Homocysteine metabolism in renal failure

Alessandra F Perna1, Diego Ingrosso, Ersilia Satta

  • 1First Division of Nephrology/Department of Pediatrics, School of Medicine, Second University of Naples, Naples, Italy. alessandra.perna@unina2.it

Insights

Hyperhomocysteinemia, linked to cardiovascular disease, is common in renal failure. New research explores its causes and consequences, including DNA hypomethylation, with ongoing trials investigating its role in kidney patients.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Biochemistry

Background:

  • Hyperhomocysteinemia is a known risk factor for cardiovascular disease in the general population.
  • Renal failure is characterized by a high prevalence of both hyperhomocysteinemia and cardiovascular disease.

Purpose of the Study:

  • To review recent findings on homocysteine metabolism in renal failure.
  • To explore the association between homocysteine and cardiovascular disease in kidney patients.

Main Methods:

  • Review of prospective studies and meta-analyses.
  • Analysis of ongoing intervention trials in transplant patients.
  • Investigation of factors influencing homocysteine levels in uremia.

Main Results:

  • Hyperhomocysteinemia is confirmed as a cardiovascular disease risk factor.
  • Renal metabolic extraction of homocysteine depends on renal plasma flow.
  • Riboflavin influences plasma homocysteine levels in uremia.
  • Consequences include DNA hypomethylation and altered gene expression.

Conclusions:

  • The exact causes of hyperhomocysteinemia in renal failure remain unclear, possibly due to uraemic toxicity affecting metabolism.
  • Renal plasma flow plays a significant role in homocysteine metabolism.
  • Hyperhomocysteinemia in renal failure impairs methylation processes, affecting gene expression.
  • Intervention trials are evaluating the causal link between hyperhomocysteinemia and cardiovascular disease in this population.
Abstract

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