Acidose métabolique et insuffisance rénale en réanimation

The kidney plays an essential role in acid-base regulation by reabsorbing the filtered bicarbonate and excreting a net acid load by titrating the phosphate and ammonia buffers present in the urine. Metabolic acidosis is defined by the accumulation of non-volatile acids, resulting from a deficit in urinary acidification, an increased acid generation or acid load, or a digestive or renal bicarbonate loss. The anion gap, which reflects the amount of unmeasured anions in the serum, is increased in anion gap metabolic acidosis but remains normal in hyperchloremic metabolic acidosis. The renal causes of hyperchloremic metabolic acidosis include proximal (type 2), distal (type 1), and hyperkalemic (type 4) renal tubular acidoses, as well as moderate renal failure. Advanced renal failure is associated with a marked decrease in the excretion of organic acids, thereby leading to anion gap metabolic acidosis. Treatment of metabolic acidosis primarily depends on its cause. The administration of sodium bicarbonate is reserved to severe metabolic acidosis (blood pH < 7,20). This treatment may induce extracellular-fluid volume overload and is associated with an increase in the CO2 partial pressure in tissues. © 2003 Éditions scientifiques et médicales Elsevier SAS. Tous droits réservés.