Metabolic acidosis is a major risk factor of kidney disease progression as a consequence of impaired H+ urinary excretion by the decreased kidney NH3 synthesis. Two key enzymes participate: a) Phosphate-dependent glutaminase under the genomic control of metabolic acidosis and b) Phosphate independent glutaminase localized on proximal tubule microvili under the nongenomic control. Two types of kidney disease metabolic acidoses are dominant: a) Hyperchloremic metabolic acidosis usually on the basis of hereditary or toxic alterations, isolated or as a part of Fanconi syndrome. b) Hyperphosphatemic metabolic acidosis of renal insufficiency. Metabolic acidosis shares serious consequences: metabolic acidosis increases protein catabolism of amino acids, inhibits proteosynthesis (albumin!), accelerates renal osteodystrophy development, modulates calcidiol and parathormone plasma levels and evokes insulin resistance. The present therapy requires full correction of metabolic acidosis!

Keywords: Acidosis, Renal Tubular /complications/; Glutamine /physiology/; Humans; Kidney /physiopathology/