Hyperoxaluria is the main factor leading to the development of nephrolithiasis. Hyperoxaluria in children can be asymptomatic for a long time, leading to secondary oxalate nephropathy, to urolithiasis and chronic kidney disease. The vast majority of kidney stones are calcium oxalate. Limiting the intake of products containing oxalic acid is not the main way to prevent calcium oxalate microlites. In this regard, scientists were interested in the bacterium Oxalobacter formigenes, which exhibits a symbiotic relationship with the human body by reducing the absorption of oxalates in the intestinal lumen with a further decrease in their concentration in plasma and urine. Oxalobacter formigenes is currently the most effective intestinal absorbent microbial oxalate.

The diagnosis of secondary oxalate nephropathy was made according to the classification developed by M. S. Ignatova et al. and N.V. Voronina: moderate hyperoxaluria, pronounced oxalate-calcium crystalluria, microhematuria and/or proteinuria, increased microalbumin in the urine (tubular dysfunction). Children has to underwent a general clinical examination: Oxalates in daily urine, microalbumin in urine, bacteriological examination of feces for quantitative and qualitative composition of microflora, PCR identification of Oxalobacter formigenes in feces were determined.

It was observed, out of 35, all children in the main study group had higher levels of oxalate in daily urine of 1.2 mg/kg/ day (at a rate of 0-0.5 mg/kg/day) than in the comparison group (0.5 mg/kg/day). Gross or microscopic hematuria is found in 65% to 90% of children who have urolithiasis. All children in the main group showed a violation of the quantitative and qualitative composition of the intestinal microbiota. In the comparison group, no signs of intestinal microbiota disturbance were noted. Grade 2 dysbiosis predominated in severity in 18 children, in 2 children dysbiosis of 3 degrees was detected, in 4 children dysbiosis of 1 degree was noted. In 6 children with secondary oxalate nephropathy, Oxalobacter formigenes was not detected. It was found that children in whom Oxalobacter formigenes was not determined received a history of antibiotics of the 3rd generation cephalosporins group, Co-trimaxazole, more than 6 times for 12 months. In 21 children, Oxalobacter formigenes were identified.

In most cases, in children with secondary oxalate nephropathy, the use of antibiotics was detected and a violation of the intestinal microbiota was found. In 5 children, Oxalobacter formigenes was not identified in feces.

Regards,
Angelina Matthew
Journal Coordinator

Pediatrics & Therapeutics
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