I have a very obese patient with a past history of nephrolithiasis who had
a gastric stapling procedure done about one year ago, and who now has flank
pain and hematuria. There are oxalate crystals present in the urine. Is
there any risk of oxalate stones after this procedure?
Answer by David S. Goldfarb, M.D. (NYU School of
Nephrolithiasis and gastric stapling
There are no reports of enteric hyperoxaluria I can find associated with
gastric stapling. However, it would be worth considering whether changes in
the patient's diet or fluid intake might contribute to calcium oxalate
precipitation. If early satiety for instance results in diminished water or
food intake, perhaps urinary concentration has increased. Dietary changes,
such as a shift towards a high protein intake for example, might contribute
to calciuria. The use of high doses of calcium containing antacids could
contribute to hypercalciuria as well. It is important to point out
however, that since calcium oxalate is present in all urine at
supersaturated concentrations, the presence of calcium oxalate crystals in
the urine is not at all indicative of stone formation or symptomatic
The incidence of stones in patients with inflammatory bowel disease and/or
bowel resection is perhaps twice that of the general population. 69% of
these stones are calcium-containing and 29% composed of uric acid (1). The
proportion with uric acid stones increases in patients with ileostomies.
Approximately five percent of dietary oxalate is absorbed across the
intestinal mucosa and is eliminated unchanged in the urine. Unabsorbed
oxalate occurs in stool, for the most part, complexed with calcium. The
calcium oxalate complex is poorly absorbed and for this reason the
proportion of dietary oxalate absorbed (and excreted in the urine) is
inversely proportional to the level of dietary calcium. Oxalate absorption
is significantly augmented when luminal calcium is reduced by
precipitation. This mechanism is important in diseases associated with
steatorrhea, such as jejunoileal bypass, Crohn's disease, chronic
pancreatitis, ileal resection, and biliary obstruction. Malabsorbed fatty
acids precipitate with luminal calcium leaving dietary oxalate uncomplexed,
soluble, and absorbable.
The reverse also occurs: urinary oxalate excretion decreases when patients
receive low fat diets. Several other factors are important in causing
enteric hyperoxaluria. Patients with ileostomies and steatorrhea, for
instance, do not have hyperoxaluria (3). Therefore the colon is the
predominant site of oxalate absorption. Furthermore, steatorrhea may not be
necessary for development of the syndrome. Laboratory and clinical evidence
suggests that malabsorbed bile salts may increase the colonic permeability
of many solutes, including oxalate (4).
Changes in the characteristics of urine of patients with gastrointestinal
disease contribute to the tendency of patients with enteric hyperoxaluria
to develop kidney stones. Diminished urine volume and increased urinary
solute concentration caused by chronic diarrhea and extracellular volume
depletion increase the urinary saturation and decrease the solubility of
calcium and oxalate. Diminished urine volume, along with the low urinary pH
associated with stool bicarbonate losses and urinary acidification
associated with renal sodium conservation also account for the significant
incidence of uric acid stones in patients with ileostomies. Hypocitraturia
and hypomagnesuria also occur in many patients with malbsorption (5).
Citrate and magnesium are important inhibitors of stone formation.
Decreases in urinary sulfate and phosphate because of protein malabsorption
are also associated with increased crystal growth. Treatment includes
correction of low urine volume (increased water intake, control of
diarrhea, eventual ileal adaptation leading to diminished ileal losses);
dietary oxalate restriction; dietary fat restriction; and binding of
oxalate. This latter can be accomplished with cholestyramine, calcium, or
perhaps organic marine hydrocolloid polymers (seaweed derived) (6).
Treatment of other stone-forming risks is also important: e.g. thiazides
for hypercalciuria, and alkalinization with citrate for hypocitraturia and
uric acid stones.
1. Worcester, E. Stones due to bowel disease in Kidney Stones: Medical and
Surgical Management. Coe, F.L., Favus, M.J., Pak, C.Y.C., Parks, J.H.,
Preminger, G.M. Lippincott-Raven, New York, 1996.
2. Charney, A.N., Goldfarb, D.S., Dagher, P.C. Metabolic disorders
associated with gastrointestinal disease, in Fluid, Electrolyte and
Acid-Base Disorders. Eds., A.I. Arieff, R.A. DeFronzo, Churchill
Livingstone, New York, 1995.
3. Dobbins, J.W., Binder, H.J. Importance of the colon in enteric
hyperoxaluria. NEJM 196:298 (77).
4. Dobbins, J.W., Binder, H.J. Effect of bile salts and faty acids on the
colonic absorption of oxalate. Gastroenterology 70:1096 (80).
5. Rudman, D., Dedonis, J.L, Fountain, M.T. et al Hypocitraturia in
patients with gastrointestinal malabsorption. NEJM 303:657 (80).
6. Lindsjo, M., Fellstrom, B., Ljunghall, S. et al. Treatment of enteric
hyperoxaluria with calcium-containing organic marine hydrocolloid.
Lancet 2:701 (89).