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Effects of therapeutic agents on the inflammatory and fibrogenic factors in IgA nephropathy
Author(s) -
IHM CHUNGYOO,
JEONG KYUNG WHAN,
LEE SANG HO,
LEE TAE WON,
PARK JAE KYUNG
Publication year - 2007
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2007.00878.x
Subject(s) - medicine , endocrinology , nephropathy , angiotensin receptor , transforming growth factor beta , mesangial proliferative glomerulonephritis , transforming growth factor , receptor , angiotensin ii , diabetes mellitus
SUMMARY: It is desirable in the treatment of IgA nephropathy (IgAN) to prevent the downstream events after the immune response has involved the glomerulus. We and others observed that IgA itself could directly activate mesangial cells to produce monocyte chemotactic peptide‐1 (MCP‐1), interleukin‐6 (IL‐6) and transforming growth factor‐β (TGF‐β) and this was suppressed by the treatment with steroid or angiotensin receptor blocker (ARB). It was shown in mesangial cells that the increased expression of TGF‐β and plasminogen activator inhibitor‐1 induced by angiotensin II was suppressed by the treatment with ARB, calcium channel blocker (CCB), spironolactone or peroxisome proliferator‐activated‐receptor‐γ (PPAR‐γ) agonist. It was well known in the patients with IgAN that renal or intraglomerular TGF‐β1 gene expression was increased. Interestingly, treatment with angiotensin‐converting enzyme (ACE) inhibitors induced significantly lower renal TGF‐β1 gene expression in patients with IgAN. It was reported in several studies that urinary levels of IL‐6, IL‐8, MCP‐1 or TGF‐β were increased in patients with IgAN. The increase was suppressed by the treatment with steroid, ARB or ACE inhibitor. More effective agents are necessary to ameliorate pathogenetic abnormalities and so to prevent the progression of IgAN.