The kidney plays the major role in the maintenance of acid-base balance by reabsorbing the daily filtered load of bicarbonate and generating sufficient base to neutralize the acid produced by metabolism of ingested foodstuffs. Therefore, damage to the kidney caused by chronic kidney disease can be associated with a decrease in kidney ammonium excretion causing net acid excretion to fall below net acid production resulting in a positive acid balance. The acid retention can lead to eubicarbonatemic metabolic acidosis (tissue retention of acid without a change in systemic acid-base balance) or metabolic acidosis with or without acidemia. The acidosis can be associated with muscle wasting, bone disease, hypoalbuminemia, tissue inflammation, progression of chronic kidney disease (CKD), and increased mortality. Administration of base in the form of sodium bicarbonate, or sodium citrate may improve acid base balance and improve cellular function. However, recent large-scale trials have questioned its efficacy in slowing CKD progression, adding complexity to treatment decisions. Evidence that serum bicarbonate concentration >25 mEq/L might be associated with increased cardiovascular disease adds complexity to treatment decisions. Further study is warranted to determine whether sustained correction of CKD-related metabolic acidosis, with meaningful bicarbonate separation between study arms, improves hard clinical outcomes and to identify which patient subgroups derive net benefit.
Kraut et al. (Mon,) studied this question.