Oxalate stones after gastric stapling?

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 Medicine)

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 crystal deposition.

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).

(January, 1997)

Since writing the above response, I did come across an interesting and possibly relevant paper: Hautmann, RE. The stomach: a new and powerful oxalate absorption site in man. J. Urol 149:1401 (93). This study was done in patients with chronic NG tube feeding, with pyloric blockade as part of the study technique, not exactly a physiologic condition. But perhaps this simulates gastric stapling in some way! Whether the stomach is a relevant site of absorption of oxalate in normal humans is unclear: the emphasis in the GI transport literature has been on distal ileum and colon, which have clearly been established as important sites of oxalate absorption.
David S. Goldfarb (74357.1665@compuserve.com)
New York, NY -Tuesday, January 28, 1997 at 20:48:37 (PST)

I have taken responsibility for a patient aged 52 who for 25 years have formed numerous calcium oxalate stones in both kidneys. No family history, oxalate excretion always above 1.3 mmol per day, most times about 2 mmol per day. L-glycerate and glycolate excretion normal, no gastrointestinal symptoms, well explained about diet and fluid intake. Without instruction given to reduce calcium intake, ca excretion a little low: 1.2 mmol (adult male). Urine acid (5-5.5), kidney function unimpaired. Se uric acid high normal, urate excretion normal. Has tried for a couple of years K citrate with no obvious effect on recurrence rate. Plan to give orthophosphate and thiamine according to the Mayo clinic paper (N Engl J Med 1994) on primary hyperoxalurics, and perhaps add allopurinol. I have not found any references to excretion in that range (measurements should be OK) without explanation. PH1 could still be present ? How could we test ? would it make a difference ? Sincerely Troels Ring
Troels Ring (ring@post1.tele.dk)
Aalborg, Denmark-Friday, April 25, 1997 at 00:15:54 (PDT)