Increased plasma levels of Urotensin-II in preeclampsia-eclampsia: a new mediator in pathogenesis?

OBJECTIVE: To assess the possible role of human Urotensin-II (hU-II), a vasoactive peptide, in the pathophysiology of preeclampsia-eclampsia prospectively. STUDY DESIGN: Sixty subjects, 30 with a diagnosis of preeclampsia-eclampsia (group I) and 30 control subjects (group II), who had been admitted between January, 2002 and December, 2002, were taken into the study. Patients in group I had an increase in blood pressure after 28th week of gestation, without any history of hypertensive disease and/or preeclampsia or eclampsia. hU-II levels were assessed using a radioimmunoassay method. RESULTS: No statistically significant difference in terms of age, gestational age, gravidity, abortion and parity was detected among groups (P > 0.05). Plasma hU-II levels in the preeclampsia-eclampsia and control groups were 10.11 +/- 5.94 pg/mL and 3.93 +/- 1.73 pg/mL, respectively. Difference between plasma hU-II levels of the two groups was found to be statistically significant (P < 0.00001). Also there was correlation between hU-II levels and mean arterial pressures in both groups (r = 0.73, P < 0.0001 and r = 0.72, P < 0.0001 for groups I and II, respectively). CONCLUSION: Results of our study strongly suggest an important role for hU-II in the pathophysiology of preeclampsia-eclampsia. Further studies concerning placenta and cord blood samples will more clearly elucidate the role of Urotensin-II in the pathogenesis of preeclampsia-eclampsia, and its feto-maternal effects.

Urotensin-II levels in children with minimal change nephrotic syndrome.

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 syndrome (MCNS). Considering the renal synthesis and vasoactive role of U-II, we aimed to measure the plasma and urinary levels of U-II in children with MCNS, and investigate the correlation with other clinical and laboratory findings. Twenty-six children with clinical MCNS, ranging 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 measured 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 relapse, 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.