DIETARY OXALATE AND ITS INFLUENCE ON URINARY OXALATE EXCRETION

1999 ◽  
pp. 251
Author(s):  
Ross P. Holmes ◽  
Dean G. Assimos
Author(s):  
J. C. Dijcker ◽  
E. A. Hagen-Plantinga ◽  
D. G. Thomas ◽  
Y. Queau ◽  
V. Biourge ◽  
...  

2015 ◽  
Vol 81 (15) ◽  
pp. 5048-5054 ◽  
Author(s):  
Xingsheng Li ◽  
Melissa L. Ellis ◽  
John Knight

ABSTRACTAnimal and human studies have provided compelling evidence that colonization of the intestine withOxalobacter formigenesreduces urinary oxalate excretion and lowers the risk of forming calcium oxalate kidney stones. The mechanism providing protection appears to be related to the unique ability ofO. formigenesto rely on oxalate as a major source of carbon and energy for growth. However, much is not known about the factors that influence colonization and host-bacterium interactions. We have colonized mice withO. formigenesOxCC13 and systematically investigated the impacts of diets with different levels of calcium and oxalate onO. formigenesintestinal densities and urinary and intestinal oxalate levels. Measurement of intestinal oxalate levels in mice colonized or not colonized withO. formigenesdemonstrated the highly efficient degradation of soluble oxalate byO. formigenesrelative to other microbiota. The ratio of calcium to oxalate in diets was important in determining colonization densities and conditions where urinary oxalate and fecal oxalate excretion were modified, and the results were consistent with those from studies we have performed with colonized and noncolonized humans. The use of low-oxalate purified diets showed that 80% of animals retainedO. formigenescolonization after a 1-week dietary oxalate deprivation. Animals not colonized withO. formigenesexcreted two times more oxalate in feces than they had ingested. This nondietary source of oxalate may play an important role in the survival ofO. formigenesduring periods of dietary oxalate deprivation. These studies suggest that the mouse will be a useful model to further characterize interactions betweenO. formigenesand the host and factors that impact colonization.


2019 ◽  
Vol 316 (3) ◽  
pp. F409-F413 ◽  
Author(s):  
Tanecia Mitchell ◽  
Parveen Kumar ◽  
Thanmaya Reddy ◽  
Kyle D. Wood ◽  
John Knight ◽  
...  

Dietary oxalate is plant-derived and may be a component of vegetables, nuts, fruits, and grains. In normal individuals, approximately half of urinary oxalate is derived from the diet and half from endogenous synthesis. The amount of oxalate excreted in urine plays an important role in calcium oxalate stone formation. Large epidemiological cohort studies have demonstrated that urinary oxalate excretion is a continuous variable when indexed to stone risk. Thus, individuals with oxalate excretions >25 mg/day may benefit from a reduction of urinary oxalate output. The 24-h urine assessment may miss periods of transient surges in urinary oxalate excretion, which may promote stone growth and is a limitation of this analysis. In this review we describe the impact of dietary oxalate and its contribution to stone growth. To limit calcium oxalate stone growth, we advocate that patients maintain appropriate hydration, avoid oxalate-rich foods, and consume an adequate amount of calcium.


2014 ◽  
Vol 92 (2) ◽  
pp. 577-584 ◽  
Author(s):  
J. C. Dijcker ◽  
E. A. Hagen-Plantinga ◽  
D. G. Thomas ◽  
Y. Queau ◽  
V. Biourge ◽  
...  

2016 ◽  
Vol 44 (2) ◽  
pp. 150-158 ◽  
Author(s):  
Craig B. Langman ◽  
Danica Grujic ◽  
Rita M. Pease ◽  
Linda Easter ◽  
Jennifer Nezzer ◽  
...  

Background: Hyperoxaluria may result from increased endogenous production or overabsorption of dietary oxalate in the gastrointestinal tract leading to nephrolithiasis and, in some, to oxalate nephropathy and chronic kidney disease. ALLN-177 is an oral formulation of a recombinant, oxalate specific, microbial enzyme oxalate decarboxylase intended to treat secondary hyperoxaluria by degrading dietary oxalate in the gastrointestinal tract, thereby reducing its absorption and subsequent excretion in the urine. Methods: This double-blind, placebo controlled, randomized, cross-over, phase 1 study of ALLN-177 evaluated the tolerability of ALLN-177 and its effect on urinary oxalate excretion in 30 healthy volunteers with hyperoxaluria induced by ingestion of a high oxalate, low calcium (HOLC) diet. The primary end point was the difference in the mean 24-hour urinary oxalate excretion during the ALLN-177 treatment period compared with the placebo treatment period. Results: The daily urinary oxalate excretion increased in the study population from 27.2 ± 9.5 mg/day during screening to 80.8 ± 24.1 mg/day (mean ± SD) on the HOLC diet before introducing ALLN-177 or placebo therapy for 7 days. Compared to placebo, ALLN-177 treatment reduced urinary oxalate by 11.6 ± 2.7 mg/day, p = 0.0002 (least squares mean ± SD). Conclusions: In healthy volunteers, with diet-induced hyperoxaluria treatment with ALLN-177, when compared to placebo, significantly reduced urinary oxalate excretion by degrading dietary oxalate in the gastrointestinal tract and thereby reducing its absorption. ALLN-177 may represent a new approach for managing secondary hyperoxaluria and its complications.


2001 ◽  
Vol 59 (1) ◽  
pp. 270-276 ◽  
Author(s):  
Ross P. Holmes ◽  
Harold O. Goodman ◽  
Dean G. Assimos

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 62
Author(s):  
Joseph J. Crivelli ◽  
Tanecia Mitchell ◽  
John Knight ◽  
Kyle D. Wood ◽  
Dean G. Assimos ◽  
...  

Kidney stone disease is increasing in prevalence, and the most common stone composition is calcium oxalate. Dietary oxalate intake and endogenous production of oxalate are important in the pathophysiology of calcium oxalate stone disease. The impact of dietary oxalate intake on urinary oxalate excretion and kidney stone disease risk has been assessed through large cohort studies as well as smaller studies with dietary control. Net gastrointestinal oxalate absorption influences urinary oxalate excretion. Oxalate-degrading bacteria in the gut microbiome, especially Oxalobacter formigenes, may mitigate stone risk through reducing net oxalate absorption. Ascorbic acid (vitamin C) is the main dietary precursor for endogenous production of oxalate with several other compounds playing a lesser role. Renal handling of oxalate and, potentially, renal synthesis of oxalate may contribute to stone formation. In this review, we discuss dietary oxalate and precursors of oxalate, their pertinent physiology in humans, and what is known about their role in kidney stone disease.


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