WJET  Vol.6 No.3 , August 2018
Homocysteine, Vitamin B12 and Folic Acid in Children with Acute Glomerulonephritis
ABSTRACT
Homocysteine (Hcy) is an intermediate product of methionine formed by its demethylation. Hcy can be metabolized via remethylation to methionine or transsulfuration to cysteine which is dependent on several enzymes and cofactors. It is deleterious to blood vessel including glomeruli. Kidney is a major organ that metabolizes Hcy. More than 80% of patients with chronic renal disease develop hyperhomocysteinemia (hHcy). Accessible data of plasma Hcy in nephritic syndrome (NS) patients are controversial with increased, decreased and unchanged values reported. In renal patients, plasma Hcy concentration can be reduced by administration of folic acid. Absolute or relative deficiencies of folate, vitamin B6, or vitamin B12 may also play a role. Therefore, plasma Hcy, folic acid, vitamin B6, and vitamin B12 in children with acute glomerulonephritis (AGN) were accessed in this study. Hcy, folic acid vitamin B12, B6 and renal function such as blood urea nitrogen (BUN), creatinine (Cr) were analyzed 12 pediatric patients with AGN and 15 age and sex matched healthy children served as controls. The results revealed that a significant increase in plasma Hcy in children with acute AGN when compared with controls. For simple regression analysis, Hcy was positively correlated with BUN, Cr, ferritin and uric acid but negatively correlated with serum glutathione. This research indicated hHcy suggests enhanced risks for inflammation and endothelial injury, which lead to kidney disease. Folic acid has also been shown to improve endothelial function, suggesting an alternative explanation for the effect of folic acid on endothelial function. Careful considerations of not only dietary measures are necessary but also folate and vitamin B supplementation for reducing hHcy in AGN need to be investigated.
Cite this paper
Viroonudomphol, D. , Kanjanachumpol, S. and Sirisate, S. (2018) Homocysteine, Vitamin B12 and Folic Acid in Children with Acute Glomerulonephritis. World Journal of Engineering and Technology, 6, 661-670. doi: 10.4236/wjet.2018.63042.
References
[1]   Kang, S.S., Wong, P.W., Susmano, A., et al. (1991) Thermoabile Methylenetetrahydrofolate Reductase: An Inherited Risk Factor for Coronary Artery Disease. American Journal of Human Genetics, 48, 536-545.

[2]   Foley, R.N., Parfrey, P.S. and Sarnak, M.J. (1998) Clinical Epidemiology of Cardiovascular Disease in Chronic Renal Disease. American Journal of Kidney Disease, 32, S112-S119.
https://doi.org/10.1053/ajkd.1998.v32.pm9820470

[3]   Guttormsen, A.B., Ueland, P.M., Svastad, E., et al. (1997) Kinetic Basis of Hyperhomocysteinemia in Patients with Chronic Renal Failure. Kidney International, 52, 495-502.
https://doi.org/10.1038/ki.1997.359

[4]   Van Guldener, C., Kulik, W., Berger, R., et al. (1999) Homocysteine and Methionine Metabolism in ESRD: A Stable Isotope Study. Kidney International, 56, 1064-1071.
https://doi.org/10.1046/j.1523-1755.1999.00624.x

[5]   Stam, F., van Guldener, C., ter Wee, P.M., et al. (2004) Homocysteine Clearance and Methylation Flux Rates in Healthy and End-Stage Renal Disease: Association with S-Adenosylhomocysteine. American Journal of Physiology-Renal Physiology, 287, F215-F223.
https://doi.org/10.1152/ajprenal.00376.2003

[6]   Chen, P., Poddar, R., Tipa, E.V., et al. (1999) Homocysteine Metabolism in Cardiovascular Cells and Tissues: Implication for Hyperhomocysteinemia and Cardiovascular Disease. Advances in Enzyme Regulation, 39, 93-109.
https://doi.org/10.1016/S0065-2571(98)00029-6

[7]   Diamond, J.R. (1991) Analogous Pathobiologic Mechanism in Glomerulosclerosis and Atherosclerosis. Kidney International, 31, S29-S34.

