Folic acid supplementation and homocyst(e)ine level in renal transplant recipients

2001 ◽  
Vol 33 (1-2) ◽  
pp. 2049-2050 ◽  
Author(s):  
B Grandtnerová ◽  
L Laca ◽  
D Gábor ◽  
E Gregová ◽  
S Korónyi
Keyword(s):  
Folic Acid ◽  
Renal Transplant ◽  
Folic Acid Supplementation ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Acid Supplementation

Homocysteine in the Plasma of Renal Transplant Recipients: Effects of Cofactors for Methionine Metabolism

1981 ◽  
Vol 61 (6) ◽  
pp. 743-749 ◽  
Author(s):  
D. E. L. Wilcken ◽  
Vatsala J. Gupta ◽  
A. K. Betts
Keyword(s):  
Folic Acid ◽  
Amino Acid ◽  
Renal Transplant ◽  
Serum Creatinine ◽  
Vitamin B12 ◽  
Normal Subjects ◽  
Serum Folate ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Erythrocyte Folate

1. Homocysteine which is formed during the metabolism of methionine is readily oxidized and is measured by the amino acid analyser as cysteine—homocysteine mixed disulphide and homocystine. We measured plasma amino acid concentrations after an overnight fast in 27 stable long-term renal transplant recipients and 25 age-and sex-matched normal subjects with particular emphasis on sulphur-containing amino acids. 2. Plasma cysteine—homocysteine mixed disulphide was increased in the patients (mean 6.0 ± sd 3.2 μmol/l; normal 3.1 ± 0.9 μmol/l, P < 0.001) and homocystine was detectable in low concentration (< 1.0 μmol/l) in 24; the elevation in cysteine—homocysteine was related to serum creatinine (r = 0.60, P < 0.002). Cystine was also increased (91.6 ± 29.3 μmol/l; normal subjects 64.0 ± 16.7 μmol/l, P < 0.001), but methionine concentrations were normal. 3. When pyridoxine, folic acid and vitamin B12, cofactors for homocysteine metabolism, were administered sequentially to 11 arbitrarily selected transplant recipients cysteine—homocysteine decreased from 7.3 ± 2.1 to 4.3 ± 0.8 μmol/l (P < 0.001) and homocystine became undetectable. the response coincided with the giving of folic acid and occurred without alteration in serum creatinine and with normal serum folate and vitamin B12 concentrations. 4. in eight patients in whom pretreatment erythrocyte folate was measured, folic acid therapy reduced cysteine—homocysteine from 9.0 ± 3.1 to 5.4 ± 1.6 μmol/l over a 4 week period (P < 0.001), the largest response being in the one patient with subnormal erythrocyte folate; values were in the low-normal or normal range in the other seven. 5. We conclude that plasma homocysteine is increased in renal transplant recipients when serum creatinine is only moderately elevated and that the homocysteine concentrations are decreased by treatment with folic acid, suggesting that both reduced homocysteine excretion and relative shortages of folic acid are responsible.

Treatment of hyperhomocysteinemia with folic acid reduces oxidative stress in renal transplant recipients

2002 ◽  
Vol 73 (4) ◽  
pp. 663-665 ◽  
Author(s):  
Aboubakr Abdelfatah ◽  
Didier Ducloux ◽  
G??rard Toubin ◽  
G??rard Motte ◽  
Daniel Alber ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Renal Transplant ◽  
Renal Transplant Recipients ◽  
Transplant Recipients

scholarly journals SP755MARINE n-3 FATTY ACID SUPPLEMENTATION INCREASE TACROLIMUS EXPOSURE IN RENAL TRANSPLANT RECIPIENTS

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i603-i603
Author(s):  
Ivar Eide ◽  
Anders Åsberg ◽  
Karsten Midtvedt ◽  
Nils Vethe ◽  
Anders Hartmann ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Renal Transplant ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Fatty Acid Supplementation ◽  
Acid Supplementation

scholarly journals Hyperhomocyst(e)inemia in chronic stable renal transplant patients

2000 ◽  
Vol 55 (5) ◽  
pp. 161-168 ◽  
Author(s):  
David José de Barros Machado ◽  
Flávio Jota de Paula ◽  
Emil Sabbaga ◽  
Luiz Estevan Ianhez
Keyword(s):  
Folic Acid ◽  
Renal Transplant ◽  
Serum Creatinine ◽  
Renal Transplant Recipients ◽  
Transplant Recipients ◽  
Group Iii ◽  
Transplant Patients ◽  
Group I ◽  
Renal Transplant Patients ◽  
Group Ii

PURPOSE: Hyperhomocyst(e)inaemia is an important risk factor for atherosclerosis, which is currently a major cause of death in renal transplant patients. The aim of this study was to assess the influence of immunosuppressive therapy on homocyst(e)inemia in renal transplant recipients. METHODS: Total serum homocysteine (by high performance liquid chromatography), creatinine, lipid profile, folic acid (by radioimmunoassay-RIA) and vitamin B12 (by RIA) concentrations were measured in 3 groups. Group I patients (n=20) were under treatment with cyclosporine, azathioprine, and prednisone; group II (n=9) were under treatment with azathioprine and prednisone; and group III (n=7) were composed of renal graft donors for groups I and II. Creatinine, estimated creatinine clearance, cyclosporine trough level, lipid profile, folic acid, and vitamin B12 concentrations and clinical characteristics of patients were assessed with the aim of ascertaining determinants of hyperhomocyst(e)inemia. RESULTS: Patient ages were 48.8 ± 15.1 yr (group I), 43.3 ± 11.3 yr (group II); and 46.5 ± 14.8 yr (group III). Mean serum homocyst(e)ine (tHcy) concentrations were 18.07 ± 8.29 mmol/l in renal transplant recipients; 16.55 ± 5.6 mmol/l and 21.44 ± 12.1 mmol/l respectively for group I (with cyclosporine) and group II (without cyclosporine) (NS). In renal donors, tHcy was significantly lower (9.07 ± 3.06 mmol/l; group I + group II vs. group III, p<0.008). There was an unadjusted correlation (p<0.10) between age (r=0.427; p<0.005) body weight (r=0.412; p<0.05), serum creatinine (r=0.427; p<0.05), estimated creatinine clearance (r=0.316; p<0.10), and tHcy in renal recipients (group I +II). Independent regressors (r²=0.46) identified in the multiple regression model were age (coefficient= 0.253; p=0.009) and serum creatinine (coefficient=8.07; p=0.045). We found no cases of hyperhomocyst(e)inemia in the control group. In contrast, 38% of renal recipients had hyperhomocyst(e)inemia: 7 cases (35%) on cyclosporine and 4 (45%) without cyclosporine, based on serum normal levels. CONCLUSIONS: Renal transplant recipients frequently have hyperhomocyst(e)inemia. Hyperhomocyst(e)inemia in renal transplant patients is independent of the scheme of immunosuppression they are taking. The older the patients are and the higher are their serum creatinine levels, the more susceptible they are to hyperhomocyst(e)inemia following renal transplantation.

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