Abstract
Metabolic acidosis (MAC) is a constant symptom of chronic kidney disease (CKD) in advanced stages. However, its onset and degree do not depend only on the decrease of glomerular filtration but also on tubular functions.
Therefore, in patients with predominant tubulointerstitial involvement it may already appear in earlier stages of CKD, usually as MAC with normal anion gap. The progressive decrease of glomerular filtration leads to acid retention that develops in a MAC with an increased anion gap.
MAC has many adverse clinical impacts, including the progression of the underlying CKD. The development and degree of MAC in CKD is usually influenced by a combination of several pathophysiological mechanisms and a number of external factors, the most important of them being the diet - the intake and type of proteins - and hydration status.
A correct identification of the factors contributing to MAC determines the therapeutic possibilities of its correction. However, optimal serum concentrations of bicarbonate in conservatively treated patients are still subject to debate.
Opinions are even more divided on the question of optimal serum concentration of bicarbonate before and after dialysis, in particular due to the risk of post-dialysis meta-bolic alkalosis