[8]   Keane, W.F., Kasiske, B.L. and O’Donnell, M.P. (1988) Lipids and Progressive Glomerulosclerosis. A Model Analogous to Atherosclerosis. American Journal of Nephrology, 8, 261-271.
https://doi.org/10.1159/000167599

[9]   Jacques, P.F., Selhub, J., Bostom, A.G., et al. (1999) The Effect of Folic Acid Fortification on Plasma Folate and Total Homocysteine Concentrations. New England Journal of Medicine, 340, 1449-1454.
https://doi.org/10.1056/NEJM199905133401901

[10]   Suliman, M.E., Qureshi, A.R., Stenvinkel, P., et al. (2005) Inflammation Contributes to Low Plasma Amino Acid Concentrations in Patients with Chronic Kidney Disease. The American Journal of Clinical Nutrition, 82, 342-349.
https://doi.org/10.1093/ajcn/82.2.342

[11]   Sawy, M.A., Zaki, M.M., El-Hakim, I.L., Mowafy, M.E., et al. (2012) Serum Amino Acid Abnormalities in Mind Renal Insufficiency Patients with Chronic Renal Failure with and without History of Thromboebolic Manifestations. The Egyptian Journal of Medical Human Genetics, 13, 73-80.
https://doi.org/10.1016/j.ejmhg.2011.06.007

[12]   Saifan, C., EI-Chalabaty and EI-Sayegh, S. (2013) Hyperhomocysteinemia and Vascular Access Thrombosis in Hemodialysis Patients: A Retrospective Study. Vascular Health and Risk Management, 9, 361-364.
https://doi.org/10.2147/VHRM.S47255

[13]   Suliman, M.E., Divino Filho, J.C., Barany, P., Anderstam, B., et al. (1999) Effect of High Dose Folic Acid and Pyridoxine on Plasma and Erythrocyte Sulfur Amino Acid in Hemodialysis Patients. Journal of American Society of Nephrology, 10, 1287-1296.

[14]   Suliman, M.E., Stevinkel, P., Heibuger, O., Barany, P., et al. (2002) Plasma Sulfur Amino Acids in Relation to Cardiovascular Disease, Nutritional Status, and Diabetes Mellitus in Patients with Chronic Renal Failure at Start of Dialysis Therapy. American Journal of Kidney Disease, 40, 480-488.
https://doi.org/10.1053/ajkd.2002.34887

[15]   Klamroth, R., Orlovic, M., Fritsche, I., Scibt, S., et al. (2013) The Influence of Thrombophillic Risk Factors on Vascular Access Survival in Chronic Dialysis Patients in a Retrospective Evaluation. Vasa, 42, 32-39.
https://doi.org/10.1024/0301-1526/a000245

[16]   Shakeri, A., Abdi, M., Khosrosshahi, H.T. and Fouladi, R.F. (2011) Common Carotid Artery Intema-Media Thickness and Alterosclerotic Plaque in Carotid Bulb in Patients with Chronic Kidney Disease on Hemodialysis a Case-Control Study. Pakistan Journal of Biological Sciences, 14, 844-848.
https://doi.org/10.3923/pjbs.2011.844.848

[17]   Aminzadeh, M.A., Gollapudi, P. and Vaziri, N.D. (2011) Effect of Nephritic Syndrome on Homocysteine Metabolism. Nephrology Dialysis Transplantation, 26, 1244-1247.
https://doi.org/10.1093/ndt/gfq551

[18]   Alberto, C., Alba, C., et al. (2003) Homocysteine, Folate, Vitamin B12 Levels and C677T MTHFR Mutation in Children with Renal Failure. Pediatric Nephrology, 18, 225-229.

