Anemia frequently complicates chronic kidney disease (CKD). We investigated here the effect of adenine-induced CKD in rats on erythrocyte count (EC), hematocrit (PCV) and hemoglobin (Hb) concentration, as well as on the activity of L-γ-glutamyl transferase (GGT) and the concentrations of iron (Fe), transferrin (Tf), ferritin (F), total iron binding capacity (TIBC) / unsaturated iron binding capacity (UIBC) and hepcidin (Hp) in serum and erythropoietin (Epo) in renal tissue. Renal damage was assessed histopathologically, and also by measuring the serum concentrations of the uremic toxin indoxyl sulfate (IS), creatinine, and urea, and by creatinine clearance. We also assessed the influence of concomitant treatment with gum acacia (GA) on the above analytes. Adenine feeding induced CKD, accompanied by significant decreases (P<0.05) in EC, PCV, and Hb, and in the serum concentrations of Fe, Tf, TIBC, UIBC and Epo. It also increased Hp and F levels. GA significantly ameliorated these changes in rats with CKD. A general improvement in the renal status of rats with CKD after GA is shown due to its antiinflammatory and anti-oxidant actions, and reduction of the uremic toxin IS, which is known to suppress Epo production, and this may be a reason for its ameliorative actions on the indices of anemia studied., B. H. Ali, M. Al Za'Abi, A. Ramkumar, J. Yasin, A. Nemmar., and Obsahuje bibliografii
Pathogenesis of adenine-induced chronic renal failure may involve inflammatory, immunological and/or oxidant mechanisms. Gum arabic (GA) is a complex po lysaccharide that acts as an anti-oxidant which can modulate inflammatory and/or immunological processes. Therefore, we tested here the effect of GA treatment (15 % in the drinking water for 4 weeks) in plasma and urine of rats, on a novel cytokine that has been shown to be pro-inflammatory, viz, DNA-binding high-mobility group box-1 protein (HMGB1). Adenine (0.75 % in the feed, 4 weeks) significantly increased indoxyl sulphate, urea and creatinine concentrations in plasma, an d significantly decreased the creatinine clearance. GA significantly abated these effects. The concentrations of HMGB1 in urine before the start of the experiment were similar in all four groups. However, 24 h after the last treatment, adenine treatment increased significantly the concentration of HMGB1 when compared with the control. GA treatment did not affect the HMGB1 concentration in urine. Moreover, the concentration of HMGB1 in plasma obtained 24 h after the last treatment in rats treated with adenine was drastically reduced compared with the control group. This may explain its significant rise in urine. In conclusion, HMGB1 can be considered a potentially useful biomarker in adenine induced CRF and its treatment., B. H. Ali, M. Al Za'abi, A. Al Shukaili, A. Nemmar., and Obsahuje bibliografii
The pathogenesis of arterial hypertension in autosomal dominant polycystic kidney disease (ADPKD) is complex and likely dependent on interaction of hemodynamic, endocrine and neurogenic factors. We decided to evaluate the role of endothelin (ET1) and nitric oxide (NO) in the regulation of arterial blood pressure (BP) and to determine plasma levels of ET1 and NO in the group of patients with ADPKD. The ADPKD group (18 patients, 6 men + 12 women, mean age 44.611.7 years, with creatinine clearancecorrig > 1.1 ml/s) was compared with a control group of 27 healthy volunteers of comparable age. Plasma levels of ET1 assessed by direct RIA determination in the group of ADPKD patients (11.03±1.8 fmol/ml) were significantly increased (p<0.001) in comparison with the control group (2.660.58 fmol/ml), while no significant differences were observed between normotensive and hypertensive patients in the ADPKD group. Serum levels of NO were evaluated according to the determination of serum levels of their metabolites - nitrites/nitrates. Serum levels of NO in the group of ADPKD patients (39.85±6.38 μmol/l) were significantly higher (p<0.05) in comparison with the control group (22.7±1.20 μmol/l), whereas in the ADPKD group no significant differences were observed between normotensive and hypertensive patients. Thus, our study supports the concept of complex alteration of both vasoconstrictor and vasodilator systems in the pathogenesis of arterial hypertension in ADPKD., M. Merta, J. Reiterová, R. Ryšavá, V. Tesař, M. Jáchymová., and Obsahuje bibliografii
Soluble leptin receptor (SLR) is the extracellular part of the leptin receptor. This protein is released into circulation and constitutes the main circulating leptin-binding protein. The aim of our study was to measure SLR concentrations in patients with chronic renal failure (CRF) and healthy subjects and to explore the relationship of SLR to other hormones and cytokines. The patients with CRF had significantly higher serum leptin, TNF-a and insulin levels than healthy subjects (25.1±23.5 vs. 9.4±7.6 ng.ml-1 (S.D.); 14.2±4.2 vs. 4.55±2.5 ng.ml-1; 39.8±36.1 vs. 20.3±11.1 mU.l-1). Serum soluble leptin receptor levels did not differ between these groups (19.1±11.3 vs. 19.6±6.1 U.ml-1). An inverse relationship between serum SLR and leptin levels was found in both groups. In patients with CRF the inverse relationship between SLR and insulin, body fat content and total protein levels were also found, while in healthy subjects only inverse relationship of SLR with insulin and albumin concentrations were detected. We conclude that soluble leptin receptor levels in patients with chronic renal failure do not differ from those of healthy subjects despite higher serum leptin levels in CRF patients. The physiological consequences of this finding require further investigation., J. Křížová, S. Sulková, V. Bednářová, E. Kotrlíková, M. Haluzík., and Obsahuje bibliografii