Abstract
Background
IgA nephropathy (IgAN) is a glomerulonephritis characterized by IgA deposition in the mesangial of the glomerulus, and it is the most common glomerulonephritis. However, many patients with inflammatory bowel disease (IBD) also have secondary IgAN. Compared with primary IgAN, the secondary IgAN may be more complex. Many novel therapies, such as anti-TNFα therapy, have been shown to influence IgAN while controlling IBD.
Case presentation
A 52-year-old woman had been treated with infliximab and azathioprine for Crohn's disease, and taking entecavir for hepatitis B. Recently, the patient developed gross hematuria, acute renal insufficiency, and positive blood anti-GBM antibody after the exacerbation of Crohn's disease. Renal biopsies were performed after infliximab dosage was increased. Although the patient presented clinically as rapidly progressive glomerulonephritis, renal biopsy revealed IgAN with acute tubulointerstitial injury and crescent formation. Subsequently, the patient experienced spontaneous remission with decrease in both hematuria and creatinine. We then gave the patient a routine dose of methylprednisolone, and her condition remained stable during follow-up.
Conclusion
In our case, IgAN may expose antigen by causing local inflammatory response to GBM, induce anti-GBM antibody production, and cause acute renal insufficiency in the patient. However, anti-TNF-α therapy may promote the remission of hematuria and renal insufficiency by inhibiting the inflammatory response in renal tissues. Therefore, more studies are needed to understand the specific role of anti-TNFα therapy in IgAN.
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