Dependence of Oxalate Absorption on the Daily Calcium Intake

Abstract

Abstract. Two to 20% of ingested oxalate is absorbed in the gastrointestinal tract of healthy humans with a daily 800 mg calcium intake. Calcium is the most potent modifier of the oxalate absorption. Although this has been found repeatedly, the exact correlation between calcium intake and oxalate absorption has not been assessed to date. Investigated was oxalate absorption in healthy volunteers applying 0.37 mmol of the soluble salt sodium [ 13 C 2 ]oxalate in the calcium intake range from 5 mmol (200 mg) calcium to 45 mmol (1800 mg) calcium. Within the range of 200 to 1200 mg calcium per day, oxalate absorption depended linearly on the calcium intake. With 200 mg calcium per day, the mean absorption (Ϯ SD) was 17% Ϯ 8.3%; with 1200 mg calcium per day, the mean absorption was 2.6% Ϯ 1.5%. Within this range, reduction of the calcium supply by 70 mg increased the oxalate absorption by 1% and vice versa. Calcium addition beyond 1200 mg/d reduced the oxalate absorption only one-tenth as effectively. With 1800 mg calcium per day, the mean absorption was 1.7% Ϯ 0.9%. The findings may explain why a low-calcium diet increases the risk of calcium oxalate stone formation.For decades, a mainstay in the treatment of patients with calcium (Ca) urinary stones has been a Ca-restricted diet (1). Reduction of the Ca content of the diet reliably reduced the amount of Ca excreted in urine. This reduction was believedbut never proven-to reduce the risk of Ca stone formation. By contrast, already in 1969, a Ca-restricted diet was shown to increase the gastrointestinal absorption of oxalate (2), leading to increased amounts of oxalate in the urine and an increased risk of the formation of Ca oxalate stones. Therefore, to reduce oxalate absorption and the resulting risk of formation of Ca oxalate stones, high-Ca supplements were routinely prescribed to obese patients after ileal bypass surgery (3). The reason why these contradictory and confusing recommendations persisted for so long is the lack of prospective studies and the fact that analysis of oxalate remained unreliable (4) until the mid-1980s. Consequently, the amount of dietary oxalate excreted in urine and its role for renal stone formation were underestimated (5). The fact that a low-Ca diet emerged as a risk factor for Ca oxalate calculi and that a high-Ca diet emerged as a protective factor in two large epidemiologic studies (6,7) is still frequently ignored. Hence, the advice to restrict Ca may still be given to patients with recurrent Ca oxalate urinary stones.We wanted to clear up the confusion generated by the contradictory results as well as the contradictory recommendations, and to answer the following question: To what extent does Ca intake influence the gastrointestinal oxalate absorption? Therefore, we quantitatively measured the dependence of oxalate absorption on Ca intake. The physiologic daily dietary Ca intake lies between approximately 370 and 1200 mg. Intakes of less than 300 mg Ca never occur in adults except in those who reduce food intake to lose weight. ...

Oxalate: From the Environment to Kidney Stones

“…A negative correlation was established between ingested Ca 2+ and absorption of ingested oxalate by demonstrating that a reduction in the amount of ingested Ca 2+ promoted the absorption of oxalate (31), and vice versa, higher concentrations of Ca 2+ in food reduced the absorption of oxalate (23,25,32). Ca 2+ and oxalate are largely absorbed separately, but they can also be absorbed together in the form of the small and neutral salt, CaOx, as already shown in rats (33).…”

Oxalic acid does not influence nonhaem iron absorption in humans: a comparison of kale and spinach meals

“…Formation of insoluble oxalate complexes is the most likely explanation based on the observation that addition of calcium decreased OA absorption from the diet in a dose-dependent fashion (von Unruh et al, 2004). However, surprisingly little attention has been paid to the effect of OA on iron bioavailability.…”

Response to Dietary Oxalate after Bariatric Surgery

“…The observed decrease in creatinine excretion was not only secondary to lower protein intake but was also most likely due to weight loss and decreased muscle mass (38). In addition, the usual low calcium and oxalate intake determined in this study may have also been responsible for the lower percentages of hyperoxaluria (39)(40)(41). Although the absolute lipid content in the typical diets of post-BS patients did not differ from that of the MO participants, the percentage of fat calculated from the total energy value was 37%, which far exceeds the upper limit of 30% suggested by the US dietary reference intakes.…”

“…Figure 4 shows the results of the subgroup of 10 post-BS patients (9 women and 1 man), aged 48 years (IQR, 47-51), who also underwent the OLT before the procedure. [40][41][42][43][44][45][46][47][48]). Significant intragroup (P,0.001) and intergroup (post-BS versus pre-BS; P=0.03) median uOx/uCr were observed at all periods after load, and the interaction effects of surgery versus oxalate load factors were also significant (P=0.01) ( Figure 4A).…”