Mechanism of acidosis | Increased AG | Normal AG |
Increased acid production | Lactic acidosis | |
Ketoacidosis | |
Diabetes mellitus | |
Starvation | |
Alcohol associated | |
Ingestions | |
Methanol | |
Ethylene glycol | |
Aspirin | |
Toluene (if early or if kidney function is impaired) | Toluene ingestion (if late and if kidney function is preserved; due to excretion of sodium and potassium hippurate in the urine) |
Diethylene glycol | |
Propylene glycol | |
D-lactic acidosis | A component of non-AG metabolic acidosis may coexist due to urinary excretion of D-lactate as Na and K salts (which represents potential HCO3) |
Pyroglutamic acid (5-oxoproline) | |
Loss of bicarbonate or bicarbonate precursors | | Diarrhea or other intestinal losses (eg, tube drainage) |
Type 2 (proximal) RTA |
Posttreatment of ketoacidosis |
Carbonic anhydrase inhibitors |
Ureteral diversion (eg, ileal loop) |
Decreased renal acid excretion | Severe kidney dysfunction (eGFR <15 to 20 mL/min/1.73 m2) | Moderate kidney dysfunction (eGFR >15 to 20 mL/min/1.73 m2) |
Type 1 (distal) RTA (hypokalemic) |
Hyperkalemic RTA |
Type 4 RTA (hypoaldosteronism) |
Voltage defect |
Large volume infusion of normal saline | | Diffusion acidosis |