IgA nephropathy is a chronic glomerulonephritis caused by abnormal deposition of immunoglobulin A in the glomerular thylakoid zone, which pathologically shows thylakoid hyperplasia and deposition of IgA-based immune complexes in the thylakoid zone. Treatment of mild IgA nephropathy includes disease assessment, non-immunosuppressive therapy, glucocorticoid therapy, immunosuppressive therapy, etc.
1. Disease assessment: exclude secondary factors; assess urinary protein, blood pressure and eGFR at the time of diagnosis and during follow-up to determine the risk of disease progression; assess prognosis according to pathological changes.
2. Non-immunosuppressive therapy: including ACEI/ARB drugs, specifically valsartan, chlorthalidomide, captopril, enalapril, and so on.
3. Glucocorticoid therapy: if the pathologic damage is more serious or proteinuria is high, usually choose to apply glucocorticoid therapy. Including prednisone, methylprednisolone and so on. High-dose glucocorticoid shock therapy can not only reduce urinary protein, but also improve renal function, while small-dose hormone oral therapy can reduce the patient’s proteinuria, but not enough to protect renal function.
4. Immunosuppressant therapy: including cyclophosphamide, cyclosporine, mertiomacrophenol ester and so on.
Patients with mild IgA nephropathy should go to the hospital in time and receive standardized treatment under the guidance of professional physicians. The drugs should be used according to the doctor’s prescription, do not self-medicate.