[19]   Annadottir, M., Hultberg, B. and Berg, A.L. (2001) Plasma Total Homocysteine Concentration in Nephrotic Patients with Idiopathic Membranous Nephropathy. Nephrology Dialysis Tranplantation, 16, 45-47.
https://doi.org/10.1093/ndt/16.1.45

[20]   Dogra, G., Irish, A.B. and Watts, G.F. (2001) Homocysteine and Nephritic Syndrome. Nephrology Dialysis Tranplantation, 16, 1720-1721.
https://doi.org/10.1093/ndt/16.8.1720

[21]   Joven, J., Arcelus, R., Camps, J., Ordonez-Lianos, J., et al. (2000) Determinants of Plasma Homocyst(e)ine in Patients with Nephritic Syndrome. Journal of Molecular Medicine, 78, 147-154.
https://doi.org/10.1007/s001090000093

[22]   Podda, G.M., Lussana, F., Moroni, G., Faioni, E.M., Lombardi, R., Fontana, G., Ponticelli, C. and Cattaneo, M. (2007) Abnormalities of Homocysteine and B Vitamins in the Nephritic Syndrome. Thrombosis Research, 120, 647-652.
https://doi.org/10.1016/j.thromres.2006.12.011

[23]   Terderenda, E., Korzeniecka-Kozerska, A., Polowski, T., Wasilewska, A. and Zoch-Zwierz, W. (2011) Serum and Urinary Homocysteine in Children with Steroid-Dependent Nephritic Syndrome. Polski Merkuriusz Lekarski, 31, 204-208.

[24]   Yi, F. and Li, P.-L. (2008) Mechanism of Hcy-Induced Glomerular Injury and Sclerosis. American Journal of Nephrology, 28, 254-264.
https://doi.org/10.1159/000110876

[25]   Meister, A. (1994) Glutathione-Ascorbic Acid Antioxidant System in Animals. The Journal of Biological Chemistry, 269, 9937-9400.

[26]   Bates, C.J. and Mansoor, M.A. (2002) Correlates of Plasma Homocysteine, Cysteine and Cyateinyl-Glycine in Respondents in the British National Diet and Nutrition Survey of Young People Aged 4-18 Years, and a Comparison with the Survey of People Aged 65 Years and over. British Journal of Nutrition, 87, 71-79.
https://doi.org/10.1079/BJN2001479

[27]   Osganian, S.K., Stampfer, M.J., Spiegelman, D., et al. (1999) Distribution of and Factors Associated with Serum Homocysteine Levels in Children: Child and Adolescent Trial for Cardiovascular Health. Journal of American Medical Association, 281, 1189-1196.
https://doi.org/10.1001/jama.281.13.1189

[28]   Bjorke, M.A.L., Refsum, H., Markestad, T. and Ueland, P.M. (2003) Cobalamin Status and Its Biochemical Markers Methylmalonic Acid and Homocysteine in Different Age Groups from 4 Days to 19 Years. Clinical Chemistry, 49, 2067-2075.
https://doi.org/10.1373/clinchem.2003.019869

[29]   Stanger, O., Herrman, W., Pietrzik, K., Fowler, B., Geisel, J., Dierkes, J. and Weger, M. (2003) DACH-LIGA Homocysteine (German, Austrian and Swiss Homocysteine Society), Consensus Paper on the Rational Clinical Use of Homocysteine, Folic Acid and B-Vitamins in Cardiovascular and Thrombotic Diseases: Guidelines and Recommendations. Clinical Chemistry and Laboratory Medicine, 41, 1392-1403.
https://doi.org/10.1515/CCLM.2003.214

[30]   Silva, L.S., Oliveira, R.A., Silva, G.B., Lima, J.W., Silva, R.P., Liborio, A.B., Daher, E.F. and Sobrinho, C.R. (2012) Cardiovascular Disease in Patients with End-Stage Renal Disease on Hemodialysis in Developing Country. Saudi Journal of Kidney Disease and Transplantation, 23, 262-266.

 
 
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