The ideal treatment for IgAN would remove IgA from the glomerulus and prevent further IgA deposition. This goal still remains a remote prospect. There are a few additional caveats that have to be considered while treating IgA nephropathy. IgA nephropathy has a very variable course, ranging from a benign recurrent hematuria up to a rapid progression to chronic kidney failure . Hence the decision on which patients to treat should be based on the prognostic factors and the risk of progression. Also, IgA nephropathy recurs in transplants despite the use of ciclosporin , azathioprine or mycophenolate mofetil and steroids in these patients. There are persisting uncertainties, due to the limited number of patients included in the few controlled randomized studies performed to date, which hardly produce statistically significant evidence regarding the heterogeneity of IgA nephropathy patients, the diversity of study treatment protocols, and the length of follow-up.
Biotin is mainly required as a coenzyme for carboxylation reactions and the main examples are carboxylation of-i) pyruvate to oxaloacetate (first step of gluconeogenesis); ii) Acetyl co A to Malonyl co A (first step of fatty acid synthesis) and iii) Propionyl co A to D-Methyl malonyl co A (in the conversion of propionyl co A to Succinyl co A to gain entry to TCA cycle). In biotin deficiency, out of the given options, defective fatty acid synthesis is the most suited option because of the impaired conversion of acetyl co A to malonyl co A.