Corticosteroid therapy in IgA nephropathy with minimal proteinuria and high renal pathological score: A single‑center cohort study.

Currently, there is no clear evidence that advocates the widespread use of corticosteroids for the treatment of immunoglobulin A nephropathy (IgAN) with minimal proteinuria (<1 g/day). The recent Kidney Disease: Improving Global Outcomes Clinical Practice Guideline recommends supportive corticosteroid treatment. In the present study, 45 IgAN patients with high renal pathological scores and minimal proteinuria were enrolled. The patients were randomly divided into two groups. The treatment group received methylprednisolone tablets in addition to angiotensin‑converting‑enzyme inhibitor (ACE‑I) and/or angiotensin‑receptor blocker (ARB) treatment. The control group only received ACE‑I and/or ARB treatment. In the treatment group, a single dose of 1 mg/kg (maximum 60 mg/day) methylprednisolone tablets was given daily followed by gradually decreasing dosage. The follow‑up time of the patients was 3 years. In addition, the underlying mechanisms were investigated. The results indicated that there was a significant reduction in the amount of urinary proteins in the treatment group compared with the control group. At the end of the follow‑up, the endpoint event rate of moderate or severe proteinuria and decrease in estimated glomerular filtration rate (eGFR) in the treatment group was significantly lower than the control group. Furthermore, higher levels of serum cytokines, interleukin (IL)‑4, IL‑17, transforming growth factor‑β1 and IL‑21, were detected in patients with IgAN compared with a group of healthy controls. There was no significant difference in IFN‑γ expression between the IgAN and healthy control groups. Furthermore, the expression of Janus kinase (Jak)1, Jak3, signal transducer and activator of transcription (STAT)3 and STAT6 was significantly upregulated in patients with IgAN compared with healthy controls. However, the expression levels of STAT5 and chaperone protein, C1GALT1 specific chaperone 1, in IgAN patients were significantly reduced compared with healthy controls. In addition, there was no significant difference in the expression of Jak2, tyrosine kinase 2, STAT1 and STAT4 between the two groups. In conclusion, for IgAN patients with minimal proteinuria and high renal pathological score corticosteroid therapy is likely to be effective. The dysregulation of serum cytokine levels in these patients with IgAN may have a role in the pathogenesis and progression of disease, which is associated with the activation of the JAK/STAT signaling pathway.