Fig. 8.1.
Decision tool and guide for the dietary management of high urine oxalate. [Reprinted from Penniston KL, Nakada SY. Diet and alternative therapies in the management of stone disease. Urol Clin North Am. 2013;40(1):31–46. With permission from Elsevier]
As with other medical conditions, treatment of the underlying cause(s) or contributor(s) is recommended. With dietary recommendations, the tendency is often to provide all recommendations to all patients, regardless of variable dietary contributions and, often, without regard to how the patient may already be eating. Few other medical therapies encourage such a “blanket” approach to medical management. Nutrition therapy for stones is best applied when targeted to address a specific dietary cause(s) for a patient’s increased stone risk. Some means of assessing patients’ current diets are usually required in order to determine whether there are contributors to stone risk factors. If dietary factors are well-controlled despite the persistence of biochemical aberration(s), then non-dietary etiologies are considered.
Controlling Oxalate Biosynthesis
There is no medication to reduce oxalate synthesis. For patients with one of the three known variants of primary hyperoxaluria (PH), a combined liver/kidney transplant corrects overproduction of oxalate by eliminating the respective enzyme deficiency or dysfunction. The subset of patients with PH type 1 who are deficient in alanine-glyoxylate aminotransferase (AGXT) may respond favorably to supraphysiologic doses of vitamin B6 (pyridoxine), 100–500 mg/day [2]. The vitamin is a co-enzyme for AGXT, which converts glyoxylic acid to glycine, thus diverting it away from oxalate production. But patients with a functional absence of AGXT would not be expected to benefit from vitamin B6 supplementation as even the highest of co-enzyme concentrations would be useless in the setting of complete enzyme inactivity.
Recently, reduced urinary oxalate excretion in patients with idiopathic hyperoxaluria has been reported with vitamin B6 [3]. Deficiency is very uncommon in the US and in other developed nations, and it is therefore unlikely that vitamin B6 deficiency accounts in any appreciable way for hyperoxaluria. However, with 146 known AGXT mutations [4] and possibly more yet undiscovered, patients with subtle forms of undiagnosed PH could exist due to mutations that may interfere with cofactor binding [5]. In this scenario, vitamin B6 supplementation could be useful in ramping up enzyme activity rendered abnormal due to a mutation. This may explain the favorable effects from pyridoxine observed in some, but not all, patients with idiopathic hyperoxaluria.
Controlling GI Oxalate Absorption
Oxalate is absorbed throughout the GI tract, mostly in the small intestine. Typically, only 5–10 % of the oxalate consumed is absorbed. This is due, in part, to the fact that much of the oxalate consumed is in the form of insoluble oxalate, e.g., calcium oxalate. Evidence in the literature supports the appropriate use of dietary calcium and, to a lesser extent, magnesium, as a way to control oxalate absorption [6]. When oxalate binds with these and other divalent cations in the GI tract, an insoluble complex is formed, resulting in the absorption of neither constituent. The amount of calcium or other mineral required to bind a known amount of oxalate varies depending on the form in which the oxalate was initially consumed, on the presence and type of dietary fats, on GI transit time, and other factors.
Role of Calcium and Magnesium
Assuming normal GI functioning, the Recommended Dietary Allowance (RDA) for calcium, in the range of 1,000–1,300 mg/day (depending on gender and life-stage group), is sufficient to provide optimal GI binding potential for oxalate. Most evidence recommends this be distributed more-or-less equally at meals throughout the day; but other data suggest that intake need not be divided at meals [7]. Calcium from foods and beverages, as opposed to supplements, is strongly recommended as it is difficult to consume excessive calcium from diet alone. A multitude of dietary calcium sources exist, both dairy and non-dairy (Table 8.1). The RDA for adults for magnesium is in the range of 310–420 mg/day; multiple dietary sources are available to meet this need. In patients with already appropriate calcium and magnesium intakes, further investigation to determine the contributor(s) to high urine oxalate is required.
Table 8.1.
Calcium content of some foods and beverages providing >100 mg calcium per typical household serving (footnotes categorize as dairy or non-dairy, lactose-free or lactose-containing).
Food item | Amount | Calcium (mg) |
|---|---|---|
Calcium-fortified, ready-to-consume breakfast cerealsa | 1 cup (30–50 g, depending on cereal) | Can be up to 1,000 |
Tofu, firm, processed with calciuma | ½ cup (about 124 g) | 430 |
Calcium-fortified orange and other fruit juicesa | 1 cup (8 fluid ozs; 240 mL) | 300–500 |
Calcium-fortified non-dairy milks (rice, soy, almond, coconut, flaxseed, hemp)a | 1 cup (8 fluid ozs; 240 mL) | 300–450 (brands vary) |
Dairy milk (cow, goat, camel)a | 1 cup (8 fluid ozs; 240 mL) | 300–400 |
Kefir (made from cow, goat, or sheep milk)b | 1 cup (8 fluid ozs; 240 mL) | 300
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