Comparison of the prophylactic antithrombotic effect of indobufen and warfarin in patients with nephrotic syndrome: a randomized controlled trial.

PURPOSE: The risk of thromboembolic events is elevated in patients with nephrotic syndrome, and warfarin use has been associated with an increased risk of bleeding. Indobufen, a selective cyclooxygenase-1 inhibitor, is currently being evaluated for the prevention of thromboembolic events in nephrotic syndrome. This study aimed to compare the efficacy and safety of indobufen with that of warfarin in patients with nephrotic syndrome. MATERIALS AND METHODS: This multicenter, randomized, three-arm, open-label, parallel controlled trial involved a total of 180 adult patients with nephrotic syndrome from four centers in China. Patients were randomly assigned to receive 100 mg indobufen (bid), 200 mg indobufen (bid), and 3 mg warfarin (qd) daily for 12 weeks. The primary endpoints included thromboembolic and bleeding events, while laboratory results and adverse events constituted secondary endpoints. RESULTS: No thromboembolic events occurred in the high-/low-dose indobufen and warfarin groups. Moreover, the use of a low dose of indobufen significantly reduced the risk of minor bleeding events compared with warfarin use (2% versus 18%, p < .05). Finally, adverse events were more frequent in warfarin-treated patients. CONCLUSIONS: This study found that indobufen therapy provided equivalent effects in preventing thromboembolic events compared with warfarin therapy, while low dose of indobufen was associated with a reduced risk of bleeding events, thus it should be recommended for the prevention of thromboembolic events in clinical practice in patients with nephrotic syndrome. TRIAL REGISTRATION NUMBER: ChiCTR-IPR-17013428.

Extralobar pulmonary sequestration in the right lower thoracic region associated with esophageal fistula.

Extralobar pulmonary sequestrations (ELS) are most commonly found within the left thoracic cavity. We report the case of a 10-year-old girl with ELS in the right thoracic cavity, associated with esophageal fistula. Chest computed tomography scans revealed a parenchymal mass between the right lower lobe and the diaphragm. At last, successful resection of the mass and repair of the esophageal fistula were performed. The girl recovered uneventfully.

Irbesartan attenuates contrast media-induced NRK-52E cells apoptosis.

BACKGROUND: Radiocontrast nephropathy (RCN) is a major complication after radiographic examination. The precise mechanisms underlying RCN are not well understood. Renal tubular cell apoptosis is a feature of RCN, but hyperosmolality cannot fully explain the cytotoxicity of contrast media. There is accumulating evidence that reactive oxygen species (ROS) is involved in the pathophysiology of RCN, whereas the correlation between oxidative stress and contrast media-induced cell apoptosis is not clear. We hypothesized that ROS mediated apoptosis in renal tubular cells exposed to contrast media. Irbesartan, a selective AT(1) receptor antagonist has been demonstrated an antioxidative effect. The present study was designed to determine whether irbesartan attenuated the contrast media-induced renal tubular cell apoptosis. METHODS: NRK-52E cells were exposed to increasing concentration (25, 50, 100, 150 mgiodinemL(-1), 335, 384, 420, 521 mOsmkg(-1)) of ioversol (a non-ionic contrast media) for 1h or incubated in ioversol (100 mgiodinemL(-1), 420 mOsmkg(-1)) for 15 min, 30 min, 60 min, 120 min, 240 min, respectively. Mannitol with the same osmolality as ioversol (420 mOsmkg(-1)) also treated NRK-52E cells for 1h. In separate experiment, irbesartan (0.01, 0.1, 1 mmolL(-1)) was added 1h before incubation with ioversol (100 mgiodinemL(-1), 420 mOsmkg(-1)) for 1h. Apoptosis was determined by Hoechst staining and flow cytometry with annexinV-FITC and propidium iodide. The intracellular formation of ROS was detected by confocal microscopy with fluorescent probe CM-H2DCFDA. Bax and bcl-2 mRNA expression were determined by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Ioversol induced NRK-52E cells apoptosis in a concentration- and time-dependent manner. The intracellular ROS generation was greatly increased following ioversol stimulus. Furthermore, ioversol induced a decrease in the expression for bcl-2 mRNA and an increase for bax mRNA. Irbesartan attenuated the ioversol-induced apoptosis in NRK-52E cells in a dose-dependent manner, in which the protective effect of irbesartan was dependent on decreasing intracellular ROS formation. In addition, irbesartan reversed the ioversol-induced increase in bax mRNA and decrease in bcl-2 mRNA. CONCLUSION: Ioversol induced NRK-52E cells apoptosis in a concentration- and time-dependant manner via an increase in oxidative stress and subsequent to the increase in mRNA expression for bax and reduction in bcl-2 mRNA. Irbesartan attenuated the ioversol-induced apoptosis in NRK-52E cells by reducing oxidative stress and reversing the enhancement of bax mRNA and the reduction in bcl-2 mRNA.