Effects of therapeutic agents on the inflammatory and fibrogenic factors in IgA nephropathy.
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-beta (TGF-beta) 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-beta 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-gamma (PPAR-gamma) agonist. It was well known in the patients with IgAN that renal or intraglomerular TGF-beta1 gene expression was increased. Interestingly, treatment with angiotensin-converting enzyme (ACE) inhibitors induced significantly lower renal TGF-beta1 gene expression in patients with IgAN. It was reported in several studies that urinary levels of IL-6, IL-8, MCP-1 or TGF-beta 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.
Ihm
Chun-Gyoo
CG
Division of Nephrology, Kyung Hee University Medical Centre, Seoul, Korea. cgihm@yahoo.co.kr
Jeong
Kyung Whan
KW
Lee
Sang Ho
SH
Lee
Tae Won
TW
Park
Jae Kyung
JK
D000959:Antihypertensive Agents / Q000627:therapeutic use*; D004232:Diuretics / Q000627:therapeutic use*; D005922:Glomerulonephritis, IGA / Q000188:drug therapy* / Q000276:immunology* / Q000473:pathology; D006801:Humans; D013256:Steroids / Q000627:therapeutic use*
D000959:Antihypertensive Agents; D004232:Diuretics; D013256:Steroids