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- W2090422257 abstract "Background: The pathophysiology of hyperhomocysteinaemia in chronic renal failure (CRF) is unknown. Possible mechanisms are decreased renal homocysteine (Hcy) catabolism or inhibition of extrarenal Hcy metabolism by uraemic toxins.Methods: We studied the short-term effect on plasma Hcy concentration of improvement of renal function after successful kidney transplantation (n=8), and determined renal Hcy extraction by measurement of total Hcy in arterial and renal venous blood in 7 cardiac patients with normal renal function.Results: Post-transplantation, plasma Hcy decreased with improving renal function. In the cardiac patients, no significant renal Hcy extraction could be demonstrated, but tubular disposal of the filtered load could not be excluded.Conclusions: Because loss of such renal metabolism could lead to hyperhomocysteinaemia in CRF, it is necessary to determine the renal extraction of free Hcy in subjects with normal renal function to further investigate renal homocysteine metabolism." @default.
- W2090422257 created "2016-06-24" @default.
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- W2090422257 date "2006-01-01" @default.
- W2090422257 modified "2023-10-16" @default.
- W2090422257 title "Th-S17:3 Early emerging studies of the atherogenicity of lipoproteins (a European perspective)" @default.
- W2090422257 doi "https://doi.org/10.1016/s1567-5688(06)81960-4" @default.
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