The kidneys play a major role in the regulation of acid-base balance by reabsorbing bicarbonate filtered by the glomeruli and excreting titratable acids and ammonia into the urine. In CKD, with declining kidney function, acid retention and metabolic acidosis occur, but the extent of acid retention depends not only on the degree of kidney impairment but also on the dietary acid load. Acid retention can occur even when the serum bicarbonate level is apparently normal. With reduced kidney function, acid transport processes in the surviving nephrons are augmented but as disease progresses ammonia excretion and, in some individuals, the ability to reabsorb bicarbonate falls, whereas titratable acid excretion is preserved until kidney function is severely impaired. Urinary ammonia levels are used to gauge the renal response to acid loads and are best assessed by direct measurement of urinary ammonia levels rather than by indirect assessments. In individuals with acidosis from CKD, an inappropriately low degree of ammonia excretion points to the pathogenic role of impaired urinary acid excretion. The presence of a normal bicarbonate level in CKD complicates the interpretation of the urinary ammonia excretion as such individuals could be in acid-base balance or could be retaining acid without manifesting a low bicarbonate level. At this time, the decision to give bicarbonate supplementation in CKD is reserved for those with a bicarbonate level of 22 mEq/L, but because of potential harm of overtreatment, supplementation should be adjusted to maintain a bicarbonate level of <26 mEq/L.
Keywords: Acid-base equilibrium; Acidosis; Ammonia metabolism; Bicarbonates; Renal insufficiency.
Published by Elsevier Inc.