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微生物与草酸钙结石病

Microorganisms and calcium oxalate stone disease.

作者信息

Goldfarb David S

机构信息

New York Harbor VA Medical Center and NYU School of Medicine, New York, NY 10010, USA.

出版信息

Nephron Physiol. 2004;98(2):p48-54. doi: 10.1159/000080264.

DOI:10.1159/000080264
PMID:15499215
Abstract

Microorganisms may have a role in the pathogenesis and prevention of kidney stones. The subjects of this review include nanobacteria, Oxalobacter formigenes, and lactic acid bacteria. Not reviewed here is the well-described role of infections of the urinary tract with Proteus species and other urease-producing organisms associated with struvite stone formation. Nanobacteria have been proposed to be very small (0.08-0.5 nm), ubiquitous organisms that could play a role in stone formation. The theory is that nanobacteria can nucleate carbonate apatite on their surfaces and thereby provide the nidus for stone formation. However, their existence remains uncertain and many investigators are openly skeptical. Recent investigations suggest that they are artifacts, and not actually living organisms, but their proponents continue to study them. O. formigenes is an obligate anaerobe which may be important in the prevention of stone formation. Its sole substrate for generation of ATP is oxalate. It may thereby metabolize its human host's dietary oxalate and diminish intestinal absorption and subsequent urinary excretion of oxalate. There is evidence that the organism's absence, perhaps sometimes due to courses of antibiotics, may be a cause of hyperoxaluria and stone formation. In early investigations, patients not colonized with the organism can be recolonized. Urinary oxalate can be diminished by accompanying an oxalate-containing meal with the organism. One study demonstrated that a preparation of lactic acid bacteria successfully reduced urinary oxalate excretion in 6 patients with calcium oxalate stones and hyperoxaluria. The mechanism of this effect is uncertain since these bacteria lacked the gene possessed by O. formigenes which codes for that organism's oxalate uptake mechanism. The author is currently completing a small randomized controlled clinical trial with this preparation in calcium stone-forming patients with idiopathic hyperoxaluria.

摘要

微生物可能在肾结石的发病机制及预防中发挥作用。本综述的主题包括纳米细菌、产甲酸草酸杆菌和乳酸菌。本文未对变形杆菌属及其他与鸟粪石形成相关的产脲酶微生物引起的尿路感染的明确作用进行综述。纳米细菌被认为是非常小(0.08 - 0.5纳米)、无处不在的生物体,可能在结石形成中起作用。理论是纳米细菌能在其表面使碳酸磷灰石成核,从而为结石形成提供核心。然而,它们的存在仍不确定,许多研究者公开表示怀疑。近期研究表明它们是人为产物,并非真正的生物体,但它们的支持者仍在继续研究。产甲酸草酸杆菌是一种专性厌氧菌,可能在预防结石形成中起重要作用。其产生ATP的唯一底物是草酸盐。因此它可能代谢人类宿主饮食中的草酸盐,减少肠道对草酸盐的吸收及随后的尿草酸盐排泄。有证据表明该生物体的缺失,可能有时是由于抗生素疗程,可能是高草酸尿症和结石形成的一个原因。在早期研究中,未被该生物体定植的患者可以重新定植。伴随含草酸盐的膳食摄入该生物体可减少尿草酸盐。一项研究表明,一种乳酸菌制剂成功降低了6例草酸钙结石和高草酸尿症患者的尿草酸盐排泄。这种作用的机制尚不确定,因为这些细菌缺乏产甲酸草酸杆菌所拥有的编码该生物体草酸盐摄取机制的基因。作者目前正在对这种制剂在特发性高草酸尿症的草酸钙结石形成患者中进行一项小型随机对照临床试验。

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引用本文的文献

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Metabolic and metagenomic outcomes from early-life pulsed antibiotic treatment.早期脉冲式抗生素治疗的代谢和宏基因组学结果。
Nat Commun. 2015 Jun 30;6:7486. doi: 10.1038/ncomms8486.
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Oral antibiotic treatment of Helicobacter pylori leads to persistently reduced intestinal colonization rates with Oxalobacter formigenes.口服抗生素治疗幽门螺杆菌可导致产甲酸草酸杆菌在肠道内持续定植率降低。
J Endourol. 2011 Nov;25(11):1781-5. doi: 10.1089/end.2011.0243. Epub 2011 Oct 21.
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Factors related to colonization with Oxalobacter formigenes in U.S. adults.美国成年人中产甲酸草酸杆菌定植相关因素。
J Endourol. 2011 Apr;25(4):673-9. doi: 10.1089/end.2010.0462. Epub 2011 Mar 7.
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Diet, but not oral probiotics, effectively reduces urinary oxalate excretion and calcium oxalate supersaturation.饮食,而非口服益生菌,能有效降低尿草酸盐排泄和草酸钙过饱和度。
Kidney Int. 2010 Dec;78(11):1178-85. doi: 10.1038/ki.2010.310. Epub 2010 Aug 25.
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