lysine hydrochloride/proteinuria

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Proteinuria is reduced by inhibition of inducible nitric oxide synthase in rat renal ischemia-reperfusion injury.

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BACKGROUND Ischemia-reperfusion (IR)-induced nephrotoxicity is associated with proteinuria. There are reports on the involvement of inducible nitric oxide synthase (iNOS) in proteinuria in conjunction with renal disease. This study was designed to investigate the effect of N6-(1-iminoethyl)-L-lysine

Renal disposition of amylase, lipase, and lysozyme in the dog.

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Normal adult dogs were given intravenously lysine hydrochloride to abolish renal tubular reabsorption. The treatment caused tubular proteinuria. Once forced diuresis was established, fractional clearances for amylase, lipase, and lysozyme increased five-, 18-, and 857-fold over the baseline values,

(-)-Epicatechin 3-O-gallate ameliorates the damages related to peroxynitrite production by mechanisms distinct from those of other free radical inhibitors.

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This study was carried out to elucidate whether the protective activity of (-)-epicatechin 3-O-gallate (ECg) against excessive peroxynitrite (ONOO(-)) production, is distinct from the activity of several well-known free radical inhibitors, the ONOO(-) inhibitors ebselen and uric acid, the superoxide

Evaluation of inducible nitric oxide synthase inhibition on kidney function and structure in high-fat diet-induced kidney disease.

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What is the central question of this study? The metabolic pathways regulating the effects of obesity on the kidney remain unknown. We sought to determine whether inducible nitric oxide synthase (iNOS) is involved in the underlying mechanisms of high-fat diet-induced kidney disease using a specific

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