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INTRODUCTION: Making an early diagnosis of acute kidney injury (AKI) is crucial. Classical biomarkers are not capable of early detection of AKI, but novel biomarkers that do have this capability are expensive and not universally available. This prospective study attempts to mitigate these limitations through the evaluation of daily urine analysis on patient admitted to a critical care unit in order to detect early AKI. METHODS: Daily urinary indices were measured on every patient admitted to the intensive care unit (ICU) from the time of admission until his/her discharge from the ICU or death. This renal monitoring consisted of daily blood and spot morning urine samples in order to measure creatinine, urea, sodium, chloride and potassium in order to calculate the fractional excretion of sodium (FENa), chloride, urea and potassium. The data collected on these patients in the previous days was analyzed to determine whether or not there was a significant statistical difference in the urinary indices one day before the clinical diagnosis of AKI (day - 1) and 2 days before the diagnosis (day - 2). The statistical test applied was a single rank test, using as a limit of significance a value of P < 0.05. RESULTS: Of the 203 patients included, 61 developed AKI. A statistical significant difference was documented only in the value of urinary sodium (UNa) and FENa between day-1 (one day before AKI clinical diagnosis) and day-2 (two days before AKI clinical diagnosis). CONCLUSION: Daily monitoring of UNa and FENa detected a significant change in their basal values 24 hours before clinical diagnosis of AKI was made.
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Overstimulation of ionotropic glutamate receptors causes excitotoxic neuronal death contributing to neurodegenerative disorders. Massive influx of calcium in excitotoxicity provokes alterations in the membrane potential of mitochondria and increases the production of reactive oxygen species. Here we report that Mangifera indica L. extracts (MiE) prevent glutamate-induced excitotoxicity in primary cultured neurons of the rat cerebral cortex. To evaluate the effects of MiE on excitotoxicity, cells were stimulated with L-glutamic acid (50 microM; 10 min) alone or in the presence of MiE. Maximal protection (56%) was obtained with 2.5 microg/mL of MiE. In turn, we measured the effects of MiE on excitotoxic-induced oxidative stress and mitochondrial depolarization by fluorimetry using 5,6-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate and tetramethylrhodamine, respectively. Both parameters were effectively reduced by MiE at concentrations which showed neuroprotection. Mangiferin, an antioxidant polyphenol which is a major component of MiE, was also effective in preventing neuronal death, oxidative stress and mitochondrial depolarization. Maximal protection (64%) was obtained at 12.5 microg/mL of mangiferin which also attenuated oxidative stress and mitochondrial depolarization at the neuroprotective concentrations. Together, these results indicate that MiE is an efficient neuroprotector of excitotoxic neuronal death, indicates that mangiferin carries a substantial part of the antioxidant and neuroprotective activity of MiE, and that this natural extract has therapeutic potential to treat neurodegenerative disorders.
