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Malignant ureteral obstruction can result in renal dysfunction or urosepsis and can limit the physician's ability to treat the underlying cancer. There are multiple methods to deal with ureteral obstruction including regular polymeric double J stents (DJS), tandem DJS, nephrostomy tubes, and then more specialized products such as solid metal stents (e.g., Resonance Stent, Cook Medical) and polyurethane stents reinforced with nickel-titanium (e.g., UVENTA stents, TaeWoong Medical). In patients who require long-term stenting, a nephrostomy tube could be transformed subcutaneously into an extra-anatomic stent that is then inserted into the bladder subcutaneously. We outline the most recent developments published since 2012 and report on identifiable risk factors that predict for failure of urinary drainage. These failures are typically a sign of cancer progression and the natural history of the disease rather than the individual type of drainage device. Factors that were identified to predict drainage failure included low serum albumin, bilateral hydronephrosis, elevated C-reactive protein, and the presence of pleural effusion. Head-to-head studies show that metal stents are superior to polymeric DJS in terms of maintaining patency. Discussions with the patient should take into consideration the frequency that exchanges will be needed, the need for externalized hardware (with nephrostomy tubes), or severe urinary symptoms in the case of internal DJS. This review will highlight the current state of diversions in the setting of malignant ureteral obstruction.
Self-expanding metallic stents (Wallstents) were implanted in 44 ureters in 31 patients suffering from malignant ureteral obstruction. The causes of obstruction were lymph node metastases or primary tumors of the pelvis. During the first 4 weeks, reversible thickening of the mucosa occurred. After 4 to 6 weeks, the stents were incorporated into the wall of the ureter. In a follow-up period from 1 to 27 months, tumor-associated hydronephrosis was prevented in all patients by implantation of the Wallstents.
Renal fibrosis is a common pathological feature of chronic kidney disease (CKD) patients who progress to end-stage renal disease (ESRD). With the increasing incidence of CKD, it is of importance to develop effective therapies that blunt development of renal fibrosis. FFNT25 is a newly developed molecular compound that could be used to prevent fibrosis. In this study, we administered FFNT25 to rats following unilateral ureteral obstruction (UUO) to investigate its anti-fibrosis mechanism. Thirty-two Sprague-Dawley rats were randomly divided into four groups: (1) control (normal rats), (2) sham-operated, (3) UUO-operated + vehicle, and (4) UUO-operated + FFNT25. Two weeks after UUO, the rats were gavaged with either FFNT25 (20.6 mg/kg/day) or vehicle for two weeks. Serum, urine, and kidney samples were collected at the end of the study. FFNT25 reduced levels of renal fibrosis and decreased mRNA and protein levels of extracellular matrix (ECM) markers α-smooth muscle actin (α-SMA) and plasminogen activator inhibitor-1 (PAI-1) following UUO compared to vehicle treatment (n = 8, p<.05). The current results indicate that FFNT25 can affect both the production and degradation of collagen fibers to reduce fibrosis.
Objectives: To improve the mouse model of relief for unilateral ureteral obstruction (RUUO) and explore the pathological process of renal fibrosis after the obstruction was relieved. Methods: C57BL/6 mice in model group were randomly divided into RUUO group, improved RUUO group, and UUO group. After leaving Unilateral Ureteral Obstruction (UUO) for 3 days, the obstruction was released by reimplantation way in RUUO group and in reimplantation + catheter way in improved RUUO group. C57BL/6 mice in observation group were randomly divided into 1d RUUO group, 3d RUUO group, 7d RUUO group, and 14d RUUO group. Three days after UUO, the obstruction was released by reimplantation + catheter in four groups. We detected the renal volume, H&E, Masson staining, and immunohistochemistry of kidney pathology on the seventh day after RUUO in model group and on the 1st, 3rd, 7th, and 14th day after RUUO in observation group. Results: Comparing with mice in RUUO group, mice in improved RUUO group had lower renal volume, tubular damage score, and collagen area percentage. After the obstruction was relieved, the renal volume decreased gradually within 2 weeks. The tubular damage score in 7d RUUO group was lower than that in 1d RUUO and 3d RUUO group. However, the tubular damage score in 14d RUUO group was higher than that in 7d RUUO group. The tendency of collagen area percentage and α-SMA IOD value were consistent with the tubular damage score. Conclusions: Using the method of reimplantation + catheter, a reliable mice model of RUUO can be got. After RUUO, the de-obstructed kidneys are still in damage and fibrosis state.
