Normal anion gap acidosis (Inorganic acidosis):

Fig. Table showing metabolic acidosis with high and normal anion gaps

Normal anion gap acidosis (Inorganic acidosis):

Here the cause of acidosis in the presence of normal anion gap is the loss of bicarbonate-rich fluid from either kidney or GIT. As bicarbonate is lost, more Cl^- ions are reabsorbed with Na⁺ or K⁺ to maintain electrical neutrality so that hyperchloremia ensues. Normal anion gap acidosis can be divided into hypokalemic and normokalemic acidosis.

Diarrhea: It causes acidosis due to loss of Na⁺, K⁺, and HCO₃^-. As bicarbonate is produced by exocrine pancreas. There is hyperchloremia occurs as response to replacement of lost bicarbonate to maintain electrical balance. This is associated with hypokalaemia.

Renal tubular Acidosis, Type I and II: These is characterized by loss of bicarbonate due to decreased tubular secretion of hydrogen ion (distal or type I RTA) or decreased reabsorption of bicarbonate (Proximal or type II RTA). Since, the major urine-acidifying power of kidney rests in distal tubules, the proximal and distal RTA may be differentiated by measuring urine pH. In proximal RTA, urine pH becomes <5.5, whereas in distal RTA the distal tubules are compromised and urine pH is >5.5. These acidosis are associated with hypokalaemia.

Carbonic anhydrase inhibitors: Acetazolamide is the most commonly used. It is used as diuretic and for Alkalinization of urine in patients with open-angle glaucoma or acute mountain sickness. Inhibition of CA cause wasting of Na, K and HCO₃ in proximal tubule.

Hyperkalaemic Normal AG acidosis (Renal tubular acidosis Type IV): Failure of kidney to synthesize renin, failure of adrenal cortex to secrete aldosterone, and renal tubular resistance to aldosterone are the most common cause of this type of acidosis (Type IV RTA). This inhibits Na reabsorption, and both K and H are thus abnormally retained. The result is decreased renal ammonia formation and therefore decreased elimination of H.