Metabolic acidosis in chronic kidney disease: cause and bicarbonate treatment
As chronic kidney disease (CKD, a long-term loss of kidney function) advances, it can slowly make the blood too acidic, a metabolic acidosis, which oral sodium bicarbonate treats.
Remember
In CKD, fewer nephrons mean less acid is excreted and less new bicarbonate is made, so the buffer is used up. Oral sodium bicarbonate replaces it, and its sodium load can limit the dose.
Healthy kidneys keep the blood at the right pH by passing acid into the urine, largely as ammonium (ammonia carrying acid). They also make new bicarbonate to replace the bicarbonate used up in soaking up the acid that normal metabolism produces. Bicarbonate is the main buffer in the blood, a chemical that soaks up excess acid and so keeps the pH steady.
In CKD there are fewer working nephrons (the tiny filtering and processing units of the kidney). Less ammonium is made, so less acid is excreted and hydrogen ions (the particles that make a fluid acidic) build up. Bicarbonate is used up faster than the kidneys can replace it, so blood bicarbonate falls and the pH drifts down. Blood bicarbonate usually falls only once the glomerular filtration rate (the volume of plasma the kidneys filter each minute) is quite low, although it can fall earlier.
A slow metabolic acidosis follows. Because nephrons are lost gradually, it develops over months or years, so the symptoms (headache, drowsiness, muscle weakness, breathlessness) are vague and it can go unnoticed. It still matters, because untreated acidosis is linked with muscle breakdown, loss of bone mineral and worsening kidney function.
The main treatment is oral sodium bicarbonate, which replaces the buffer that failing kidneys can no longer make enough of. It may reduce the loss of bone mineral and the breakdown of muscle, and may slow the decline in kidney function, but it does not restore lost nephrons. Sodium bicarbonate carries a sodium load that can raise blood pressure, so the dose is increased gradually.
Key facts
- Mechanism
- Fewer nephrons mean less ammonium is made, so less acid is excreted and bicarbonate is consumed.
- Onset
- The acidosis builds slowly, so early symptoms are vague and easily missed.
- Anion gap
- A calculated blood value that helps sort out the cause of a metabolic acidosis; in CKD it can be normal or raised.
- Why treat
- Untreated, the acidosis is linked with muscle breakdown, loss of bone mineral and worsening kidney function.
- Treatment
- Oral sodium bicarbonate is the main treatment, because it replaces the lost bicarbonate buffer.
- Dose limit
- Its sodium load can raise blood pressure, so the dose is increased gradually.
Exam traps
- Lactic acid made by oxygen-starved tissue is a real cause of metabolic acidosis, most seriously in shock, but in CKD the acid builds up slowly because the kidneys cannot excrete it.
- Acid from the diet adds to the load, but healthy kidneys excrete the acid produced by normal metabolism and diet, so the kidney failure rather than the diet is the main cause of the acidosis of CKD.
- Poor ventilation causes carbon dioxide retention, which also lowers blood pH, but that is a respiratory acidosis with a raised carbon dioxide level; the acidosis of chronic kidney disease is metabolic, with a low bicarbonate level.
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