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Nees, B.J. Perry, M. Choi, M. Bodria, Y. Liu, P.L. Weng, V.J. Lozanovski, M. Verbitsky, F. Lugani, R. Sterken, N. Paragas, G. Caridi, A. Carrea, M. Dagnino, A. Materna-Kiryluk, G. Santamaria, C. Murtas, N. Ristoska-Bojkovska, C. Izzi, N. Kacak, B. Bianco, S. Giberti, M. Gigante, G. Piaggio, L. Gesualdo, D. Kosuljandic Vukic, K. Vukojevic, M. Saraga-Babic, M. Saraga, Z. Gucev, L. Allegri, A. Latos-Bielenska, D. Casu, M. State, F. Scolari, R. Ravazzolo, K. Kiryluk, Q. Al-Awqati, V.D. D’Agati, I.A. Drummond, V. Tasic, R.P. Lifton, G.M. Ghiggeri, and A.G. Gharavi: Mutations in DSTYK and Dominant URINARY SYSTEM Malformations Congenital malformations of the kidney and urinary system donate to 23 percent of birth defects1,2 and account for 40 to 50 percent of pediatric cases and 7 percent of adult instances of end-stage renal disease worldwide.3,4 These disorders are heterogeneous and encompass a wide range of anatomical defects genetically, such as for example renal agenesis, renal hypodysplasia, ureteropelvic junction obstruction, or vesicoureteral reflux.5 Mutations in genes that cause syndromic disorders, such as PAX2 and HNF1B mutations, are detected in only 5 to 10 percent of cases.6,7 Familial types of nonsyndromic disease have been reported, further supporting genetic determination8,9; however, owing to locus heterogeneity and small pedigree size, the genetic reason behind most familial or sporadic situations remains unknown.