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Urolithiasis
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Thomas Johnston, James Armitage, Oliver Wiseman
Oxalobacter formigenes is an anaerobic bacterium which colonises the large intestine of humans and causes the degradation of oxalate. It is important in the metabolism of calcium oxalate and its absence in the intestine following treatment with broad spectrum antibiotics such as quinolones may increase the risk of calcium stone formation.
Cholelithiasis and Nephrolithiasis
Published in John K. DiBaise, Carol Rees Parrish, Jon S. Thompson, Short Bowel Syndrome Practical Approach to Management, 2017
The risk of nephrolithiasis increases as a result of enhanced absorption of enteric oxalate in those with colon remaining. Oxalate absorption in the colon is increased by high oxalate intake in the diet. Up to 40% of the daily excretion of oxalate in the urine is from a dietary source; however, oxalate absorption in the intestine depends linearly on the concomitant dietary intake of calcium and is influenced by the bacterial degradation by several bacterial species of intestinal microbiota. The gut-dwelling obligate anaerobe Oxalobacter formigenes has been an area of research interest because of its oxalate-degrading property [54]. A reduction in bacterial breakdown of oxalate due to decreased O. formigenes in the colon of SBS patients has been described [55]. By altering the intestinal bacterial population, probiotics may have the potential to lower oxalate absorption and urinary excretion and may be beneficial in the treatment or prevention of oxalate stones as shown in healthy subjects [56].
Azithromycin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Among the Gram-negative anaerobic bacteria, the Prevotella spp., Porphyromonas spp., Fusobacterium spp., Aggregatibacter actinomycetemcomitans, Peptostreptococcus micros, Oxalobacter formigenes, and Eikenella corrodens are azithromycin-susceptible (Japoni et al., 2011; Kuriyama et al., 2007; Lange et al., 2012; Muller et al., 2002). Veillonela spp., Bacteroides fragilis, and other members of the B. fragilis group are moderately resistant (Barry et al., 1988; Chen et al., 1992; Kitzis et al., 1990; Pajukanta et al., 1992).
Why is diagnosis, investigation, and improved management of kidney stone disease important? Non-pharmacological and pharmacological treatments for nephrolithiasis
Published in Expert Review of Clinical Pharmacology, 2022
Viola D’Ambrosio, Shabbir Moochhala, Robert J Unwin, Pietro Manuel Ferraro
Another way of reducing urinary oxalate excretion and/or its absorption from the gut, although not its production, has also been tried and is still being explored. This is the idea of using a gram-negative anaerobic bacterial species known as Oxalobacter formigenes that is part of the normal gut microbiome present mainly in the large intestine and metabolizes oxalate. One study reported that colonization with Oxalobacter is reduced in calcium oxalate stone formers, although this did not correlate with oxalate excretion [73]. Another suggestion was that in addition to oxalate metabolism, these bacteria may also promote oxalate secretion, which is now recognized as an important pathway for oxalate excretion in stool [74]. However, results so far have been less striking in clinical practice [75], but it may still be of benefit as adjunctive therapy in PH and as an additional treatment for stone-formers with the more common idiopathic calcium oxalate stones and mild hyperoxaluria. Moreover, other gut bacteria may be involved in oxalate metabolism [76] and might also account for the association of oral antibiotic use and loss of these bacteria, with an increased renal stone risk, especially in females [77].
From pathogenesis to novel therapies in primary hyperoxaluria
Published in Expert Opinion on Orphan Drugs, 2019
Gill Rumsby, Sally-Anne Hulton
While only a small percentage of the total oxalate in PH comes from the diet, animal studies suggest that there may be secretion of oxalate into the gut once renal failure occurs [69]. There are two experimental therapies that have targeted degradation of oxalate. One of these is the use of recombinant oxalate decarboxylase to degrade oxalate within the gastrointestinal tract. This treatment, ALLN-177, was shown to reduce urinary oxalate in diet-induced hyperoxaluria although only 15% of these had a reduction greater than 30% [70]. This drug is currently undergoing phase 2 clinical trials for primary and secondary hyperoxaluria (NCT03391804). The second treatment is colonization of the gut with the naturally occurring oxalate-degrading anaerobe Oxalobacter formigenes. Initial early optimism with this treatment has not been borne out by subsequent trials [71] but assessments of plasma oxalate in PH1 patients with advanced CKD receiving Oxalobacter formigenes are being undertaken following reported improvements in two infants [72].
Novel therapeutic approaches in primary hyperoxaluria
Published in Expert Opinion on Emerging Drugs, 2018
Alexander Weigert, Christina Martin-Higueras, Bernd Hoppe
Oxalobacter formigenes (Oxabact®, Oxthera AB, Stockholm, Sweden), an anerobic bacterium, normally localized in the intestinal tract of humans, uses oxalate as its sole carbon source [32]. Orally applied, it reduces oxalate concentration in the patient’s intestine, leading to a relevant concentration gradient between blood and intestinal lumen, but also to activation of the intestinal oxalate transporter SLC26A6 [33,34]. Both effects can lead to a significant shift of oxalate from patient’s blood into the intestinal lumen, where it is being degraded by O. formigenes and thus excreted via the feces.