Immunomodulatory agents against IgA nephropathy

Synthesis of aberrant IgA molecules as the key pathogenetic mechanism of immunoglobulin A nephropathy (IgAN) apparently forms a potential scientific rationale for applying immunomodulatory agents in the treatment of IgAN. There is evidence that corticosteroids can steadily reduce proteinuria and slow down renal progression. Evidence that pulse steroid plus intravenous or oral cyclophosphamide can retard the rate of progression of advanced IgAN was provided by several groups worldwide. Cyclosporin is generally not used to treat IgAN. The efficacy of azathioprine is equivocal. Mycophenolate mofetil reduces proteinuria by up to 30% and favorably impacts renal survival in Chinese patients with mild histologic lesions, but these results were not achieved in Caucasians with more advanced disease. In conclusion, the choice of immunomodulatory therapy remains controversial. We advocate the use of immunomodulatory agents as an adjunctive therapy in patients with proteinuria>1 g/day despite achieving target blood pressure with full renin-angiotensin blockade. More aggressive therapy should be reserved for patients with nephrotic-range proteinuria, crescentic lesions and/or rapidly progressive renal failure.