Serum TGF-Beta 1 and TNF-Alpha Levels and Cardiac Fibrosis in Experimental Chronic Renal Failure

2005 ◽  
Vol 34 (2) ◽  
pp. 143-152 ◽  
Author(s):  
Alexey V. Fedulov ◽  
T. P. Ses ◽  
N. A. Gavrisheva ◽  
M. G. Rybakova ◽  
J. G. Vassilyeva ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cardiac Fibrosis ◽  
Tnf Alpha ◽  
Tgf Beta

Serum TGF-Beta 1 and TNF-Alpha Levels and Cardiac Fibrosis in Experimental Chronic Renal Failure

2005 ◽  
Vol 34 (2) ◽  
pp. 143-152 ◽  
Author(s):  
Alexey Fedulov ◽  
T. P. Ses ◽  
N. A. Gavrisheva ◽  
M. G. Rybakova ◽  
J. G. Vassilyeva ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cardiac Fibrosis ◽  
Tnf Alpha ◽  
Tgf Beta

ANALYSIS OF THE ROLE OF MTHFR C677T AND TGF-BETA C-509T POLYMORPHISMS IN TYPE 1 DIABETIC PATIENTS WITH CHRONIC RENAL FAILURE

2008 ◽  
Vol 9 (1) ◽  
pp. 109
Author(s):  
C.I. Tecuceanu ◽  
D. Cimponeriu ◽  
P. Apostol ◽  
M. Stavarachi ◽  
M. Toma ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Mthfr C677t ◽  
Diabetic Patients ◽  
Tgf Beta ◽  
Type 1 Diabetic Patients

ACE Inhibition in Experimental Chronic Renal Failure Improves Renal Function but not Cardiac Fibrosis or Function

2008 ◽  
Vol 17 ◽  
pp. S15-S16
Author(s):  
Luke J. Burchill ◽  
Elena Velksoka ◽  
Rachael Dean ◽  
Karen Griggs ◽  
Louise Burrell
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Chronic Renal Failure ◽  
Cardiac Fibrosis ◽  
Ace Inhibition

scholarly journals Interaction of angiotensin II and TGF-beta 1 in the rat remnant kidney.

1997 ◽  
Vol 8 (11) ◽  
pp. 1732-1738 ◽  
Author(s):  
A Junaid ◽  
M E Rosenberg ◽  
T H Hostetter
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Transforming Growth Factor ◽  
Renin Angiotensin System ◽  
Renal Tissue ◽  
Negative Influence ◽  
Ang Ii ◽  
Tgf Beta ◽  
Renal Ablation ◽  
Remnant Kidney

An interaction between angiotensin (Ang) II and transforming growth factor (TGF)-beta 1 is gaining increasing recognition. Ang II has been implicated in the progression of renal disease, and TGF-beta 1 is a potent fibrosis-promoting cytokine. We sought to determine whether the beneficial effects of renin-angiotensin system blockade on remnant kidney function were associated with a reduction in renal TGF-beta 1 in this model of chronic renal failure. After subtotal renal ablation, rats fed a 40% protein diet and treated with losartan not only had a reduction in systolic BP (96 +/- 8 versus 130 +/- 8 mmHg, P < 0.05, losartan versus control) and urinary protein excretion (4 +/- 5 versus 23 +/- 20 g/d, P < 0.05, losartan versus control), but also exhibited a reduction in renal TGF-beta 1 mRNA (194 +/- 64 versus 411 +/- 101 optical density units, P < 0.05, losartan versus control) and TGF-beta 1 protein levels (9.8 +/- 2.5 versus 18.6 +/- 5.8 ng/g of renal tissue, P < 0.05, losartan versus control). The elevation of TGF-beta 1 in the remnant kidney was most pronounced in the scar region (22.9 +/- 13.1 versus 5.8 +/- 3.7 ng/g, P < 0.05, scar versus nonscar). A combination of reserpine, hydralazine, and hydrochlorothiazide, although effective in lowering systemic BP in this model of chronic renal failure, was not associated with a reduction in proteinuria or TGF-beta 1. We conclude that in this model of progressive renal injury, Ang II antagonism may exert a beneficial effect in part by its negative influence on TGF-beta 1.

scholarly journals Monoclonal antibody against marinobufagenin reverses cardiac fibrosis in rats with chronic renal failure

2012 ◽  
Vol 25 (6) ◽  
pp. 690-696 ◽  
Author(s):  
S. T. Haller ◽  
D. J. Kennedy ◽  
A. Shidyak ◽  
G. V. Budny ◽  
D. Malhotra ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cardiac Fibrosis

scholarly journals Lack of plasma interleukin-1 beta or tumor necrosis factor-alpha elevation during unfavorable hemodialysis conditions.

