Absence of Oxalobacter Formigenes in Cystic Fibrosis Patients: A Risk Factor for Hyperoxaluria

Sidhu, H.; Höppe, Bernd; Hesse, Albrecht; Tenbrock, Klaus; Brömme, Sabine; Rietschel, Ernst; Peck, Ammon B.

doi:10.1016/s0022-5347(05)69046-5

Cited by 23 publications

(27 citation statements)

References 19 publications

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“…The absence of the intestinal oxalate-degrading bacterium Oxalobacter formigenes has been found to be associated with hyperoxaluria [40], so that a colonization of the gut by direct administration of the bacteria in capsule form may HD to clear oxalate 3. K-Tx CAD: needs two different donors-loss of immunological benefit.…”

Section: Future Trendsmentioning

confidence: 99%

Primary hyperoxaluria type 1: still challenging!

et al. 2006

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Primary hyperoxaluria type 1, the most common form of primary hyperoxaluria, is an autosomal recessive disorder caused by a deficiency of the liver-specific enzyme alanine: glyoxylate aminotransferase (AGT). This results in increased synthesis and subsequent urinary excretion of the metabolic end product oxalate and the deposition of insoluble calcium oxalate in the kidney and urinary tract. As glomerular filtration rate (GFR) decreases due to progressive renal involvement, oxalate accumulates and results in systemic oxalosis. Diagnosis is still often delayed. It may be established on the basis of clinical and sonographic findings, urinary oxalate +/- glycolate assessment, DNA analysis and, sometimes, direct AGT activity measurement in liver biopsy tissue. The initiation of conservative measures, based on hydration, citrate and/or phosphate, and pyridoxine, in responsive cases at an early stage to minimize oxalate crystal formation will help to maintain renal function in compliant subjects. Patients with established urolithiasis may benefit from extracorporeal shock-wave lithotripsy and/or JJ stent insertion. Correction of the enzyme defect by liver transplantation should be planned, before systemic oxalosis develops, to optimize outcomes and may be either sequential (biochemical benefit) or simultaneous (immunological benefit) liver-kidney transplantation, depending on facilities and access to cadaveric or living donors. Aggressive dialysis therapies are required to avoid progressive oxalate deposition in established end-stage renal disease (ESRD), and minimization of the time on dialysis will improve both the patient's quality of life and survival.

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Section: Future Trendsmentioning

confidence: 99%

Primary hyperoxaluria type 1: still challenging!

et al. 2006

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“…Oxalobacter formigenes, the best-known oxalate-degrading bacteria that derive metabolic energy solely from oxalate, appear to begin to colonize the colon at ages 6-8 y; however, only 60-80% of the adults test positive for these bacteria, with the use of antibiotics a possible contributing factor to this reduction [3]. Several studies have linked the absence of O. formigenes to higher urinary oxalate levels [4][5][6]. In addition, several studies have assessed the effects of oral administration of different probiotic preparations, containing bacterial species with oxalate-degrading potential, on urinary oxalate excretion [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Acute probiotic ingestion reduces gastrointestinal oxalate absorption in healthy subjects

Al-Wahsh

Liebman

2011

Urol Res

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Both a high dietary oxalate intake and increased intestinal absorption appear to be major causes of elevated urine oxalate, a risk factor for kidney stone formation. A number of recent studies have assessed whether daily ingestion of a probiotic containing oxalate-degrading bacteria could lead to sufficient gut colonization to increase oxalate degradation, thereby reducing urinary oxalate. In contrast, the present study assessed whether simultaneous ingestion of oxalate-degrading probiotic bacteria with a 176 mg oxalate load could lead to decreased urinary oxalate in a population of 11 healthy non-stone formers (8 females, 3 males), aged 21-45 years. The results indicated that both the single and double doses of VSL#3(®) probiotic solutions were effective in reducing urinary oxalate and estimated oxalate absorption with no significant difference between the two probiotic doses. The timing of the reduction in urinary oxalate suggested a small intestinal and possibly gastric reduction in oxalate absorption. Similar to what had been reported for chronic or daily probiotic ingestion, individuals characterized by high oxalate absorption were most likely to experience clinically significant reductions in urinary oxalate in response to acute probiotic ingestion.

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“…1) (mean Ϯ SEM). CaCO 3 tended to increase Ca oxalate crystal and oxalate/Osm in urine, but AAACa did not ciated with an increased risk of hyperoxaluria and calcium oxalate nephrolithiasis, especially in patients with cystic fibrosis [12]. Urine may contain inhibitors of calcium oxalate crystal growth such as nephrocalcin, one of the Gla proteins regulated by vitamin K. Warfarin, a vitamin K antagonist, failed to change the ability of the urine to inhibit Ca oxalate crystal growth [13].…”

Section: Discussionmentioning

confidence: 99%

Heated oyster shell with algal ingredient (AAACa) decreases urinary oxalate excretion

Ohgitani

Fujita²

2000

J Bone Miner Metab

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In nine normal subjects, four men and five women between 23 and 49 years of age, 800mg calcium was orally administered as active absorbable algal calcium (AAA Ca) (A) and calcium carbonate (CaCO3) (B), to compare with non-calcium-containing placebo (C) in a crossover design. Calcium, oxalate, osmolality, creatinine, and pH were measured in the first three morning urine samples and Ca/osmolality, Ca/osmolality/body weight, Ca/creatinine, and oxalate/ osmolality were calculated to correct for urine dilution. Ca x oxalate product was also calculated, and Ca oxalate crystal in the sediment was microscopically examined, semiquantitatively estimated as -, +, ++, or , and numerically expressed as 0, 1, 2, or 3, respectively. Urinary Ca excretion was similar in groups A and B, but significantly larger than in group C, regardless of the method of correction for dilution. Urinary oxalate excretion with correction for osmolality, however, was significantly lower in A than in B and C, which gave similar values. Urine pH was similar among all three groups. Ca x oxalate product was significantly higher in C than in A, but A and B were not significantly different. AAA Ca appeared to decrease urinary oxalate excretion and Ca x oxalate product more efficiently than CaCO3, suggesting the possibility of inhibiting the formation of Ca x oxalate kidney stones.

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Absence of Oxalobacter Formigenes in Cystic Fibrosis Patients: A Risk Factor for Hyperoxaluria

Cited by 23 publications

References 19 publications

Primary hyperoxaluria type 1: still challenging!

Primary hyperoxaluria type 1: still challenging!

Acute probiotic ingestion reduces gastrointestinal oxalate absorption in healthy subjects

Heated oyster shell with algal ingredient (AAACa) decreases urinary oxalate excretion

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