Urine activity of cathepsin B, collagenase and urine excretion of TGF-β 1 and fibronectin in membranous glomerulonephritis

Senatorski, G; Pączek, Leszek; Sułowicz, Władysław; Gradowska, L; Bartlomiejczyk, I

doi:10.1007/s004330050103

Cited by 17 publications

(11 citation statements)

References 15 publications

(22 reference statements)

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“…A role for MMPs in the alteration of basement membrane permeability has been postulated in patients with membranous GN, which reveal elevated levels of TGF-β and collagenase activity in urine [23]. Moreover, collagen IV and fibronectin, which are the major components of ECM, and MMP and TIMP expressions were all altered in diabetic and other nephropathies [24,25,26,27,28,29].…”

Section: Discussionmentioning

confidence: 99%

Doxycycline: A Pilot Study to Reduce Diabetic Proteinuria

Naini

Harandi²,

Bastani³

et al. 2007

Am J Nephrol

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Background: Activity of matrix metalloproteinases (MMPs), the enzymes primarily responsible for the deposition of extracellular matrix proteins, contributes to the pathogenesis of diabetic proteinuria. We evaluated the effect of doxycycline, a potent nonselective MMPs inhibitor, on reduction of proteinuria in diabetic patients. Material and Methods: In a self-control clinical trial, 35 patients with overt diabetic nephropathy (proteinuria >300 mg/24 h) received oral doxycycline 100 mg/day for 2 months. Twenty-four-hour urine volume, Cr and protein excretion were measured at baseline, after 1 and 2 months of treatment, and after 4 months of its discontinuation. Treatment-related side effects were closely monitored and documented. Results: Mean (±SD) 24-hour urine protein was 888 ± 419 mg at baseline, 884 ± 368 mg after 1 month, and 643 ± 386 mg after the 2 months of doxycycline treatment. There was statistically significant reduction in proteinuria at 2 months of treatment vs. at the baseline (p < 0.001). Mean 24-hour urine protein excretion increased to 1,021 ± 422 mg 4 months after doxycycline was discontinued. The changes in serum sodium, potassium, BUN and Cr concentrations, and blood pressure measurements during the 2 months of treatment and follow-up period were not statistically significant. Conclusion: Proteinuria in patients with diabetic nephropathy can be reduced with low dose doxycycline therapy over a 2-month period of drug administration. Further studies are necessary to determine the long-term effect, the optimal dose, and the optimal duration of this potentially novel therapy.

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Section: Discussionmentioning

confidence: 99%

Doxycycline: A Pilot Study to Reduce Diabetic Proteinuria

Naini

Harandi²,

Bastani³

et al. 2007

Am J Nephrol

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“…Fibronectin is excreted in the urine of patients with proteinuria and glomerular disease such as membranous nephropathy [30][31][32][33]. To determine the potential proinflammatory effect of this protein on renal epithelium, confluent monolayers of TECs were exposed to increasing concentrations of soluble fibronectin (50 to 150 lg/mL).…”

Section: Chemokine Induction By Soluble Fibronectinmentioning

confidence: 99%

“…Soluble fibronectin is also reported in clinical and experimental renal disease. Urinary fibronectin levels are increased in patients with diabetic nephropathy and glomerular diseases, including membranous nephropathy [30][31][32][33][34]. Soluble fibronectin is also seen in the tubular lumen and urine of rats in various experimental models of renal injury [28,35,36].…”

mentioning

confidence: 99%

Soluble fibronectin induces chemokine gene expression in renal tubular epithelial cells

Ren

Blanchette

White

et al. 2005

Kidney International

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“…Our results obtained at the time of relapse of proteinuria (A) also showed a positive correlation between protein and TGF-b1 in the urine. Our study was performed in a homogenous group of children with histopathological signs of FSGS in 10%-30% of glomeruli, which might also influence the urinary TGF-b1 level, as FSGS is related to intensified fibrosis and glomerulosclerosis [5,8,20,21].…”

Section: Discussionmentioning

confidence: 99%

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

Wasilewska

Zoch-Zwierz

2004

Pediatr Nephrol

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The aim of the study was to assess urinary transforming growth factor (TGF)-beta1 in children with steroid-dependent nephrotic syndrome (SDNS) treated with cyclosporine A (CyA) and ACE inhibitors (ACEI). The study involved 24 children (14 boys and 10 girls) with SDNS and signs of focal segmental glomerulosclerosis. The children were treated with prednisone, CyA, and ACEI. All children were examined four times: A during relapse of proteinuria, before treatment with CyA and ACEI, and B after 3 months, C 6 months, and D 12 months of treatment. The control group consisted of 20 healthy children of the same age. The urinary TGF-beta1 level was determined by ELISA (R and D Quantikine). The serum CyA level was measured by monoclonal antibody fluorescence polarization immunoassay. Prior to CyA treatment, the urinary TGF-beta1 level was the highest (135.61+/-38.31 pg/mg creatinine). During CyA treatment, TGF-beta1 was reduced to 117.96+/-81.57 after 3 months, to 80.26+/-49.52 after 6 months, and to 44.00+/-31.83 pg/mg creatinine after 12 months, but it was still higher than in the control group. At 3 months there was a positive linear correlation between urinary TGF-beta1 and proteinuria (r=0.654, P<0.01). These results indicate that the urinary TGF-beta1 level increases in proportion to proteinuria during relapse of NS. Treatment with CyA and ACEI also influences urinary TGF-beta1, which is still higher after 12 months of treatment than in healthy children.

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Urine activity of cathepsin B, collagenase and urine excretion of TGF-β 1 and fibronectin in membranous glomerulonephritis

Cited by 17 publications

References 15 publications

Doxycycline: A Pilot Study to Reduce Diabetic Proteinuria

Doxycycline: A Pilot Study to Reduce Diabetic Proteinuria

Soluble fibronectin induces chemokine gene expression in renal tubular epithelial cells

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

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