Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android


Typically, patients with chronic kidney disease have low HCO3 levels, high creatinine levels (often > 4–5 mg/dL), and elevated BUN and phosphate levels. Patients often complain of a variety of constitutional symptoms secondary to their kidney disease, including fatigue, nausea, vomiting, anorexia, and pruritus.


  1. Pathophysiology

    1. Each day, ingested nonvolatile acids neutralize HCO3.

    2. In health, the kidneys regenerate the HCO3 and maintain the acid-base equilibrium.

    3. Kidney impairment results in failed HCO3 regeneration and a metabolic acidosis.

  2. Acidosis in patients with kidney disease may be of the anion gap type or nonanion gap type.

    1. In early kidney disease, ammonia-genesis is impaired, resulting in reduced acid secretion and a nonanion gap metabolic acidosis.

    2. In more advanced chronic kidney disease, the kidney remains unable to excrete the daily acid load and also becomes unable to excrete anions such as sulfates, phosphates, and urate. Therefore, an anion gap acidosis develops. HCO3 levels stabilize between 12 mEq/L and 20 mEq/L.

  3. The acidosis has several adverse effects.

    1. Increased calcium loss from bone

    2. Increased skeletal muscle breakdown


  1. NaHCO3 replacement

  2. Hemodialysis

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.