Evaluation of TGF-β1 and MCP-1 expression and tubulointerstitial fibrosis in children with Henoch-Schönlein purpura nephritis and IgA nephropathy: A clinical correlation

Abstract

OBJECTIVES:Henoch-Schönlein purpura nephritis and immunoglobulin A nephropathy are two diseases with similar clinical presentations but very different prognoses. Transforming growth factor β1 and monocyte chemoattractant protein-1 have been associated with the development of tissue fibrosis. We examined the development of tubulointerstitial fibrosis and its relationship with Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in these patients.METHODS:Renal tissue samples were collected by renal biopsy from 50 children with Henoch-Schönlein purpura nephritis and 50 children with immunoglobulin A nephropathy. Hematoxylin and eosin and Masson's trichrome-stained tissues were examined using light microscopy. Tubulointerstitial fibrosis was graded using the method described by Bohle et al. 1. The immunohistochemical detection of Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was correlated with the tubulointerstitial fibrosis grade. Clinical Trial registration number: ZJCH-2012-0105.RESULTS:Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in the renal tissues was significantly greater in the patients with immunoglobulin A nephropathy than in the patients with Henoch-Schönlein purpura nephritis (both p<0.001). The immunoglobulin A nephropathy patients had a higher tubulointerstitial fibrosis grade than the Henoch-Schönlein purpura nephritis patients (p<0.001). The tubulointerstitial fibrosis grade was in accordance with the Transforming growth factor β1 and monocyte chemoattractant protein-1 expression levels in both diseases (both p<0.001).CONCLUSION:Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was associated with the development of immunoglobulin A nephropathy and Henoch-Schönlein purpura nephritis. Further studies are needed to better evaluate this association.

Increased Abundance of Plasmacytoid Dendritic Cells and Interferon-Alpha Induces Plasma Cell Differentiation in Patients of IgA Nephropathy

“…T cells and monocytes/macrophages were reported to be predominant infiltrated leukocytes in renal interstitial of IgAN patients, which was significantly correlated with histological injury and renal dysfunction [ 85 – 87 ]. Also, increased MCP-1 expression was found in renal tissues of IgAN patients [ 88 ]. Here, we found that IFN- α strongly induces mRNA levels of IP-10 (CXCL10) and MCP-1 from mesangial cells in vitro and conditioned HMC supernatant with IFN- α pretreatment precipitates the transendothelial migration of CD14 + and CD4 + cells.…”

The Effect of Chinese Traditional Medicine Huaiqihuang (HQH) on the Protection of Nephropathy

“…Studies have shown that HQH particles can effectively downregulate the expression of TGF-β1, so as to have a good effect on allergic purpura nephritis [63,64]. Clinical studies have shown that HQH granules can maintain the integrity of the cerebral venous filtration barrier by upregulating the 5 Oxidative Medicine and Cellular Longevity expression of nephron and podocin on the septal septum, thereby reducing the leakage of urinary protein.…”

“…Reduces proteinuria by enhancing nephrin expression and inhibit the NF-κB signaling pathway, interferes with the proinflammatory and proapoptotic signaling, and promotes the nephrin and podocin protein expression [11,66,73] Renal interstitial fibrosis Reduces infiltration of myofibroblast and downregulates the expression of α-SMA [4,66] Allergic purpura nephritis Downregulates the expression of TGF-β1 mRNA and upregulates the expression of nephrin and podocin on the septal septum [65] Cisplatin nephrotoxicity Inhibits cp-induced renal tubular apoptosis and cell cycle arrest and reduces the levels of oxidative stress, inflammation and mitochondrial dysfunction [8,37] IgA nephropathy Increases the expression of nephrin and improves the anomalies of their distribution and improves the expression of CD3, CD4, and CD4/CD8 [14,64] Renal carcinoma…”

Analysis of the Clinical Effects of the Combination of Mycophenolate Mofetil with Either Tacrolimus or Cyclophosphamide

“…Moreover, bone tissues and blood platelets are its most abundant sources ( 13 ). TGF-β1, a cell factor expressed in the kidneys, is related to the development of tubulointerstitial fibrosis ( 14 ). Presently, there are only a few analyses on the influence of the combination of mycophenolate mofetil and either tacrolimus or cyclophosphamide on the serum levels of cystatin C and TGF-β1 when used for LN treatment.…”