Transforming growth factor-?1 in nephrotic syndrome treated with cyclosporine and ACE inhibitors

Wasilewska, Anna; Zoch-Zwierz, W

doi:10.1007/s00467-004-1619-5

Cited by 11 publications

(9 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Increased urinary TGF-beta is detected in patients with some forms of nephrotic syndrome (6), IgA nephropathy (7), and focal segmental glomerulosclerosis (FSGS) (7, 8). Interestingly, while detection of TGF-beta in the urine can differentiate between FSGS and the non-fibrotic process of minimal change disease (8), TGF-beta levels cannot be used predict response to corticosteroid therapy, despite the fact that some anti-fibrotic treatments may reduce these levels (9). In human FSGS (10) and in experimental models of renal fibrosis (11), TGF-beta is closely associated with ECM accumulation.…”

Section: Tgf-beta and The Pathogenesis Of Chronic Kidney Diseasementioning

confidence: 99%

TGF-beta signal transduction in chronic kidney disease

Schnaper

Jandeska

Runyan³

et al. 2009

Front Biosci

119

View full text Add to dashboard Cite

Transforming growth factor (TGF)-beta is a central stimulus of the events leading to chronic progressive kidney disease, having been implicated in the regulation of cell proliferation, hypertrophy, apoptosis and fibrogenesis. The fact that it mediates these varied events suggests that multiple mechanisms play a role in determining the outcome of TGF-beta signaling. Regulation begins with the availability and activation of TGF-beta and continues through receptor expression and localization, control of the TGF-beta family-specific Smad signaling proteins, and interaction of the Smads with multiple signaling pathways extending into the nucleus. Studies of these mechanisms in kidney cells and in whole-animal experimental models, reviewed here, are beginning to provide insight into the role of TGF-beta in the pathogenesis of renal dysfunction and its potential treatment.

show abstract

Section: Tgf-beta and The Pathogenesis Of Chronic Kidney Diseasementioning

confidence: 99%

TGF-beta signal transduction in chronic kidney disease

Schnaper

Jandeska

Runyan³

et al. 2009

Front Biosci

119

View full text Add to dashboard Cite

show abstract

“…Consistently, among our patients, baseline TGF‐β1 excretion was higher among those who underwent dialysis and also correlated well with the severity of the acute renal damage. Other authors have already reported a significant correlation between TGF‐β1 urinary levels and the magnitude of the proteinuria and the GFR drop . Activation of the TGF‐β1 axis explains many morphological alterations in chronically failing kidneys .…”

Section: Discussionmentioning

confidence: 93%

Prognostic value of urinary TGF‐β1 in hemolytic uremic syndrome: A pilot study

Balestracci¹,

Roy

Caletti³

2020

Pediatrics International

View full text Add to dashboard Cite

Background Transforming growth factor β1 (TGF‐β1) is the main profibrotic cytokine. Its urinary excretion reflects intrarenal production; thus, we conjectured that it is elevated during hemolytic uremic syndrome related to Shiga‐toxin‐producing Escherichia coli (STEC‐HUS). In this pilot study, we explored the ability of baseline TGF‐β1 excretion (exposure variable) to predict renal prognosis at 6 months (outcome variable). In a secondary investigation, we compared changes in cytokine levels during the study period between patients with opposite renal outcomes. Methods Urinary TGF‐β1 concentrations were measured prospectively in 24 children with STEC‐HUS on admission, and at 15, 30, 60, 90, and 180 days. Normal values were obtained from 20 healthy subjects. Results Baseline TGF‐β1 concentrations predicted renal outcomes with an area under the curve of 1 (95%CI 0.85–1; sensitivity 100%, specificity 100%) with the best cutoff level >293.7 pg/mg uCr. All patients with high TGF‐β1 levels developed persistent renal impairment, unlike none with low concentrations (4/4 vs. 20/0 respectively, P = 0.0001). The latter had higher cytokine levels (P < 0.05) at each time point without reaching normal concentrations (<45 pg/mg uCr). Conclusions Baseline urinary TGF‐β1 levels accurately predicted short‐term renal outcomes in STEC‐HUS children, and cytokine excretion during the first 6 months after diagnosis was higher among those with worse evolution. Larger studies are needed to validate these findings.

show abstract

“…In patients with primary and secondary glomerulopathies, renal glomeruli contain a few times more mRNA TGF-β1 than in healthy subjects [40,41]. Wasilewska and ZochZwierz found that urinary TGF-β1 level increased in proportion to proteinuria during relapse of NS [42]. Zhang et al showed an increase in TGF-β1 expression in the kidneys of rats with adriamycin-induced nephropathy which was prevented by simvastatin [43].…”

Section: Discussionmentioning

confidence: 95%

Beneficial effect of triple treatment plus immunoglobulin in experimental nephrotic syndrome

et al. 2009

View full text Add to dashboard Cite

Combinations of antiproteinurics, including angiotensin I-converting enzyme inhibitors + angiotensin II receptor antagonist + statins, are promising choices in the treatment of steroid-resistant nephrotic syndrome. We aimed to investigate the effects of high doses of immunoglobulin in addition to these combinations in rats with adriamycin-induced nephrosis. The study included 40 rats allocated into five groups: control, nephrotic syndrome without treatment, dual therapy (DT) with enalapril + losartan, triple therapy (TT) with enalapril + losartan + simvastatin, and quadruple therapy (QT) with enalapril + losartan + simvastatin + a high dose of immunoglobulin. The proteinuria levels were not statistically different between DT, TT and QT groups at weeks 5, 8, 12 and 16. At week 16, serum creatinine levels in the QT group were significantly lower than those in the control, DT and TT groups. The glomerulosclerosis index in the DT group was significantly lower than in the TT and QT groups. The scores for interstitial fibrosis and TGF-beta staining were similar among treatment groups. In conclusion, we showed that quadruple therapy including immunoglobulin had a beneficial effect on renal function in the late phase, but it had no additional effects in reducing proteinuria or in glomerulosclerosis score in experimental nephrotic syndrome. Further studies with angiotensin I-converting enzyme inhibitors (ACEIs), angiotensin II receptor antagonists (AIIRAs) and immunoglobulin combinations would offer some benefits in the treatment of nephrotic syndrome.

show abstract

Transforming growth factor-?1 in nephrotic syndrome treated with cyclosporine and ACE inhibitors

Cited by 11 publications

References 27 publications

TGF-beta signal transduction in chronic kidney disease

TGF-beta signal transduction in chronic kidney disease

Prognostic value of urinary TGF‐β1 in hemolytic uremic syndrome: A pilot study

Beneficial effect of triple treatment plus immunoglobulin in experimental nephrotic syndrome

Contact Info

Product

Resources

About