The Variability and Dietary Dependence of Urinary Oxalate Excretion in Recurrent Calcium Stone Formers

Abstract

Twenty-two recurrent calcium stone formers had 24-h urinary oxalate excretions on their home diets which were significantly greater than those of 30 normal subjects «()·4X±()·23 rnrnol/d; mean±SD compared with 0·31±0·11; P<IHII). The stone formers also demonstrated marked day to day variability in oxalate excretion indicating that a single normal urinary oxalate measurement did not exclude significant hyperoxaluria at other times.On a hospital diet containing J()()() mg calcium per day, urinary oxalate excretion fell significantly from 0·4X±0·23 mmol/d to ()·32±O·12; P<O·Ol. As the urinary calcium excretion in and out of hospital was similar, it seems unlikely that low calcium intake at home was responsible for the hyperoxaluria.All patients had recurrent symptomatic stone disease and had been advised to avoid foods rich in oxalate. Whilst poor compliance is a possible explanation for the variability in oxalate excretion. we believe it is more likely that there is an inadvertent intake of oxalogenic precursors in their diet. As normal subjects do not demonstrate hypcroxaluria on similar home diets, stone formers may have a metabolic defect in the handling of these precursors.Approximately XO-YO'X. of renal stones in westernised societies contain calcium. I. 2 Calcium oxalate is a major constituent of these stones and increased urinary oxalate excretion is one of the major factors predisposing an individual to calcium nephrolithiasis.' For this reason 24-h urinary oxalate excretion is often measured routinely in patients with renal calculi. However. the factors which modulate oxalate excretion in these patients remain poorly defined.In the current study the daily urinary excretion of oxalate was measured in recurrent calcium stone formers on their usual diets at home at about monthly intervals to determine its variability and therefore its clinical usefulness. In addition. oxalate excretion was assessed in these patients on controlled hospital diets containing ISO and J()()() mg of calcium. The IOI)() rng/d diet approximates the mean normal daily calcium intake. This has enabled us to compare the effect of dietary calcium with other dietary constituents on urinary oxalate excretion. Methods SUBJECTSThe 22 patients studied had a history of recurrent calcium nephrolithiasis. This group comprised 16 men and six women with ages ranging from 22 to 66 years. All patients had recent radio-opaque stones demonstrable on abdominal X-rays. Stones obtained from nine of the patients and analysed by a wet chemical method" indicated the presence of mixed calcium phosphate/oxalate calculi. None of the patients had evidence of hyperparathyroidism. enteric hyperoxaluria or vitamin D intoxication. All could acidify their urine to a urinary pH<5·3. following a standard ammonium chloride loading test thereby excluding renal tubular acidosis", At the time of the experiments, all patients were healthy and had normal renal function as assessed by plasma creatinine concentration. 385

Oral Antibiotic Treatment of Helicobacter pylori Leads to Persistently Reduced Intestinal Colonization Rates with Oxalobacter formigenes

“…In studying persons who were not selected for having hyperoxaluria, after elimination of colonization with OF there was a low likelihood of demonstrating a change in urinary oxalate, a highly variable measure under even wellcontrolled circumstances. 19 We did not achieve our planned sample size in part because we found a lower prevalence of OF colonization than expected and ended the study. Because our interim analysis showed a strong difference between the groups, we terminated enrollment before reaching our planned sample size.…”

Human SLC26A1 Gene Variants: A Pilot Study

“…This exchange process is proposed to be important for the removal of oxalate from the blood (via the intestine), as well as for maintaining circulating (via the kidneys) and hepatic levels of nutrient sulfate [4, 6, 24, 29–31]. Loss of SAT1 in mice led to disturbances in sulfate homeostasis (hyposulfataemia and hypersulfaturia), as well as hyperoxalaemia and hyperoxaluria [24].…”

Microbial degradation of oxalate in the gastrointestinal tracts of rodents and ruminants

“…Some of these abnormalities or risk factors include: decreased urine volume due to water malabsorption; reduced ionic strength of urine because of electrolyte malabsorption; magnesium and citrate depletion; reduced urine pH; and reduced urinary sulfate and pyrophosphate resulting from protein malabsorption (Bambach et al. 1981;Nordenvall et al, 1983;Smith et al, 1980 intestinal oxalate absorption and urinary oxalate excretion are slightly, but significantly, increased when compared to normal subjects (Brown et al, 1987;Robertson et al, 1978;Tiselius et al, 1981;Zarembski and Hodgkinson, 1969). In addition, Broadus and Thier (1979) found that approximately 50% of the stone-formers exhibited hypercalciuria.…”