Plasma amino acid abnormalities in chronic renal failure

Robins, Alexander; Milewczyk, B.K.; Booth, Elizabeth; Mallick, N. P.

doi:10.1016/0009-8981(72)90401-9

Cited by 28 publications

(11 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There are several reports on abnormalities of plasma sulfur-containing amino acid composition, such as cystine and homocysteinecysteine mixed disulfide in chronic renal failure on hemodialysis (22, 23) (see references in Robins et al (22) and Wilcken et al (23)). The concentration of cystine was extremely high in hemodialysis patients and was decreased by hemodialysis (22,23). When decreasing cystine concentration by hemodialysis, HNA might be converted to HMA by certain organs and dissociated cysteine might be removed from blood during hemodialysis.…”

Section: Resultsmentioning

confidence: 99%

HPLC‐studies on nonmercapt‐mercapt conversion of human serum albumin

Sogami

Era

Nagaoka

et al. 1985

International Journal of Peptide and Protein Research

View full text Add to dashboard Cite

Human mercaptalbumin (HMA) and nonmercaptalbumin (HNA) could be separated by high‐performance liquid chromatography (HPLC) at neutral pH. Using HPLC, the present authors found the nonmercapt‐mercapt conversion (HNA ← HMA) during hemodialysis and the mercapt‐nonmercapt conversion (HMA ← HNA) after hemodialysis in chronic renal failure, indicating HMA as the covalent carrier protein for sulfur‐containing amino acids.

show abstract

Section: Resultsmentioning

confidence: 99%

HPLC‐studies on nonmercapt‐mercapt conversion of human serum albumin

Sogami

Era

Nagaoka

et al. 1985

International Journal of Peptide and Protein Research

View full text Add to dashboard Cite

show abstract

“…Anemia, a typical characteristic of end-stage renal disease, was recently shown to develop earlier in the course of disease. 2 The high homocysteine levels in persons with CKD, described more than 30 years ago, 31,32 are known to correlate inversely with GFR. Similar patterns are emerging for Creactive protein level and other markers of inflammation, as shown to date in cross-sectional analyses.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Risk Factor Profiles and Kidney Function Stage in the US General Population: The NHANES III Study

Foley

Wang²,

Collins

2005

Mayo Clinic Proceedings

133

View full text Add to dashboard Cite

“…[59] Patients with renal failure have elevated plasma homocysteine and a high incidence of cardiovascular disease. [60,61] Although the pathophysiology is not well understood, the homocysteine elevation is influenced by the MTHFR variant [62] as well as by poor nutritional status and other undetermined factors. [63] As in other populations, folate-responsiveness in patients with renal disease is most pronounced in homozygotes for 677T, but folate supplementation often does not normalize homocysteine levels.…”

Section: Vascular Diseasementioning

confidence: 99%

Polymorphisms in the Methylenetetrahydrofolate Reductase Gene

Schwahn

Rozen

2001

American Journal of PharmacoGenomics

186

151

View full text Add to dashboard Cite

5,10-Methylenetetrahydrofolate reductase (MTHFR) plays a key role in folate metabolism by channeling one-carbon units between nucleotide synthesis and methylation reactions. Severe enzyme deficiency leads to hyperhomocysteinemia and homocystinuria, with altered folate distribution and a phenotype that is characterized by damage to the nervous and vascular systems. Two frequent polymorphisms in the human MTHFR gene confer moderate functional impairment of MTHFR activity for homozygous mutant individuals. The C to T change at nucleotide position 677, whose functional consequences are dependent on folate status, has been extensively studied for its clinical consequences. A second polymorphism, an A to C change at nucleotide position 1298, is not as well characterized. Still equivocal are associations between MTHFR polymorphisms and vascular arteriosclerotic or thrombotic disease. Neural tube defects and pregnancy complications appear to be linked to impaired MTHFR function. Colonic cancer and acute leukemia, however, appear to be less frequent in individuals homozygous for the 677T polymorphism.MTHFR polymorphisms influence the homocysteine-lowering effect of folates and could modify the pharmacodynamics of antifolates and many other drugs whose metabolism, biochemical effects, or target structures require methylation reactions. However, only preliminary evidence exists for gene-drug interactions. This review summarizes the biochemical basis and clinical evidence for interactions between MTHFR polymorphisms and several disease entities, as well as potential interactions with drug therapies. Future investigations of MTHFR in disease should consider the influence of other variants of functionally-related genes as well as the medication regimen of the patients. Animal models for genetic deficiencies in folate metabolism will likely play a greater role in our understanding of folate-dependent disorders.

show abstract

Plasma amino acid abnormalities in chronic renal failure

Cited by 28 publications

References 7 publications

HPLC‐studies on nonmercapt‐mercapt conversion of human serum albumin

HPLC‐studies on nonmercapt‐mercapt conversion of human serum albumin

Cardiovascular Risk Factor Profiles and Kidney Function Stage in the US General Population: The NHANES III Study

Polymorphisms in the Methylenetetrahydrofolate Reductase Gene

Contact Info

Product

Resources

About