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INTRODUCTION: Henoch-Schönlein purpura nephritis (HSN) is defined as Henoch-Schönlein purpura with kidney involvement, including hematuria and/or proteinuria. The aim of this study was to evaluate the data of HSN patients who underwent renal biopsy, and compare the main clinical and laboratory parameters that may affect renal biopsy findings, treatment protocols, and short- and long-term outcome of those patients. METHODS: Biopsies performed in 72 HSN patients between January 2007 to January 2017 were retrospectively evaluated. They were divided into two groups according to renal biopsy classification of the International Study of Kidney Disease in Children. Renal outcome, clinical and laboratory parameters, treatment protocols, and outcome were compared between groups. Short- and long-term follow-up of patients were evaluated. RESULTS: Of 72 patients, 47 were male (65.3%) and 44 (61.1%) were ≤10 years of age. Neutrophil-lymphocyte ratio was found higher in patients with scrotal involvement (p=0.042). Short-term unfavorable outcome was significantly higher in patients with scrotal involvement (p=0.038). Patients with hypertension and decreased creatinine clearance were found to have more unfavorable outcomes in long-term follow-up (p=0.029, p=0.040). CONCLUSION: Cyclosporin-A and cyclophosphamide could be effective in steroid unresponsive HSN patients. Patients with scrotal involvement, decreased creatinine clearance, and hypertension should be closely monitored for sequelae of HSN.

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Human urotensin-II (hU-II) is one of the most potent vasoconstrictors in mammals, even more potent than endothelin. It has a wide range of vasoactive properties dependent on the anatomic site and the species studied. Although it is expressed mainly in the brain and spinal cord, it is also detected in other tissues, such as the kidney. It has been recognized for over 30 years, however only recently it has become a major focus of clinical researches. It has been suggested that U-II may have a possible autocrine/paracrine functions in kidney, and may be an important target molecule in studying renal pathophsiology. Previously, we investigated the level of U-II in children with minimal change nephrotic syndrome (MCNS), and to our knowledge there is no study about the possible role of U-II in other childhood glomerulonephritis. We firstly determined the expression of h U-II in kidneys of children with several glomerular diseases. In the lights of literature and our findings, this review describes mainly the possible role of U-II in children with renal diseases and summarizes what is known, and what must be known about the U-II

La urotensina II (U-II) humana es uno de los vasoconstrictores más fuertes en los mamíferos, es incluso más potente que la endotelina. Tiene un amplio espectro de propiedades vasoactivas según su localización anatómica y las especies estudiadas. Si bien se expresa fundamentalmente en el cerebro y en la médula espinal, también se la detecta en otros tejidos como el riñón. Aunque se la conoce desde hace más de 30 años, sólo recientemente se transformó en un objetivo principal de las investigaciones clínicas. Se sugirió que la U-II podría tener funciones autocrinas/paracrinas en el riñón y que podría ser una importante molécula blanco en el estudio de la fisiopatología renal. Con anterioridad investigamos el nivel de U-II en niños con síndrome nefrótico de cambios mínimos (SNCM) y según nuestro conocimiento no existe ningún estudio acerca del posible papel de la U-II en otras glomerulonefritis infantiles. En primer lugar determinamos la expresión de la U-II en riñones de niños con varias enfermedades glomerulares. En función de la literatura y de nuestros hallazgos, en esta revisión se describe esencialmente el posible papel de la U-II en niños con enfermedades renales y se resumen los conocimientos disponibles y lo que resta saber acerca de la U-II.

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