The importance of homocysteine levels in the prognosis of patients with chronic renal disease and in hemodialysis patients

Bruna M Martella,Glaucia Raquel L Veiga,Flavia S Gehrkei,Ligia A Azzalis,Virginia B C Junqueira,Beatriz C A Alves,Fernando Luiz A Fonseca,Marcelo R Bacci

doi:10.5935/1676-2444.20180030

Abstract

ABSTRACT Introduction: Homocysteine (Hcy) is one of the metabolites of methionine (Met), an essential diet-derived amino acid. There is a close relationship between high plasma Hcy levels and declining renal function. Plasma and urinary Hcy level has been the target of studies as a biomarker that forecasts poor outcome in renal patients and in hemodialysis patients. This review evaluates the main studies that sought to correlate Hcy and poor prognosis in renal disease as well as the treatments proposed for the reduction of plasma Hcy levels in these patients. Conclusion: Hcy could be an important biomarker of renal disease progression mainly in hemodialysis patients. We emphasize the importance of normalizing plasma levels of this amino acid to ensure a better prognosis in kidney disease.

Highlights

Homocysteine (Hcy) is one of the metabolites of methionine (Met), an essential diet-derived amino acid
This review evaluates the main studies that sought to correlate Hcy and poor prognosis in renal disease as well as the treatments proposed for the reduction of plasma Hcy levels in these patients
We emphasize the importance of normalizing plasma levels of this amino acid to ensure a better prognosis in kidney disease

Summary

Introduction

Homocysteine (Hcy) is one of the metabolites of methionine (Met), an essential diet-derived amino acid. Homocysteine (Hcy) is a sulfur-containing non-proteinogenic amino acid derived from the demethylation of an essential amino acid, methionine (Met). Mostly found in the liver, is converted to Hcy via S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), which are released in numerous methylation reactions[1] This molecule originates from catabolism of proteins or varied dietary sources, and its metabolism occurs by two main pathways: remethylation and transsulphuration[2,3,4]. An enzyme action occurs both from methyltetrahydrofolate and betaine for methyl donation to this molecule, with cobalamin (vitamin B12) being one of the precursors of this activation that originates Met. On the other hand, in transsulphuration, there is an irreversible reaction in which Hcy condensates along with the serine molecule, which is catalyzed by cystathionine-β-synthase, forming cystathionine. This reaction occurs by direct action of pyridoxine cofactor (pyridoxal 5-phosfate, vitamin B6) from dietary sources[1]

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