Nephrology Dialysis Transplantation, Vol 12, Issue 3 430-437, Copyright © 1997 by Oxford University Press
B Schiller and J Moran
BACKGROUND: The mechanism of progression of established renal disease
remains unclear. While a low protein diet slows this progression, the role
of cytokines in this process has been little investigated. METHODS: We
investigated cytokine expression by Northern blot and immunohistochemistry
in two groups of 5/6 nephrectomized rats (5/6 Nx) fed a normal (24%) or low
(6%) protein diet and compared them with sham operated controls. RESULTS:
The rats on 6% protein diet had significantly less focal glomerulosclerosis
(FGS) (17.4 +/- 4.4 vs 27.4 +/- 8.8%, P < 0.05) and global sclerosis
(GGS) after 7 weeks (0.4 +/- 0.8 vs 3.5 +/- 2.1% of glomeruli P < 0.05).
Both experimental groups showed three times control levels of MCP-I
expression after 2 weeks. However in the 5/6 Nx 6% protein group the
expression decreased at 4 weeks (1.5 times controls) and reached control
levels after 7 weeks. In contrast, the 5/6 Nx 24% protein group exhibited a
further marked increase after 4 weeks (5.6 times controls) and was still
two-fold higher after 7 weeks. TGF-beta expression was modestly but
consistently increased at all time points (120-160% of controls), with no
difference between the two study groups. Neither IL-1 beta or TNF-alpha was
detectable at any time. Immunohistochemistry demonstrated TGF-beta
intracellularly in distal tubular cells in both experimental and control
animals, while MCP-1 protein was found in the area of FGS and in the apical
pole of distal tubular cells in both experimental groups. Glomerular and
interstitial ED1 positive cells were significantly increased after four
weeks in the 5/6 Nx 24% protein group (P < 0.05). CONCLUSIONS: A
'mechanical' injury to the kidney clearly results in an inflammatory
response associated with the upregulation of MCP-1. A low protein diet
modulates the expression of MCP-1 and improves the morphological sequelae
seen after renal ablation.
ORIGINAL ARTICLES
Focal glomerulosclerosis in the remnant kidney model--an inflammatory disease mediated by cytokines
Section of Nephrology, Rush Presbyterian St Luke's Medical Center, Chicago, IL, USA.
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