A. Szczawińska-Popłonyk – study design, data collection and interpretation, literature search, A. Bręborowicz – acceptance of final manuscript version, L. Ossowska – data collection and interpretation. None declared. ”
“Hyperuricemia plays an important role in the pathogenesis of acute and chronic diseases including gout, tumor lysis syndrome (TLS), arterial hypertension, renal failure, coronary heart disease, left ventricular hypertrophy and metabolic syndrome [1]. In acute kidney injury (AKI), when the urine flow is low and pH is acidic, uric acid as the substance poorly soluble in water precipitates into Selleckchem CH5424802 crystals in renal tubules. This

results in increased risk of tubular obstruction. Additionally hyperuricemia is the cause of enhanced synthesis of reactive oxygen species, renin–angiotensin–aldosterone system activation,

increased endothelin-1 production and nitric oxide system inhibition, which contributes to the pathogenesis of AKI [2]. Rasburicase (recombinant urate oxidase) is an efficient protease in urate depletion, which plays a valuable role in the treatment of malignancy – associated TLS [3]. Its action includes uric acid (UA) conversion GDC-0199 cost to more soluble allantoine. This drug does not cause the accumulation of intermediate products of purine metabolism pathway such as xanthine. Intraluminal obstruction of renal tubules by precipitating uric acid has been avoided [4]. Urate oxidase was produced from cultures of Aspergillus flavus. It was introduced to the treatment of TLS in Europe in 1974. Now it is used as the recombinant form – rasburicase – Fasturtec (Sanofi-Aventis, Molecular motor Paris, France). The usage of

rasburicase has eliminated serious immunological complications caused by non-recombinant compound [5]. There is not much data in literature on rasburicase usage in AKI in children [4]. In this manuscript authors describe the application of rasburicase in the treatment of AKI in a child with acute non-malignancy associated hyperuricemia and combined congenital abnormalities. A 5-year-old boy was admitted to pediatric department with a 4-day history of vomiting, dehydratation and oliguria in the course of gastro-intestinal infection. Past history was remarkable. He had multiply congenital malformations [face dysmorphy and limb deformation with muscular contractures, hypostature, organic heart disease – significant mitral insufficiency (+ + +) with ventricular septal defect, corneal and scleral staphylomas, amaurotic right bulb, congenital cataract of left eye]. He suffered from AKI 10 months prior to current hospitalization. He developed multiorgan dysfunction syndrome after the reimplantation of artificial mitral valve. He required dialysis for 11 days (2 days on peritoneal dialysis, 9 days on continuous hemodiafiltration).