CHAPTER 47. Cobalamin and Nutritional Implications in Kidney Disease

Abstract

This chapter primarily describes how the metabolism of vitamin B12 is influenced by the progression of chronic kidney disease (CKD), i.e. decreased kidney function, and what happens subsequently in the biological process. Vitamin B12 must be converted into its coenzyme forms, adenosylcobalamin and methylcobalamin, in the cell. These coenzymes function as the cofactors of methylmalonyl-CoA mutase and methionine synthase, respectively. CKD may affect the conversion from vitamin B12 to the coenzyme forms and this may be why CKD induces vitamin B12 deficiency by reducing the availability of this coenzyme. The best known biomarker associated with vitamin B12 is homocysteine. Given that homocysteine metabolism is involved both in the synthesis and degradation of asymmetric dimethylarginine (ADMA), a potent endogenous NO-synthase inhibitor which is thought to be an independent predictor of cardiovascular mortality in end-stage renal disease, homocysteine management is clinically important in CKD patients. Since human vascular cells lack cystathionine beta-synthase, vascular endothelium may be extremely vulnerable to homocysteine loading induced by impaired remethylation. Thus homocysteine metabolism disorder should not be ignored in these patients. When vitamin B12 and vitamin B6 are viewed in terms of homocysteine metabolism, both vitamins may be linked with each other in the degradation of homocysteine.