Acidosis, Metabolic, Decreased or Normal Anion Gap

Key Features

Essentials of Diagnosis

• Decreased HCO₃^– and hyperchloremia (usually) with acidemia

• Normal anion gap acidosis is mainly caused by gastrointestinal HCO₃^– loss or RTA. Urinary anion gap may help distinguish between these causes

General Considerations

• Most common causes

  • Gastrointestinal (GI) HCO₃^– loss

  • Defects in renal acidification (renal tubular acidoses)

• The urinary anion gap can differentiate between these two causes

• Table 21–12 outlines anion gap in metabolic acidosis

Renal tubular acidosis (RTA)

• Hyperchloremic acidosis with a normal anion gap and normal or near normal glomerular filtration rate, in the absence of diarrhea

• Three major types of RTA can be differentiated by the clinical setting: urinary pH, urinary anion gap, serum K⁺ level

• Type I (distal H⁺ secretion defect)

  • Characterized by selective deficiency in H⁺ secretion by alpha intercalated cells in the collecting tubule

  • Enhanced K⁺ excretion occurs probably due to less competition from H⁺ in the distal nephron transport system

  • Develops as a consequence of paraproteinemias, autoimmune disease, and drugs and toxins such as amphotericin

• Type II (proximal HCO₃^– reabsorption defect)

  • Due to a defect in the ability of the proximal tubule to reabsorb filtered HCO₃^–

  • Hypokalemia results when a patient is treated with HCO₃^– without adequate K⁺ supplementation

  • Can exist with other proximal reabsorption defects resulting in glucosuria, aminoaciduria, phosphaturia, and uricosuria (Fanconi syndrome)

  • Causes include plasma cell myeloma and nephrotoxic drugs and carbonic anhydrase inhibitors (acetazolamide)

• Type IV (hyporeninemic hypoaldosteronism)

  • Most common RTA in clinical practice

  • Due to a defect in aldosterone action that impairs distal nephron Na⁺ reabsorption and therefore K⁺ and H⁺ excretion

  • Common causes include diabetic nephropathy and tubulointerstitial renal ...