Abstract
Hyperhomocysteinemia, an independent, modifiable risk factor for cardiovascular disease, is found in most patients with end-stage renal disease. In this issue, Perna et al. examine the extent of protein-S-linked and protein-N-linked homocysteinylation in uremic patients on hemodialysis and the effect of folate treatment on protein homocysteinylation. Their findings show that protein-N-linked homocysteinylation, but not S-linked homocysteinylation, can be normalized by folate therapy.
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