We performed differential display analysis to determine transcriptional activity in the rat kidney, following unilateral ureteral obstruction and found a 12-fold increase in the expression of Growth Arrest and DNA Damage-45gamma (GADD45gamma), a stress-responsive molecule that interacts with cell-cycle proteins. GADD45gamma was strongly expressed in as little as 6 h following ureteric obstruction in the renal tubules, and was also found in kidney tissue of patients with chronic glomerulonephritis. Adenovirus-mediated expression of GADD45gamma in cultured renal tubular cells activated p38 along with a significant upregulation of C-C and C-X3-C chemokine ligands and fibrosis-related factors such as several matrix metalloproteinases, transforming growth factor-beta1, decorin, and bone morphogenetic protein 2. Silencing of GADD45gamma expression significantly blunted the upregulation of these inflammatory and fibrogenic mediators and monocyte infiltration in the ureteral obstructed rat kidney. Our study shows that GADD45gamma is quickly upregulated in the kidney with an obstructed ureter, enhancing the production of factors regulating the pathogenesis of kidney disease.
Although the primary organ has been the subject of intense investigation in the field of organ fibrosis over the past several decades, the presence of lymph node fibrosis due to persistent activation of the immune response in its partner organ remains largely unknown. Previously, we demonstrated that activation of the immune response following ischemia-reperfusion injury (IRI) and crescentic glomerulonephritis (CGN) in the kidney was associated with extracellular matrix (ECM) production by fibroblastic reticular cells (FRCs) of the kidney-draining lymph node (KLN). Here, we sought to determine whether FRCs in the KLN become similarly fibrogenic following unilateral ureteral obstruction (UUO) of the kidney. We subjected 6-8-week-old C57BL/6J mice to UUO for 2, 7, and 14 days. We examined the microarchitecture of the kidney and KLN by immunofluorescence staining at each timepoint, and we quantified immune cell populations in the KLN by flow cytometry. The contralateral kidney unaffected by UUO and its partner KLN were used as controls. We found through immunofluorescence staining that FRCs increased production of ECM fibers and remodeled the microarchitecture of the UUO KLN, contributing to fibrosis that mirrored the changes in the kidney. We also observed by flow cytometry that the populations of CD11b+ antigen-presenting cells, CD11c+ dendritic cells, and activated CD4+ and CD8+ T cells were significantly higher in the UUO KLN than the KLN draining the unaffected contralateral kidney. Expression of the TGFβ/TGFβR signaling pathway was upregulated and colocalized with FRCs in the UUO KLNs, suggesting a possible mechanism behind the fibrosis. Both release of ureteral ligation at 2 days following UUO and depletion of FRCs at the time of injury onset halted the progression of fibrosis in both the kidney and the KLN. These findings for the first time highlight the association between fibrosis both in the kidney and the KLN during UUO, and they lay the groundwork for future studies that will investigate more deeply the mechanisms behind the connection between FRCs and KLN fibrosis.
Cognitive impairment is a common complication in chronic kidney disease (CKD) patients. Currently, limited types of animal models are available for studying cognitive impairment in CKD. We used unilateral ureteral obstruction (UUO) in mice as an animal model to study the cognitive changes and related pathology under prolonged renal impairment METHODS: UUO was performed in 8-week-old male C57BL/6 N mice with double-ligation of their left ureter. A sham group was subjected to the same experimental procedure without ureteral obstruction. Cognitive and behavioral tests were performed to examine potential changes in cognition and behavior at 2, 4 and 12 weeks after surgery. Sera were collected, and kidneys and brains were harvested for the detection of systemic inflammation markers and neurodegenerative changes.
