Chapter 4-13: Uremic Acidosis

TEXTBOOK PRESENTATION

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.

DISEASE HIGHLIGHTS

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

TREATMENT

1. NaHCO₃⁻ replacement

2. Hemodialysis