1991 ◽  
Vol 2 (5) ◽  
pp. 1007-1013
Author(s):  
A C Powell ◽  
L E Bland ◽  
C W Oettinger ◽  
S K McAllister ◽  
J C Oliver ◽  
...  
Keyword(s):  
Renal Failure ◽  
Peritoneal Dialysis ◽  
Chronic Renal Failure ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Interleukin 1 ◽  
Cellulose Triacetate ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Plasma interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) were determined by ELISA in 17 healthy controls, 23 HD patients, 10 continuous ambulatory peritoneal dialysis patients, and 15 chronic renal failure patients, as well as in 2 HD patients experiencing pyrogenic reactions. Another group of 10 chronic HD patients were dialyzed for 2.5 h, 5 with first-use Cuprophan membranes and 5 with first-use high-flux cellulose triacetate membranes. The mean bacterial and endotoxin concentrations of the dialysate used for HD treatments during the study period were 18,440 +/- 530 CFU/mL (mean +/- SEM) and 976 +/- 205 pg/mL, respectively. Blood specimens were obtained intradialysis and postdialysis for cytokine assay and were incubated to augment cytokine production. There was no difference in plasma IL-1 beta or TNF-alpha concentrations among the healthy controls, continuous ambulatory peritoneal dialysis patients, chronic renal failure patients, or HD patients. Neither cytokine increased significantly during or after HD. Two patients experiencing pyrogenic reactions had plasma TNF-alpha concentrations of 537 and 413 pg/mL, compared with matched controls of 6 and 0 pg/mL. Il-1 beta concentration did not differ from controls. We conclude that: (1) plasma IL-1 beta and TNF-alpha are not chronically elevated in chronic renal failure, continuous ambulatory peritoneal dialysis, or HD patients; (2) HD with new Cuprophan or cellulose triacetate membranes and high concentrations of dialysate endotoxin and bacteria does not cause elevation of circulating IL-1 beta or TNF-alpha; and (3) pyrogenic reactions might be mediated by TNF-alpha.

scholarly journals The effect of uremia on tumor necrosis factor-alpha release after an in vitro whole-blood endotoxin challenge.

1994 ◽  
Vol 4 (11) ◽  
pp. 1890-1895
Author(s):  
C W Oettinger ◽  
L A Bland ◽  
J C Oliver ◽  
M J Arduino ◽  
S K McAllister ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Hemodialysis Patients ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Uremia has been associated with immunologic aberrations, including anergy, increased susceptibility to infections, and reduced phagocytic activity of polymorphonuclear leukocytes. In this study, cytokine release in uremic and nonuremic blood after in vitro endotoxin stimulation was studied. Blood from nonuremic controls, chronic renal failure patients not on dialysis, and chronic hemodialysis patients predialysis and postdialysis was spiked with 10 ng/mL of Escherichia coli endotoxin and incubated for 2 and 26 h. Plasma tumor necrosis factor-alpha (TNF alpha) concentrations were determined by ELISA after each incubation period. To further study which uremic blood component may be responsible for enhanced release of TNF alpha, plasma and cellular components of chronic renal failure patients and controls were switched and then given an in vitro endotoxin stimulation (1 ng/mL). It was found that (1) TNF alpha release is enhanced by uremia and is exacerbated with progressive declines in renal function, (2) enhanced TNF alpha release is related to a blood cellular phenomenon induced by uremia, and (3) enhanced TNF alpha release in hemodialysis patients is associated with a prolonged stimulation and/or reduced plasma elimination of TNF alpha.

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