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Homocysteine and cardiovascular disease in renal disease
Simon K Austen1, Jeff S Coombes, Rob G Fassett
1School of Human Movement Studies, University of Queensland, St Lucia, Queensland, Australia.
Insights
Elevated homocysteine (hyperhomocysteinaemia) is common in renal patients and linked to cardiovascular disease (CVD). Further trials are needed to confirm if treating hyperhomocysteinaemia in renal patients prevents CVD events.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Elevated homocysteine (hyperhomocysteinaemia) is a significant concern in patients with renal disease.
- A strong association exists between hyperhomocysteinaemia and cardiovascular disease (CVD), though causality is not definitively established in renal populations.
Purpose of the Study:
- To explore the relationship between hyperhomocysteinaemia and CVD in renal patients.
- To investigate potential mechanisms linking elevated homocysteine to cardiovascular events.
Main Methods:
- Review of existing evidence on homocysteine metabolism and CVD in renal patients.
- Analysis of purported pathophysiological mechanisms.
Main Results:
- Renal patients exhibit a higher prevalence of hyperhomocysteinaemia.
- Potential contributing factors include reduced renal and extrarenal metabolism of homocysteine.
- Proposed mechanisms involve endothelial injury, smooth muscle cell proliferation, LDL oxidation, and altered hemostasis.
Conclusions:
- Long-term, placebo-controlled trials are essential to ascertain if hyperhomocysteinaemia causes CVD events in renal patients.
- The necessity of therapeutic targeting for hyperhomocysteinaemia in this population requires further investigation.
Abstract:
Elevated homocysteine (hyperhomocysteinaemia) in renal patients is a major concern for physicians. Although cause and effect between homocysteine and cardiovascular disease (CVD) has not been established in either the general population or renal patients, there is much evidence that this relationship does exist. Purported mechanisms that may explain this effect include increases in endothelial injury, smooth muscle cell proliferation, low-density lipoprotein oxidation and changes in haemostatic balance. Renal patients have a much greater incidence of hyperhomocysteinaemia and this may be explained by decreases in either the renal or extrarenal metabolism of the compound. We conclude that data from long-term placebo-controlled trials are urgently required to determine whether hyperhomocysteinaemia in renal patients is a cause of CVD events and requires therapeutic targeting.
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