Hyperoxaluria

Definition > 40 mg / day.

Small amount is dietary – vast majority is by-product of metabolism.

 

Primary hyperoxaluria

Congenital, rare. Deficiency of liver enzyme AGT.

 

Enteric hyperoxaluria

Chronic diarrhoeal states / bariatric surgery

Fat malabsorption -> saponification of fatty acids with available cations (calcium and magnesium)

Less calcium for calcium oxalate complexation, more oxalate available to reabsorbed

 

Dietary hyperoxaluria

Cola, nuts, chocolate, brewed tea, spinach, potatoes, beets and rhubarb

Vitamin C is a pre-cursor for oxalate metabolism – excessive vitamin C supplementation can lead to significant hyperoxaluria (vitamin C itself also upregulates oxalate absorption).

 

Oxalate absorption from the gut is dependent on:

1. Complexing with cations (calcium and magnesium) in the gut -> less oxalate absorbed and then excreted in urine
   1. Low calcium diet -> less calcium to bind to oxalate -> more free oxalate absorbed and excreted in urine
   2. Malabsorption of fats -> fats preferentially bind to calcium/magnesium -> more free oxalate absorbed and excreted
2. Oxalate-degrading bacteria in urine
   1. Oxalobacter formigenes metabolise oxalate in the gut, meaning less oxalate is absorbed and excreted in urine

 

 

Treatment of hyperoxaluria:

• Primary hyperoxaluria – treated with pyridoxine, renal physician management as leads to ESRF
• Low oxalate diet
• Stop vitamin C supplementation
• Reduce dietary fat
• Dietary calcium and magnesium supplementation to bond with oxalate in the gut
  • Calcium citrate may have dual effect
  • Give with meals
• Alkaline citrates (potassium citrate) may help calcium oxalate stone formation