Pediatr Nephrol (2005) 20:42–45 DOI 10.1007/s00467-004-1716-5 ORIGINAL ARTICLE Ayse Balat · I. Halil Pakir · Faysak Gok · Ruksen Anarat · Saime Sahinoz Urotensin-II levels in children with minimal change nephrotic syndrome Received: 19 March 2004 / Revised: 14 September 2004 / Accepted: 20 September 2004 / Published online: 25 November 2004  IPNA 2004 Abstract Human urotensin-II (hU-II) is the most potent mammalian vasoconstrictor identified to date. 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 speculated that U-II might be an important physiological mediator of vascular tone and blood pressure in humans. To our knowledge, no studies have investigated the level of U-II in children with minimal change nephrotic syn- drome (MCNS). Considering the renal synthesis and va- soactive role of U-II, we aimed to measure the plasma and urinary levels of U-II in children with MCNS, and in- vestigate the correlation with other clinical and laboratory findings. Twenty-six children with clinical MCNS, rang- ing in age from 2 to 7 years, were compared with 16 healthy age- and sex-matched controls. The median age of the children was 4.73€2.36 years. U-II level was mea- sured by RIA. Plasma U-II concentrations (pg/ml) were decreased during relapse (20.11€14.43 in relapse, 38.94€23.86 in remission, P<0.05), whereas urinary U-II levels (pg/mg urinary creatinine) were significantly higher in relapse than in remission (37.31€28.43 in re- lapse, 31.09€21.10 in remission, P<0.05). We could not detect any relationship between U-II levels and other clinical and laboratory parameters. Our data indicate that the important changes in plasma and urinary U-II levels during relapse may be the result of heavy proteinuria rather than playing a role in mediating the clinical and laboratory manifestations of MCNS in children. Keywords Minimal change nephrotic syndrome · Urotensin-II Introduction Human urotensin-II (hU-II) is a cyclic peptide of 11 amino acids cleaved from a larger prepro-U-II precursor peptide of about 130 amino acids [1, 2]. It is a ligand for the orphan G-protein-coupled receptor, GPR14 [2]. Al- though human prepro-U-II mRNA is expressed mainly in the brain and spinal cord, it is also detected in other tis- sues, such as kidney, spleen, small intestine, thymus, prostate, pituitary, and adrenal gland [1]. U-II is the most potent mammalian vasoconstrictor identified to date [2], being tenfold more potent than endothelin-I. It circulates in the plasma of healthy indi- viduals, and acts as a circulating vasoactive hormone [3] and as a locally acting paracrine or autocrine factor in cardiovascular regulation [3, 4]. It may also be detected in urine [3]. It has been speculated that U-II might be an important physiological mediator of vascular tone and blood pres- sure in hums and, since its vasoconstrictor effects are modulated by endothelium-dependent vasodilators, that it may be of importance in states of endothelial dysfunction [3]. Although it is a potent mammalian vasoconstrictor [2], it also has a vasodilatory effect on the small arteries of rats [5] and on the resistance arteries of humans [6], through release of endothelium-derived hyperpolarizing factor and nitric oxide. Although it has been recognized as A. Balat · I. H. Pakir Department of Pediatrics, Medical Faculty, Gaziantep University, Gaziantep, Turkey F. Gok Department of Pediatric Nephrology, Gulhane Military Medical School, Ankara, Turkey R. Anarat Laboratory of Baskent University, Adana Hospital, Turkey S. Sahinoz Department of Public Health, Medical Faculty, Gaziantep University, Gaziantep, Turkey A. Balat ( ) ) Gaziantep University, P.T.T Subesi, P.K 34, 27310 Gaziantep, Turkey e-mail: aysebalat@hotmail.com Tel.: +90-342-3357374