Abstract
The etiology of acid-base disorder in acute kidney injury (AKI) and the mechanism of its correction using continuous renal replacement therapy (CRRT) were analyzed using the Stewart approach. AKI patients exhibited acidemia because of metabolic acidosis. This acidemia was mostly secondary to a decreased strong ion difference apparent, hyperphosphatemia, and elevated strong ion gap (SIG). These acidifying effects were offset by hypoalbuminemia. CRRT corrected the metabolic acidosis in AKI patients by reducing SIG, phosphate, and chloride. CRRT using lactate-buffered fluid resulted in an increase in the plasma lactate level with the lactate load. However, CRRT with bicarbonate-buffered fluid might decrease the plasma lactate level without the lactate load and with the removal of lactate, exerting an alkalizing effect. Moreover, caution is needed because high-volume hemofiltration with lactate-buffered fluid can induce hyperlactatemia, leading to temporally metabolic acidosis.
