Biotin status as assessed by the Activation Coefficient (AC) of the biotin-dependent enzyme PCC is significantly impaired in individuals with ESRD who have RLS compared with individuals with ESRD who do not have RLS. This difference was observed despite daily, standard-of-care, oral supplementation with biotin at five to ten times the Adequate Intake (AI). Based solely on this observed association, inferring a causal relationship between biotin deficiency and RLS in ERSD would be problematic
In addition to these pathogenic processes arising directly from ESRD and dialysis, restriction to lower protein diets might restrict biotin intake. More frequent use of antibiotics could suppress the intestinal biome and hence the production and release of biotin by intestinal microbes; the contribution of gut bacteria to net absorbed biotin remains unknown. A higher incident of therapy with medications that accelerate biotin biotransformation to inactive metabolites (e.g., antiepileptics) might also contribute to reducing biotin status in ESRD.
However, no toxicity has been reported even with doses of biotin up to 200,000 Î¼g, a dose that has been given orally for treatment of inborn errors of metabolism. Supplements of 10,000 Î¼g of biotin per day have been given intramuscularly for a year with no reported side effects and have been reported to improve symptoms of peripheral neuropathy in ESRD. Further, the catabolites of biotin are not active and apparently do not interfere with the attachment of biotin to apocarboxylases.
Last date updated on June, 2014