Fat-reduced diet in the treatment of hyperoxaluria in patients with ileopathy

Andersson, Henrik; Jagenburg, Rudolf

doi:10.1136/gut.15.5.360

Cited by 101 publications

(35 citation statements)

References 12 publications

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“…A small reduction in urinary oxalate can significantly reduce the risk of forming calcium oxalate stones (see earlier), therefore, avoiding oxalate-rich foods (spinach, rhubarb, beetroot, soya beans and tofu, nuts, peanut butter, okra, yams, sesame seeds, tahini and chocolate) is justified, even if the contribution of dietary oxalate to urinary oxalate excretion is limited [46]. A reduction in dietary fat intake can decrease urinary oxalate excretion: in 13 patients with disease of the ileum (mainly due to Crohn’s disease) who switched from a 100- to a 40-gram fat diet, oxalate excretion decreased slowly, but significantly, up to 50%, if faecal fat excretion fell to <15 g/day [47]. In patients with significant hypercalciuria and a high calcium intake (particularly if derived from dairy produce, the more absorbable form), some reduction in dietary calcium with oxalate may be justified.…”

Section: Medical Managementmentioning

confidence: 99%

An Update and Practical Guide to Renal Stone Management

et al. 2010

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Renal stone disease covers kidney and lower urinary tract stones caused by a variety of conditions, including metabolic and inherited disorders, and anatomical defects with or without chronic urinary infection. Most cases are idiopathic, in which there is undoubtedly a genetic predisposition, but where environmental and lifestyle factors play an important role. Indeed, it is becoming apparent that renal stone disease is often part of a larger ‘metabolic picture’ commonly associated with type 2 diabetes, obesity, dyslipidaemia, and hypertension. Renal stone disease is a growing problem in the UK (and other developed and developing populations) with a cross-sectional prevalence of ∼1.2%. This means that there are currently ∼720,000 individuals with a history of kidney stones in the UK. Almost 40% of first-time stone formers will form a second stone within 3 years of the first episode if no prophylactic measures are instituted to prevent stone recurrence, since removal or disintegration of the first stone does not treat the underlying cause of stones in the majority of patients. The age of onset is getting younger and the sex ratio (until recently more men than women) is becoming almost even. Metabolic screening remains an important part of investigating renal stone disease, but to the disappointment and frustration of many doctors, medical treatment is still essentially pragmatic, except perhaps in cystinuria, and to a limited extent in primary hyperoxaluria (if pyridoxine-sensitive); although newer treatments may be emerging. This review summarizes current thinking and provides a practical basis for the management of renal stone disease.

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Section: Medical Managementmentioning

confidence: 99%

An Update and Practical Guide to Renal Stone Management

et al. 2010

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“…Until recently most investigators had concluded that oxalate was absorbed by a passive, noncarrier-mediated pathway and that increased absorption resulted from increased passive permeability and/or increased solubility of oxalate (2)(3)(4)(7)(8)(9)(10)(11)(12)(13)(14). Hatch et al (15), SITS),' which suggests an anion exchange process on the brush border.…”

Section: Introductionmentioning

confidence: 99%

Oxalate transport by anion exchange across rabbit ileal brush border.

Knickelbein¹,

Aronson²,

Dobbins³

1986

J. Clin. Invest.

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This study demonstrates the presence of oxalate transporters on the brush border membrane of rabbit ileum. We found that an inside alkaline (pH = 8.5 inside, 6.5 outside) pH gradient stimulated I14Cloxalate uptake 10-fold at 1 min with a fourfold accumulation above equilibrated uptake at 5 min. 1 mM 4,4'-disothiocyanostilbene-2,2'-disulfonate (disodium salt; DIDS) profoundly inhibited the pH-gradient stimulated oxalate uptake. Using an inwardly directed K+ gradient and valinomycin, we found no evidence for potential sensitive oxalate uptake. In contrast to Cl:HCO3 exchange, HCO3 did not stimulate oxalate uptake more than was seen with a pH gradient in the absence of HCO3. An outwardly directed Cl gradient (50 mM inside, 5 mM outside) stimulated oxalate uptake 10-fold at 1 min with a fivefold accumulation above equilibrated uptake. Cl-stimulated oxalate uptake was largely inhibited by DIDS. Addition of K+ and nigericin only slightly decreased the Cl gradient-stimulated oxalate uptake, which indicates that this stimulation was not primarily due to the Cl gradient generating an inside alkaline pH gradient via Cl:OH exchange. Further, an outwardly directed oxalate gradient stimulated 36CI uptake. These results suggested that both oxalate:OH and oxalate:Cl exchange occur on the brush border membrane. To determine if one or both of these exchanges were on contaminating basolateral membrane, the vesicle preparation was further fractionated into a brush border and basolateral component using sucrose density gradient centrifugation. Both exchangers localized to the brush border component. A number of organic anions were examined (outwardly directed gradient) to determine if they could stimulate oxalate and Cl uptake. Only formate and oxaloacetate were found to stimulate oxalate and Cl uptake. An inwardly directed Na gradient only slightly stimulated oxalate uptake, which was inhibited by DIDS.

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“…The mechanisms promoting increased oxalate absorption are thought to be as follows: solubility [4,10]; permeability [11], and reduction of oxalate degradation by intestinal bacteria [12] (fig. 3).…”

Section: Discussionmentioning

confidence: 99%

Oral Calcium Supplement Decreases Urinary Oxalate Excretion in Patients with Enteric Hyperoxaluria

et al. 1998

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We studied the effect of oral calcium supplementation in patients with enteric hyperoxaluria. Three patients with renal stone events following ileal resection were given oral calcium supplement. One of the three patients was put on a low-fat diet. The treatment reduced urinary oxalate excretion to the normal range. Subsequently, 2 patients reduced the dose of calcium supplementation at their own discretion and consequently developed renal stones again together with hyperoxaluria. Based on these observations, we believe that an adequate dose of calcium can normalize urinary oxalate excretion.

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Fat-reduced diet in the treatment of hyperoxaluria in patients with ileopathy

Cited by 101 publications

References 12 publications

An Update and Practical Guide to Renal Stone Management

An Update and Practical Guide to Renal Stone Management

Oxalate transport by anion exchange across rabbit ileal brush border.

Oral Calcium Supplement Decreases Urinary Oxalate Excretion in Patients with Enteric Hyperoxaluria

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