Related Experiment Videos
Hyperhomocyst(e)inemia in chronic stable renal transplant patients
D J Machado1, F J Paula, E Sabbaga
1Division of Urology, Hospital das Clínicas, Faculty of Medicine, University of São Paulo.
Insights
Renal transplant recipients often have high homocysteine levels, a risk factor for atherosclerosis. This condition is independent of immunosuppression and linked to patient age and serum creatinine.
Area of Science:
- Nephrology
- Cardiovascular Science
- Clinical Chemistry
Background:
- Hyperhomocysteinemia is a significant risk factor for atherosclerosis, a leading cause of mortality in renal transplant patients.
- Understanding factors influencing homocysteine levels post-transplantation is crucial for patient management.
Purpose of the Study:
- To evaluate the impact of immunosuppressive therapy on homocysteine levels in renal transplant recipients.
- To identify determinants of hyperhomocysteinemia in this patient population.
Main Methods:
- Measurement of total serum homocysteine, creatinine, lipid profile, folic acid, and vitamin B12 in three groups: cyclosporine-based immunosuppression, azathioprine-prednisone immunosuppression, and healthy renal donors.
- Assessment of clinical characteristics and medication levels (cyclosporine trough level).
Main Results:
- Renal transplant recipients exhibited significantly higher mean serum homocysteine levels compared to healthy donors (18.07 ± 8.29 mmol/l vs. 9.07 ± 3.06 mmol/l).
- 38% of renal recipients had hyperhomocysteinemia, irrespective of immunosuppressive regimen (cyclosporine vs. non-cyclosporine).
- Independent predictors of hyperhomocysteinemia were patient age and elevated serum creatinine levels.
Conclusions:
- Hyperhomocysteinemia is prevalent in renal transplant recipients and is not influenced by the specific immunosuppressive therapy used.
- Increased patient age and higher serum creatinine levels are associated with a greater risk of developing hyperhomocysteinemia after renal transplantation.
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.