Abstract
Modified Huangqi Chifeng decoction (MHCD) has been used to reduce proteinuria in immunoglobulin A nephropathy (IgAN) for many years. Previously, we have demonstrated its protective role in glomerular mesangial cells. Podocyte injury, another key factor associated with proteinuria in IgAN, has also attracted increasing attention. However, whether MHCD can reduce proteinuria by protecting podocytes remains unclear. The present study aimed to investigate the protective effects of MHCD against podocyte injury in a rat model of IgAN. To establish the IgAN model, rats were administered bovine serum albumin, carbon tetrachloride, and lipopolysaccharide. MHCD in three doses or telmisartan was administered once daily for 8 weeks (n = 10 rats/group). Rats with IgAN developed proteinuria at week 6, which worsened over time until drug intervention. After drug intervention, MHCD reduced proteinuria and had no effect on liver and kidney function. Furthermore, MHCD alleviated renal pathological lesions, hyperplasia of mesangial cells, mesangial matrix expansion, and podocyte foot process fusion. Western blot analysis revealed that MHCD increased the expression of the podocyte-associated proteins nephrin and podocalyxin. Additionally, we stained podocyte nuclei with an antibody for Wilms’ tumor protein one and found that MHCD increased the podocyte number in rats with IgAN. In conclusion, these results demonstrate that MHCD attenuates proteinuria by reducing podocyte injury.
Highlights
Immunoglobulin A (IgA) nephropathy (IgAN) is a glomerular disease characterized by IgA deposition in the mesangial region
After using sodium citrate for antigen retrieval, endogenous peroxidase was quenched with 3% hydrogen peroxide, and the sections were incubated with the Wilms’ tumor protein 1 (WT1) antibody (1:100) overnight at 4°C
According to the 2012 KDIGO clinical practice guideline, we recommend long-term angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin receptor blocker (ARB) treatment when proteinuria is > 1 g/d, with uptitration of the drug depending on blood pressure (Beck et al, 2013)
Summary
Immunoglobulin A (IgA) nephropathy (IgAN) is a glomerular disease characterized by IgA deposition in the mesangial region. Its clinical manifestations include proteinuria, hematuria, acute kidney injury, hypertriglyceridemia, and hypertension. IgAN is the main cause of endstage renal disease in patients with primary glomerular disease in China (Yang et al, 2020). The majority of patients with IgAN exhibit progressive symptoms, with progression to end-stage renal disease within 10 years after diagnosis in 10–30% of cases (Liu et al, 2018). The mechanism by which podocyte injury contributes to IgAN warrants investigation and might provide a basis for therapeutic strategies to delay progression
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