Unilateral ureteral obstruction: beyond obstruction

Ucero, Álvaro C.; Benito-Martín, Alberto; Izquierdo, María C.; Sanchez-Niño, María Dolores; Sanz, Ana B.; Ramos, Adrián M.; Berzal, Sergio; Ruíz-Ortega, Marta; Egido, Jesús; Ortíz, Alberto

doi:10.1007/s11255-013-0520-1

Cited by 160 publications

(165 citation statements)

References 125 publications

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“…Its receptor, Fn14, a type I transmembrane protein and member of the fibroblast growth factor-inducible gene family, was recognized by differential display and later identified in 2001 as the TWEAK receptor. In kidney tissue, Ortiz and his group [9,10] have presented ample evidence to support the role of TWEAK activation of intrinsic renal cell Fn14 receptors in the pathogenesis of AKI and CKD. Increased expression of TWEAK and Fn14 has been observed in human and experimental models of tubulointerstitial kidney disease.…”

Section: Role Of Tweak-fn14 In Aki and Ckdmentioning

confidence: 99%

Apoptosis, Fibrosis and Senescence

Portilla¹

2014

Nephron Clin Pract

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Fibrosis is a major hallmark of progressive kidney disease. The cellular mechanisms that lead to kidney tissue fibrosis are complex and include, for example, increased inflammation, increased oxidative stress, and proximal tubule cell death in the form of apoptosis or senescence. Recent studies have identified TWEAK, a tumor necrosis factor-like weak inducer of apoptosis, as a novel cytokine that mediates kidney inflammation in models of renal fibrosis. Inhibition of apoptosis via TWEAK inhibition has been shown to reduce kidney fibrosis. Recent studies using lineage tracing suggest that interstitial pericytes/perivascular fibroblasts differentiate into myofibroblasts and undergo proliferative expansion during fibrosis. Furthermore, increased expression of nuclear peroxisome proliferator-activated receptor-α in proximal tubules can directly reduce increased expression of transforming growth factor-β1 and interstitial inflammation in models of renal fibrosis, which suggests preservation of proximal tubule cell metabolism and integrity represents an important new therapeutic target. In this review, the current evidence and potential molecular mechanisms involved in the development of kidney fibrosis are discussed.

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Section: Role Of Tweak-fn14 In Aki and Ckdmentioning

confidence: 99%

Apoptosis, Fibrosis and Senescence

Portilla¹

2014

Nephron Clin Pract

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“…UO may lead to renal impairment due to the physical blockade of urine flow causing hydronephrosis [2]. Obstructive uropathy is the cause of renal failure in 2.6% of patients [3].…”

Section: Introductionmentioning

confidence: 99%

Does a Ureteral Obstruction Affect the Contralateral Kidney Morphology? A Stereological Analysis in a Rodent Model

et al. 2018

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Objective: To investigate, in a rodent model, the influence of an obstructed kidney/ureter on the contralateral organ morphology. Methods: Thirty-six rats were randomly assigned into the following groups: untreated ureteral obstruction group (UO-U, n = 10), submitted to a ligature of the ureter at day 0; UO group (at day 0) followed by nephrectomy after 24 h (UO-N, n = 8); nephrectomy group (N, n = 9), submitted to nephrectomy at day 0; and sham group (S, n = 9), submitted to simulated surgery at day 0. All these procedures were performed on the left kidney/ureter. All animals were euthanized 30 days after surgery, and the right kidneys were collected for stereological analysis. Data were compared using a one-way analysis of variance with Bonferroni’s post test, considering p < 0.05 as significant. Results: The kidney volume, weight, and cortical volume were augmented in groups UO-N and N, compared to group S. Kidneys from the UO-U group showed only a moderate augmentation in kidney weight, with a reduction in the cortical-medullar ratio, compared to the kidneys in group S. No differences in the glomerular volumetric density, volume-weighted glomerular volume, and number of glomeruli were observed among the right kidneys of the studied groups. Conclusion: An obstructed kidney/ureter is more prejudicial to the contralateral kidney morphology than an absent kidney.

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“…If left untreated, it can lead to inflammation, atrophy, fibrosis, and irreversible renal injury ending in chronic kidney disease 2 , which can significantly burden both patients and the health care system 3 .…”

Section: Introductionmentioning

confidence: 99%

“…These leukocytes subsequently release a variety of mediators such as transforming growth factor beta-1 (TGF-β1) 2 . Regulated by angiotensin II (ANGII) 4 , TGF-β1 is an inducer of epithelial-mesenchymal transition (EMT), a key initiator of tissue fibrosis.…”

Section: Introductionmentioning

confidence: 99%