Mast cells regulate both inflammatory responses and tissue repair in human diseases but there are conflicting reports on the role of these cells in the pathogenesis of various kidney diseases. Here we measured mast cell function in unilateral ureteral obstruction, a well-characterized model of renal fibrosis, using Kit(W)/Kit(W-v) mice genetically deficient in mast cells, wild-type mice, and deficient mice reconstituted by adoptive transfer with mast cells from the wild-type animals. Mast cell-deficient mice had higher levels of renal tubular damage, more stromal fibrosis, higher numbers of infiltrating ERHR3-positive macrophages and CD3-positive T cells, and higher tissue levels of profibrotic transforming growth factor-beta1 than wild-type mice or mice reconstituted by adoptive transfer of mast cells 3 weeks after ureteral obstruction. Similarly, while wild-type and adoptively transferred mice had increased alpha-smooth muscle actin and decreased E-cadherin expression, which are indicators of epithelial-mesenchymal transition, the obstructed kidneys of the mast cell-deficient mice had significant attenuation of those indicators. Thus, our study suggests that mast cells protect the kidney against fibrosis by modulation of inflammatory cell infiltration and by transforming growth factor-beta1-driven epithelial-to-mesenchymal transitions.
Regardless of their primary causes, progressive renal fibrosis and tubular atrophy are the main predictors of progression to end-stage renal disease. Basigin/CD147 is a multifunctional molecule-it induces matrix metalloproteinases and hyaluronan, for example-and has been implicated in organ fibrosis. However, the relationship between basigin and organ fibrosis has been poorly studied. We investigated basigin's role in renal fibrosis using a unilateral ureteral obstruction model. Basigin-deficient mice (Bsg(-/-)) demonstrated significantly less fibrosis after surgery than Bsg(+/+) mice. Fewer macrophages had infiltrated in Bsg(-/-) kidneys. Consistent with these in vivo data, primary cultured tubular epithelial cells from Bsg(-/-) mice produced less matrix metalloproteinase and exhibited less motility on stimulation with transforming growth factor β. Furthermore, Bsg(-/-) embryonic fibro blasts produced less hyaluronan and α-smooth muscle actin after transforming growth factor β stimulation. Together, these results demonstrate for the first time that basigin is a key regulator of renal fibrosis. Basigin could be a candidate target molecule for the prevention of organ fibrosis.
The AXL receptor tyrosine kinase (RTK) is involved in partial epithelial-to-mesenchymal transition (EMT) and inflammation - both main promoters of renal fibrosis development. The study aim was to investigate the role of AXL inhibition in kidney fibrosis due to unilateral ureteral obstruction (UUO). Eight weeks old male C57BL/6 mice underwent UUO and were treated with oral AXL inhibitor bemcentinib (n = 22), Angiotensin-converting enzyme inhibitor (ACEI, n = 10), ACEI and bemcentinib (n = 10) or vehicle alone (n = 22). Mice were sacrificed after 7 or 15 days and kidney tissues were analyzed by immunohistochemistry (IHC), western blot, ELISA, Sirius Red (SR) staining, and hydroxyproline (Hyp) quantification. RNA was extracted from frozen kidney tissues and sequenced on an Illumina HiSeq4000 platform. After 15 days the ligated bemcentinib-treated kidneys showed less fibrosis compared to the ligated vehicle-treated kidneys in SR analyses and Hyp quantification. Reduced IHC staining for Vimentin (VIM) and alpha smooth muscle actin (αSMA), as well as reduced mRNA abundance of key regulators of fibrosis such as transforming growth factor (Tgfβ), matrix metalloproteinase 2 (Mmp2), Smad2, Smad4, myofibroblast activation (Aldh1a2, Crlf1), and EMT (Snai1,2, Twist), in ligated bemcentinib-treated kidneys was compatible with reduced (partial) EMT induction. Furthermore, less F4/80 positive cells, less activity of pathways related to the immune system and lower abundance of MCP1, MCP3, MCP5, and TARC in ligated bemcentinib-treated kidneys was compatible with reduction in inflammatory infiltrates by bemcentinib treatment. The AXL RTK pathway represents a promising target for pharmacologic therapy of kidney fibrosis.
