead of print). A cohort of 707 RTRs was recruited for the study. Researchers collected dietary intake data from 625 of these patients. They used a food frequency questionnaire to assess intake, and results related to 177 different food choices were recorded as the number of times a particular defined serving was consumed per day, week, or month. 

The results were validated by comparing the estimated protein intake with 24-hour urinary urea excretion. The validity was further assessed by analyzing the three-day food records of a subgroup of 60 patients. Dietary acid load was assessed using two formulas, the potential renal acid load (PRAL) and the estimated net endogenous acid production (NEAP).

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Net acid excretion

In all, 31% of the patients exhibited metabolic acidosis, and nearly half had a pH less than 7.35. The mean net acid excretion (NAE) was 40.7 mEq/day (range 22.2 – 60.0 mEq/d) and was positively associated with eGFR; urinary excretion of ammonia, phosphorus, sulfate, and titratable acid; use of mycophenolate; and serum chloride. NAE was negatively associated with serum and urine pH and bicarbonate, time since transplantation, and use of azathioprine. 

After adjustment, NAE, PRAL, and NEAP were all inversely associated with both serum bicarbonate and serum pH. The associations between NAE and serum pH and bicarbonate were significant regardless of whether the patients exhibited metabolic acidosis. NAE was also negatively associated with cholesterol and serum phosphate. NAE was positively associated with cheese intake and negatively associated with fruit intake. Regarding specific nutrients, NAE was positively associated with total protein, animal protein, phosphorus, and calcium.

Dietary choices and acid-base balance

Although these results are observational, there appears to be a strong correlation between the dietary choices that RTRs make and overall acid-base balance. This association has been found in the general population as well as CKD populations, and prior studies have indicated that reducing dietary load can provide positive benefits for long-term kidney health. 

The authors of the paper went on to mention that, based on their models, consuming 100 g (3.5 oz) of vegetables and 100 g (3.5 oz) of fruit while eliminated 50 g of meat (1.8 oz) and 20 g of cheese (0.7 oz) could reduce NAE by 15 mEq/day, resulting in a serum bicarbonate increase of 0.5 mmol/L. This change could theoretically lead to a 5% reduction in the metabolic acidosis prevalence. For RTRs, protein intake for stable patients should follow general guidelines of approximately 0.8 g/kg body weight. Long-term studies are needed to assess whether the general protein recommendation is adequate, but keeping protein at 0.8 g/kg body weight/day helps avoid possible negative nitrogen balance if graft rejection occurs, but also helps preserve residual renal function by avoiding excess protein intake.

The first and third tertile ranges for estimated glomerular filtration rate (eGFR) in this study were 48 and 56 mL/min/1.73 m2, respectively. Thus, many of these patients would benefit from avoiding excessive animal protein intake, especially from cheese sources, to ensure prolonged kidney function. (Note: If graft rejection occurs, a protein intake of 1.4 g/kg bodyweight/day is recommended, similar to that within four weeks post-transplant). Of note, dairy products typically have high phosphorus content, which, in addition to contributing an acidotic effect, may be a risk for cardiovascular health should serum phosphorus be elevated.

Increased intake of fruits and vegetables can be of benefit in helping reduce metabolic acidosis. This effect is typically achieved through the intake of alkaline salts such as citrate. These salts are often bound with electrolytes such as potassium, calcium, and magnesium. Meanwhile, the contributions of phosphate salts and sulfur-containing amino acids often contribute to an acidotic effect in the body.

Elevated potassium levels

For some CKD patients, potassium levels may be elevated and thus a restriction on high potassium items like fruit and vegetables may be necessary. This restriction may also reduce the potential intake of alkalinizing anions like citrate and potentially increase the risks for acidosis. As noted, the eGFR’s for the RTRs in this cohort ranged from 48-56. Patients with this level of renal function will not often have trouble with high potassium levels. Consequently, this population most likely will be able to safely consume higher intakes of fruits and vegetables to help reduce the risks of metabolic acidosis.