Isolated abnormality in up to 10 % of calcium stone formers.
Associated with other abnormalities in 20 – 60 % stone formers.
Defined < 320 mg / day.
Important stone inhibitor with multiple mechanisms:
- Complexes with calcium in the urine, reducing urinary calcium saturation
- Directly prevents spontaneous nucleation of calcium oxalate
- Inhibits agglomeration and sedimentation of calcium oxalate crystals
- Prevents heterogenous nucleation by urate on to calcium
- Enhances inhibitory effects of Tamm-Horsfall protein
The primary determinant of urinary citrate excretion is acid-base status.
Metabolic acidosis = reduced urinary citrate levels 2’ to enhanced reabsorption and reduced synthesis
RTA = associated with hypocitraturia.
Carbonic anhydrase inhibitors (topiramate, acetazolamide) – metabolic acidosis and hypocitraturia (and hypercalciuria)
Excess animal protein intake = acid load, resulting in acidosis and hypocitraturia.
Hypokalaemia – intracellular acidosis – may contribute to hypocitraturia. (Thiazides may induce hypokalaemia and subsequent intracellular acidosis and hypocitraturia)
UTIs
Treatment:
- Correction of any underlying metabolic acidosis or stopping offending medication (if on HCT, may need potassium supplementation)
- Potassium citrate
- Sodium bicarbonate
- Citrus supplementation or citrus juices
- General measures (fluid intake most important)
Oral citrate salts are metabolised to bicarbonate in the liver -> alkali load inhibits tubular reabsorption of citrate, increasing citrate levels in urine.