Toxic effects of hyperhomocysteinemia in chronic renal failure and in uremia: cardiovascular and metabolic consequences.
Hyperhomocysteinemia, highly prevalent in well-nourished patients with chronic renal failure and in uremia, causes toxic effects that can be envisioned in terms of cardiovascular risk increase. However, its effects on cellular metabolism and on gene expression, not to mention receptor regulation, only recently are being evaluated. For example, it has been shown that hypomethylation induced by hyperhomocysteinemia can alter erythrocyte membrane protein repair and gene expression. In addition, increased plasma protein L-isoaspartyl content, related to hyperhomocysteinemia and uremic toxicity, determines specific effects on protein function, with a reduced binding of homocysteine to albumin. We propose that uremia is a state in which proteins present a widespread derangement of structure-function relationships.
Perna
Alessandra F
AF
First Division of Nephrology/Department of Pediatrics, and Cardiovascular Research Center, School of Medicine, Second University of Naples, Naples, Italy. alessandra.perna@unina2.it
Capasso
Rosanna
R
Acanfora
Filomena
F
Satta
Ersilia
E
Lombardi
Cinzia
C
Ingrosso
Diego
D
Violetti
Eleonora
E
Romano
Maria Maddalena
MM
De Santo
Natale G
NG
D002318:Cardiovascular Diseases / Q000209:etiology*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000150:complications*; D007676:Kidney Failure, Chronic / Q000150:complications*; D008659:Metabolic Diseases / Q000209:etiology*; D014511:Uremia / Q000150:complications*