Amikacin is a commonly used antibacterial drug that can cause significant nephrotoxic effects in both humans and experimental animals. It has been reported that one mechanism of the toxic effects of aminoglycoside antibiotics are the result of oxidative reactions. The aim of this study is to examine the effects of N-acetylcysteine, a thiol-containing antioxidant, on renal function (serum creatinine) and morphology (renal tubular damage) in mice subjected to amikacin-induced nephrotoxicity. A total of 32 mice were equally divided into four groups that were injected with either saline, amikacin (1.2g/kg intraperitoneally), N-acetylcysteine (150mg/kg intraperitoneally for three days) plus amikacin (1.2 g/kg intraperitoneally on the third day as a single dose), or N-acetylcysteine (150mg/kg intraperitoneally). Amikacin administration led to granulovacuolar tubular degeneration in light microscopic examination and myeloid bodies, mitochondrial electron-dense material deposition, and mitochondrial swelling in the proximal tubule epithelium in the electron microscopic evaluation. N-acetylcysteine administration before amikacin injection caused significant decreases in myeloid body and mitochondrial swelling and granulovacuolar tubular degeneration formation. Serum creatinine levels did not change as a result of any treatment. The results show that N-acetylcysteine has a protective effect on nephrotoxicity induced by amikacin. Higher doses of amikacin should be tried to observe biochemical effects.
A spectrum of renal abnormalities of patients with situs inversus has been reported. Renal dysplasia is the most common. Herein is described for the first time, an association of situs inversus totalis, unilateral congenital renal hypoplasia and external ear cartilage deformity.
Arterial and venous thrombosis is a prominent feature of antiphospholipid syndrome together with antiphospholipid antibodies. We report generalised thrombosis in a 28 years old male patient with antiphospholipid syndrome associated with lupus erythematosis. Firstly the patient had myocardial infarction. Eight months later he started to complain about oedema which was found to be secondary to nephrotic syndrome. In his third hospital day he developed pulmonary emboli. Tomographic angiography revealed left renal vein thrombosis, portal vein thrombosis, right renal infarct, pulmonary emboli. His tests for antinuclear antibody, anti dsDNA antibody and antiphospholipid antibody IgM Downloaded from were positive. After anticoagulation therapy and immunosupressive therapy he could have been disconnected from mechanical ventilator and his oedema nearly disappeared. This case clearly highlights the fact that antiphospholipid syndrome with systemic lupus erythematosus can present with myocardial infarction in young patients.
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