Asiatic acid (AA) is one of the triterpenoid compounds present in Centella asiatica and it has been shown to be capable of attenuating liver fibrosis. In the present study, we investigated the effects of AA on renal tubulointerstitial fibrosis in mice with unilateral ureteral obstruction (UUO). Mice were divided randomly into five groups (n=5 per group): the sham-surgery (Sh), UUO plus vehicle treatment (UUO+V), UUO plus 1 mg/kg body weight AA treatment (UUO+A1), UUO plus 4 mg/kg body weight AA treatment (UUO+A2) and UUO plus 16 mg/kg body weight AA treatment (UUO+A3) groups. The mice were treated with AA daily by oral gavage from the day subsequent to surgery for six days. On the seventh day, the mice were sacrificed for examination. Tubular injury was observed in the renal cortex of the mice administered the vehicle, while high doses of AA were observed to exert a significant suppressive effect on tubular injury. Interstitial fibrosis, increased expression of α-smooth muscle actin (SMA) and transforming growth factor (TGF)-β1 and phosphorylation of Smad2/3 were induced by ureteral ligation; however these effects were abrogated by intermediate and high doses of AA. These results suggest that AA may ameliorate tubulointerstitial fibrosis by reducing tubular injury, fibroblast activation and extracellular matrix (ECM) accumulation mediated by Smad-dependent TGF-β1 signaling.
Obstructive nephropathy decreases renal blood flow (RBF) and glomerular filtration rate (GFR), causing tubular abnormalities, such as urinary concentrating defect, as well as increasing oxidative stress. This study aimed to evaluate the effects of N-acetylcysteine (NAC) on renal function, as well as on the protein expression of aquaporin 2 (AQP2) and endothelial nitric oxide synthase (eNOS), after the relief of bilateral ureteral obstruction (BUO).
Transforming growth factor-β (TGF-β) plays a pivotal role in renal fibrosis. Endoglin, a 180 KDa membrane glycoprotein, is a TGF-β co-receptor overexpressed in several models of chronic kidney disease, but its function in renal fibrosis remains uncertain. Two membrane isoforms generated by alternative splicing have been described, L-Endoglin (long) and S-Endoglin (short) that differ from each other in their cytoplasmic tails, being L-Endoglin the most abundant isoform. The aim of this study was to assess the effect of L-Endoglin overexpression in renal tubulo-interstitial fibrosis. For this purpose, a transgenic mouse which ubiquitously overexpresses human L-Endoglin (L-ENG+) was generated and unilateral ureteral obstruction (UUO) was performed in L-ENG+ mice and their wild type (WT) littermates. Obstructed kidneys from L-ENG+ mice showed higher amounts of type I collagen and fibronectin but similar levels of α-smooth muscle actin (α-SMA) than obstructed kidneys from WT mice. Smad1 and Smad3 phosphorylation were significantly higher in obstructed kidneys from L-ENG+ than in WT mice. Our results suggest that the higher increase of renal fibrosis observed in L-ENG+ mice is not due to a major abundance of myofibroblasts, as similar levels of α-SMA were observed in both L-ENG+ and WT mice, but to the higher collagen and fibronectin synthesis by these fibroblasts. Furthermore, in vivo L-Endoglin overexpression potentiates Smad1 and Smad3 pathways and this effect is associated with higher renal fibrosis development.
Granulocytic sarcoma is an extramedullary tumor which is composed of myeloblasts and immature myeloid cells. It usually occurs in association with acute myeloid leukemia and most commonly involves skin, soft tissue, lymph nodes, bone, and periosteum. We report a case of isolated ureteral granulocytic sarcoma without hematologic manifestations. Our patient presented with bloody urine and left-sided lumbar pain. Preoperative clinical and radiologic features raised the suspicion of an upper urinary tract transitional cell carcinoma, and he was scheduled for nephroureterectomy. However, perioperative pathologic feedback and the unusual endoscopic appearance of the tumor altered our surgical strategy towards segmental ureterectomy and ureteroneocystostomy. Eventual pathologic diagnosis was granulocytic sarcoma of the ureter. Postoperative workup failed to demonstrate any sign of an accompanying hematologic disorder. He started receiving the chemotherapy protocol of acute myeloblastic leukemia. To our knowledge, this is the first documented case of nonleukemic ureteral granulocytic sarcoma which came to attention due to urologic complaints.
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