Treatment of IgA nephropathy

Conclusion

In summary, there is still a large gap in our knowledge with regard to etiology, pathogenesis, and, most important, therapy of IgA nephropathy. Even with massive clinical trials, no therapeutic maneuvers have yet been found to be consistently effective. To find effective therapy, the underlying pathogenesis of IgA nephropathy must first be fully understood. Over-production of nephritogenic IgA or IgA-immune complexes of either mucosal or nonmucosal origin, may play a major role. In addition, impairment of clearance of circulating IgA-immune complexes by phagocytosis or complement-dependent solubilization, which may be seen in liver dysfunction, is also important. The prospective therapy must be pathogenesis oriented. At present, we use dipyridamole to improve hematuria. For patients with hematuria complicated with nephrotic range proteinuria, especially those with elevated serum IgE, combination therapy with corticosteroid, cyclophosphamide and persantin may be beneficial in preventing end-stage renal disease. For those unresponsive to combination therapy, cyclosporin therapy should be used as soon as possible. In considering the nephrotox-icity, it needs to be more precisely quantitated both from a functional and pathological perspective. FK506 and other analogues with lower nephrotoxicity may be tried clinically. The effect of Chinese herb drugs on IgA nephropathy has been vigorously investigated recently. Preliminary results have revealed that they are of value in preventing the process of renal deterioration. The long-term effect of Chinese herb drugs still needs further study and this research is in progress.