Renal ischemia/reperfusion injury is a common cause of acute kidney injury (AKI) and hypertension might contribute to the increased incidence of AKI. The purpose of this study was to investigate the effects of single and combined hyperbaric oxygen (HBO) preconditioning and NADPH oxidase inhibition on oxidative stress, kidney function and structure in spontaneously hypertensive rats (SHR) after renal ischemia reperfusion injury. HBO preconditioning was performed by exposing to pure oxygen (2.026 bar) twice a day for two consecutive days for 60 minutes, and 24h before AKI induction. For AKI induction, the right kidney was removed and ischemia was performed by clamping the left renal artery for 45 minutes. NADPH oxidase inhibition was induced by apocynin (40 mg/kg b.m., intravenously) 5 minutes before reperfusion. AKI significantly increased renal vascular resistance and reduced renal blood flow, which were significantly improved after apocynin treatment. Also, HBO preconditioning, with or without apocynin treatment showed improvement on renal hemodynamics. AKI significantly increased plasma creatinine, urea, phosphate levels and lipid peroxidation in plasma. Remarkable improvement, with decrease in creatinine, urea and phosphate levels was observed in all treated groups. HBO preconditioning, solitary or with apocynin treatment decreased lipid peroxidation in plasma caused by AKI induction. Also, combined with apocynin, it increased catalase activity and solitary, glutathione reductase enzyme activity in erythrocytes. While AKI induction significantly increased plasma KIM-1 levels, HBO preconditioning, solitary or with apocynin decreased its levels. Considering renal morphology, significant morphological alterations present after AKI induction were significantly improved in all treated groups with reduced tubular dilatation, tubular necrosis in the cortico-medullary zone and PAS positive cast formation. Our results reveal that NADPH oxidase inhibition and hyperbaric oxygen preconditioning, with or without NADPH oxidase inhibition may have beneficial effects, but their protective role should be evaluated in further studies.

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Background: Fetal serum β₂-microglobulin (β₂M) has been reported as a reliable indicator of fetal infectious diseases. Objectives: To evaluate serum β₂M as a marker of congenital toxoplasmosis or cytomegalovirus (CMV) infection in neonates. Methods: β₂M was retrospectively measured in 72 neonatal serum samples from preterm neonates. Of these, 32 originated from neonates with serological evidence of congenital toxoplasmosis (n = 12) and CMV infection (n = 20), while 40 samples from neonates in which both infections were serologically excluded served as controls. β₂M levels were compared between the infection and control groups. Results: Mean (±SEM) β₂M levels were significantly higher in the groups of neonates infected with Toxoplasma (5.64 ± 0.61 mg/l) (p = 0.014) and CMV (6.06 ± 0.66 mg/l) (p < 0.0001) than in the control group (3.80 ± 0.2). Against the cut-off level of 5 mg/l, β₂M was normal in 36 of the 40 uninfected neonates examined, indicating a specificity of 90%. In contrast, it was elevated in 66.7% (8/12) and 65% (13/20) of the Toxoplasma and CMV-infected neonates, respectively, indicating an overall sensitivity of 66%. Conclusions: In the absence of urogenital disorders, an increase in β₂M in neonates is likely to be infection-induced. We showed that serum β₂M is increased in congenital toxoplasmosis and CMV infection in the first weeks of life.

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TASK2 (K 2P 5.1, KCNK5) is a two-pore domain K + channel belonging to the TALK subgroup of the K 2P family of proteins. TASK2 expression has been reported in a variety of cells and tissues ranging from kidney to immune cells and including specific neurons, its proposed functions spanning from involvement in the regulation of cell volume to control of excitability. The purpose of this study was to determine the tubule location of the TASK2 K + channel protein in frog kidney applying polyclonal antibody against the carboxyl terminus of human TASK2 (KCNK5) protein. Immunohistochemical analysis revealed that TASK2 is expressed on distal tubules and proximal epithelial cells. TASK2 is strongly expressed predominantly on the luminal part of the proximal epithelial cells and slightly cytoplasmatic staining is expressed. Distal tubules showed diffuse cytoplasmatic staining as well as slight staining on the apical parts of the cells. These findings suggest that the TASK2 K + channel has cell-specific roles in renal potassium ion transport.

Peritubular membrane potential in kidney proximal tubular cells of spontaneously hypertensive rats (SHR-Okamoto strain adult rats) was measured with conventional 3 mol KCl microelectrodes, in vivo. Peritubular cell membrane potential was not different in SHR (-66.5 ± 0.7 mV) as compared with normotensive control Wistar rats (-67.5 ± 1.2 mV). To test the effects of possible altered sodium membrane transport in SHR on proximal tubule peritubular membrane potential, we allowed SHR and control rats to drink 1% NaCl for two weeks. Again, proximal tubule peritubular membrane potential was not different in SHR on 1% NaCl (-67.0 ± 1.0 mV) as compared with control rats on 1% NaCl (-64.7 ± 1.3 mV). From these results we concluded that peritubular membrane potential in kidney proximal tubular cells of SHR was not different from normotensive Wistar control rats, and if some alteration of sodium transport in kidney proximal tubular cells of SHR could exist, that was not possible to evaluate from the measurements of peritubular membrane potential in kidney proximal tubular cells.

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