Abstract

Sirs,We are grateful to Dr. Fujieda for suggesting anotherpossibility as the cause for uric acid stones associated withrotavirus-associated gastroenteritis [1].The pathogenesis of urate stone formation in children withhuman rotavirus (HRV)-associated gastroenteritis, which wasmainly reported from Japan, remains unknown. As formationof urolithiasis consisting of urate, which is rarely seen inchildren, is generally associated with increased urinaryexcretion of uric acid, previous reports have proposed severalpossibilities of hyperuricuria being the cause.Possible causes of hyperuricuria in this condition include:1. Hyperuricemia due to massive breakdown of intestinalcells due to HRV [2]2. Severe dehydration caused by HRV infection [2]3. Renal hypouricemia associated with mutation of humanurate transporter 1 (URAT1) gene [3]Fujieda et al. [1] suggest another intriguing hypothesis thatHRVmightinfectnotonlysmallintestinalcells,butalsorenaltubularcells,whichleadstoincreasedurinaryconcentrationofuric acid in conjunction with increased excretion of beta-2-microglobulin and N-acetyl-β-glucosaminidaseHowever, none of the possibilities mentioned above hasclearly answered the following questions:1. Why is this condition reported mainly in Japan?2. Do other viruses causing gastroenteritis, such asnorovirus or adenovirus infect renal tubular cells?3. Is an infection of the renal epithelial cells exclusivelycharacteristic of HRV?4. Why do most of the children with HRV-associatedgastroenteritis not have the complication of urateurolithiasis?Until these questions have been clarified, the pathogenesisof urolithiasis in children with HRV-associated gastroenteritiswill remain enigmatic.References

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