Calcium Oxalate Stones

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Calcium oxalate is the most common type of kidney calculi not only in IBD patients but also in the general population. However, in the latter, urinary oxalate concentration is often normal and the formation of stones is mainly secondary to the abnormalities in its solubility.

In contrast, the pathogenesis in IBD patients appears to be related to hyperoxaluria combined with fluid depletion. It has been shown that hyperox-aluria is present in two thirds of patients with ileal disease, or those that have had extensive ileal resection [18], and this condition renders these patients more prone to develop calculi. Hyperoxaluria, as demonstrated by Chadwick et al. [15] via the use of C14-labelled oxalate, is the consequence of an increased enteric absorption of dietary oxalate, which is 5 times greater in people with ileal disease compared to control population (30% vs. 6%). Since excessive oxalate is mainly absorbed by colonic mucosa, colectomy or ileostomy patients do not manifest this phenomenon [15, 19, 20]. Enteric hyperoxaluria mainly depends on two mechanisms, both of which are related to bile salt and the consequent fat malabsorption.

The first mechanism regards oxalate solubility. Under normal conditions, oxalate binds with dietary calcium to form insoluble calcium-oxalate, which is eliminated with the faeces. However, the affinity of calcium is higher for fatty acids than for oxalate. Thus, in the presence of malabsorption, calcium is mainly bound by non-absorbed fatty acids and this leads to an indirect augmentation of the soluble oxalate which can be easily absorbed by the colonic mucosa [19, 21]. It has been estimated that hyperoxaluria occurs if steatorrhea exceeds 12-15 g/day [15].

The second mechanism is an increase in permeability of colonic mucosa which is irritated by non-absorbed fatty acid and bile salts [20, 22]. A third described effect of bile salt malabsorption is the inhibition of a bacterium (Oxalobacter formigenes) which normally degrades oxalate in the colon [23-25]. Other factors such as excessive fluid loss, hypomag-nesuria and hypocitruria due to hypokalemia [26], metabolic acidosis, steroid use and prolonged bed rest, predispose to stone formation.


Treatment of urinary stones in IBD patients does not differ from treatment in the general population: extra-corporeal shock wave lithotripsy (ESWL) is the gold standard. When it fails, endoscopic procedures are an option, while open surgery is rarely required [27]. In case of complete persistent obstruction, especially if associated with infection, an immediate decompression with either a ureteral stent or nephrostomy may be necessary.


Whatever the nature of calculi, the mainstay of prevention is maintaining a good hydration and minimising diarrhoea or ostomy output in order to have a urine volume of 1 500-2 000 ml/day. Patients at risk should regularly have urinary measurements of uric acid, oxalate, calcium, citrate, phosphate and pH, to keep them in the proper range.

In the presence of low pH, potassium/sodium citrate (30-60 mEq/day) can be used to alkalinise the

Table 2. Food with high concentration of oxalate




Wheat bran Wild fruits Chocolate Tea Cola urine [28]. Sodium bicarbonate (650 mg x 3/day) is an alternative but this can increase the risk of forming calcium stones [29]. If hyperuricosuria persists despite fluid intake and correction of urinary pH, the patient can start allopurinol (300 mg/day). However, it should be kept in mind that this drug may interact with azathioprine/6MP [30].

Prevention of hyperoxaluria is mainly obtained with diet: avoiding food high in oxalate (see Table 2) may be sufficient, but generally it is more effective to assume a low-fat diet and to substitute fats with medium-chain triglycerides in order to reduce fat malabsorption.

Different cations may be added to bind excessive oxalatum resistant to dietetic measures, but all of them have side effects. In fact, extra calcium (1-2 g/day), which is often necessary in patients with malabsorption, may lead to formation of calcium-phosphate calculi [31]; aluminium may interfere with phosphate absorption, while magnesium can exacerbate diarrhoea, thus minimising its potential benefit. A good oxalate binder is cholestyramine (4-10 g/day) [14]. Still, it may also increase bile salt losses and worsen steatorrhea. To date there is not a single accepted strategy for enteric hyperoxaluria and treatment needs to be personalised on the basis of haema-tological and urinary parameters (see algorithm in Table 3).

Table 3. Treatment of enteric hyperoxaluria as adapted from Pardi et al. [30]

Phase I


Increase fluid intake for urine output of 3 L/day

Low-oxalate diet

Low-fat (50 g/day) diet

Calcium supplementation (1-2 g/day)

Needs monitoring of urinary Ca; potential high risk

of Ca-phosphate stones

Cholestyramine (4 g x 4 day)

May exacerbate steatorrhea

Phase II (if stones recur despite Phase I treatment)

Alkalinisation of urine and citrate supplementation

(K citrate or Na citrate 30 mEq x 4 day)

Mg supplementation

May exacerbate diarrhoea

Allopurinol 300 mg/day (if stone contains uric acid)

Interaction with azathioprine/6MP

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  • Antero J
    What happens with oxalate absorption in chron's diesease?
    10 months ago
  • christopher
    Why does calcium oxalate stones increase in crohns disease?
    6 months ago
  • fiammetta
    Why do people with crohn's disease get calcium oxalate stones?
    1 month ago

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