LAUSR

1. Uric acid (UA) is the end product of purine catabolism in humanoids, since the hepatocyte enzyme uricase, which degrades UA to allantoin in other mammals, is completely inactive. Approximately 65–75% of the UA produced daily is excreted by the kidneys, while the remaining 25–35% exits in the stool. Homeostasis of UA is determined by the balance between production and excretion. Hyperuricemia is caused by all conditions associated with increased purine synthesis and degradation during excessive cell breakdown and followup catabolism of nucleic acids, or an inability of the kidneys and gastrointestinal tract relative to urate excretion and clearance. During childhood, it is important to evaluate ageand sex-related serum UA concentration with respect to reference values. While gout is the most common cause of hyperuricemia in the adult population, it is rare in childhood, and if a child has symptoms of gout, it is usually associated with some other comorbidity, such as glycogen storage disease, Down syndrome, congenital heart disease, purine enzymopathy, uromodulin-associated kidney disease, or apolipoprotein E gene polymorphisms. Most of the abovementioned diseases are diagnosed early in childhood based on clinical symptoms; however, abnormalities of purine metabolism or uromodulinassociated kidney disease are often diagnosed in both adolescents and adults. Hyperuricemia has also been reported as a side effect of drug use (e.g., thiazide diuretics, valproate, phenobarbital, and cyclosporine). Hyperuricemia can also be found during acute diseases such as gastroenteritis, hemolytic anemia, or cancer (especially leukemias or lymphomas). Hyperuricemia is a typical laboratory anomaly in obese children and adolescents. In our cases, hyperuricemia presented during acute gastroenteritis, which had been accompanied by repeated vomiting and diarrhea. Due to the irritability of the gastrointestinal tract, our pediatric patients received only limited amounts of fluids by mouth during their symptomatic treatment at home and, as a result, gradually developed dehydration. This led to intravenous rehydration therapy during hospitalization. After 36 h of treatment, the patients stopped vomiting, and the intravenous solution was replaced with oral fluid intake, which was well tolerated. The laboratory values in both cases significantly improved during this time (for example, in Case 1, blood urea nitrogen decreased from 66.5 to 18.6mmol/l, serum creatinine from 369 to 132.8 μmol/l, serum uric acid from 1865 to 528 μmol/l, and her urine output was 1.2 ml/kg/h). During treatment, we did not use any medication to reduce hyperuricemia. Loss of body water subsequently led to laboratory evidence (i.e., blood urea nitrogen and serum creatinine) of acute renal failure of prerenal origin (i.e., in Case 1, urine osmolality was 750mmol/kg, urinary sodium 14mmol/l, fractional excretion of sodium < 1%) accompanied by slightly reduced diuresis (0.7 ml/kg/h during the first 16 h of hospitalization). The patients did not have any other clinical or laboratory values suggesting another underlying disease associated with hyperuricemia. We, therefore, suspected that the hyperuricemia in our patients was caused not only by acute renal injury but also by concomitant acute gastroenteritis, resulting in decreased intestinal UA excretion. 2. Hyperuricemia is a non-reference laboratory finding that often receives inadequate consideration by pediatricians. A differential diagnostic algorithm in pediatric patients with This refers to the article that can be found at https://doi.org/10.1007/ s00467-020-04491-w.