Decrease of Urotensin II activity can impact on the volume status in predialysis chronic kidney disease

Abstract

Urotensin II (U-II) was thought to be one of the mediators of primary renal sodium retention due to effects on renal sodium excretion. For this purpose, the relationship between U-II and overhydration was investigated. A total of 107 patients were enrolled in the study. According to body compositor monitor analysis, fluid overload up to 1.1 L, was considered normohydration. Patients were divided according to hydration status; overhydrate (n ¼ 42) and normohydrate (n ¼ 65) were studied in both groups. Pulse waveform velocity propagation for arterial stiffness and blood pressure analysis and echocardiographic left ventricular and left atrial indices were performed with known fluid overload-related parameters. U-II levels were measured by using Human ELISA kit. In overhydrated group, U-II levels were significantly lower. All parameters (blood pressure, arterial stiffness parameters, echocardiographic data, age, gender, diabetes, U-II, hemoglobin) correlated with overhydration, were determined by linear regression model (method ¼ enter), when considered together, U-II was found to be an independent predictor from other conventional overhydration-related parameters. Male sex, left ventricular mass index, left atrial volume index, hemoglobin value were found to be independent predictors for overhydration. Considering the association of low U-II levels with adverse cardiovascular events and its role in sodium retention, we think that low U-II levels can be accepted as a potential therapeutic target in patients with hypervolemic cardio-renal syndrome.

Plasma Urotensin II levels in children and adolescents with chronic kidney disease: a single-centre study

“…However the authors noticed an increase in UII levels at the end of the HD session [ 36 ]. Furthermore, in a recent study, predialysis of UII levels were lower in overhydrated compared to normohydrated ESKD patients [ 37 ]. Taking into consideration previous reports on the relationship between low UII concentration and the risk of cardiovascular events in patients with CKD, the authors assume that low levels may be a therapeutic target in overhydrated CKD patients [ 37 ].…”

“…It is speculated, that the removal of fluids from our patients by HD and the resulting hemoconcentration may have a role in the increase of HDII levels after the completion of HD [ 36 , 37 ]. Moreover, UII is a middle size molecule (molecular mass = 1388.6 g/mol) and is only partially removed using the convential HD [ 36 , 38 ].…”

Urotensin II enhances transforming growth factor-β1 expression and secretion in the kidney during aristolochic acid nephropathy

“…Studies have demonstrated that UII promotes the proliferation of renal tubular epithelial cells (12), activates the epidermal growth factor receptor in rat renal tubular epithelial cells via the SHP-2 signaling pathway (13), inhibits renal tubular reabsorption of potassium and sodium (14), promotes intracellular calcium release (15) and inhibits apoptosis in NRK-52E rat proximal tubular epithelial cells (16). In addition, UII has been proposed as a target for treating patients with hypervolemic cardio-renal syndrome (17). UII exerts a potent vasoconstrictive action as well as renal profibrotic effects (18).…”