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 |
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