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Ureteral Obstruction (ureteral + obstruction)

Distribution by Scientific Domains
Medical Sciences80%

Kinds of Ureteral Obstruction

  • unilateral ureteral obstruction
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    Selected Abstracts

    Ureteral obstruction caused by a duplicated anomaly of inferior vena cava

    INTERNATIONAL JOURNAL OF UROLOGY, Issue 9 2005
    LIANG-TSAI WANG
    Abstract Developmental anomalies of inferior vena cava are a rare cause of ureteral obstruction. We report a case that presented with right upper ureteral obstruction that radiologically simulated a retrocaval ureter. An aberrant vessel, which caused obstruction of the right ureter was identified at operation and surgical relief of ureteral obstruction was performed. Inferior venocavography was performed postoperatively and disclosed an unusual incomplete duplication of inferior vena cava. Our findings suggested that ureteral obstruction by incompletely duplicated anomaly of the inferior vena cava should be included in the differential diagnosis of extrinsic ureteral obstruction. [source]

    Smad3 as a mediator of the fibrotic response

    INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 2 2004
    Kathleen C. Flanders
    Summary Transforming growth factor-, (TGF-,) plays a central role in fibrosis, contributing to the influx and activation of inflammatory cells, the epithelial to mesenchymal transdifferentiation (EMT) of cells and the influx of fibroblasts and their subsequent elaboration of extracellular matrix. TGF-, signals through transmembrane receptor serine/threonine kinases to activate novel signalling intermediates called Smad proteins, which modulate the transcription of target genes. The use of mice with a targeted deletion of Smad3, one of the two homologous proteins which signals from TGF-,/activin, shows that most of the pro-fibrotic activities of TGF-, are mediated by Smad3. Smad3 null inflammatory cells and fibroblasts do not respond to the chemotactic effects of TGF-, and do not autoinduce TGF-,. The loss of Smad3 also interferes with TGF-,-mediated induction of EMT and genes for collagens, plasminogen activator inhibitor-1 and the tissue inhibitor of metalloprotease-1. Smad3 null mice are resistant to radiation-induced cutaneous fibrosis, bleomycin-induced pulmonary fibrosis, carbon tetrachloride-induced hepatic fibrosis as well as glomerular fibrosis induced by induction of type 1 diabetes with streptozotocin. In fibrotic conditions that are induced by EMT, such as proliferative vitreoretinopathy, ocular capsule injury and glomerulosclerosis resulting from unilateral ureteral obstruction, Smad3 null mice also show an abrogated fibrotic response. Animal models of scleroderma, cystic fibrosis and cirrhosis implicate involvement of Smad3 in the observed fibrosis. Additionally, inhibition of Smad3 by overexpression of the inhibitory Smad7 protein or by treatment with the small molecule, halofuginone, dramatically reduces responses in animal models of kidney, lung, liver and radiation-induced fibrosis. Small moleucule inhibitors of Smad3 may have tremendous clinical potential in the treatment of pathological fibrotic diseases. [source]

    Transient anuria requiring nephrostomy after intravesical bacillus Calmette-Guérin instillations for superficial bladder cancer

    INTERNATIONAL JOURNAL OF UROLOGY, Issue 3 2006
    TOMOYUKI KANEKO
    Abstract, A 76-year-old man received intravesical bacillus Calmette-Guérin (BCG) instillations for recurrent superficial bladder cancer. He had undergone right nephroureterectomy for right renal pelvic cancer 9 months previously. He presented with anuria and left hydronephrosis after the fourth instillation, with serum creatinine increasing up to 15.7 mg/dL. Percutaneous nephrostomy was indwelled, and antegrade pyelography showed left vesicoureteral obstruction. There was no sign of recurrent bladder cancer or ureteral cancer. He started spontaneous voiding on day 4 and the nephrostomy was removed on day 8. Most of the side-effects of intravesical BCG therapy are minor, and major adverse reactions are rare. Life-threatening ureteral obstruction would be a rare complication of BCG immunotherapy. Although BCG intravesical instillation after nephroureterectomy is a common practice, special care should be taken of renal function in patients with unilateral kidney during BCG therapy. [source]

    Ureteral obstruction caused by a duplicated anomaly of inferior vena cava

    INTERNATIONAL JOURNAL OF UROLOGY, Issue 9 2005
    LIANG-TSAI WANG
    Abstract Developmental anomalies of inferior vena cava are a rare cause of ureteral obstruction. We report a case that presented with right upper ureteral obstruction that radiologically simulated a retrocaval ureter. An aberrant vessel, which caused obstruction of the right ureter was identified at operation and surgical relief of ureteral obstruction was performed. Inferior venocavography was performed postoperatively and disclosed an unusual incomplete duplication of inferior vena cava. Our findings suggested that ureteral obstruction by incompletely duplicated anomaly of the inferior vena cava should be included in the differential diagnosis of extrinsic ureteral obstruction. [source]

    Distal ureteral atresia: Recovery of renal function after relief of obstruction at ten months old

    INTERNATIONAL JOURNAL OF UROLOGY, Issue 6 2005
    SATOSHI ASHIMINE
    Abstract A large cystic mass that occupied more than half of the abdomen was identified by ultrasound in a 10-month-old boy. Intravenous pyelography failed to visualize the right kidney, so we created a loop ureterocutaneostomy followed by temporary nephrostomy to improve renal function. Exploratory surgery revealed complete atresia of the distal right ureter. A ureteral stricture developed after ureteroneocystostomy and undiversion of the loop, so a second reconstruction procedure was required (pelvi-ureteroplasty and reimplantation of the right ureter with a psoas hitch) to free the patient from dependence on catheters. Despite the occurrence of giant hydronephrosis secondary to complete ureteral obstruction at the age of 10 months, the function of the right kidney could be preserved. Accordingly, aggressive attempts to promote functional recovery may be justified even when patients have advanced hydronephrosis. [source]

    Alterations in renal cilium length during transient complete ureteral obstruction in the mouse

    JOURNAL OF ANATOMY, Issue 2 2008
    Leanne Wang
    Abstract The renal cilium is a non-motile sensory organelle that has been implicated in the control of epithelial phenotype in the kidney. The contribution of renal cilium defects to cystic kidney disease has been the subject of intense study. However, very little is known of the behaviour of this organelle during renal injury and repair. Here we investigate the distribution and dimensions of renal cilia in a mouse model of unilateral ureteral obstruction and reversal of ureteral obstruction. An approximate doubling in the length of renal cilia was observed throughout the nephron and collecting duct of the kidney after 10 days of unilateral ureteral obstruction. A normalization of cilium length was observed during the resolution of renal injury that occurs following the release of ureteral obstruction. Thus variations in the length of the renal cilium appear to be a previously unappreciated indicator of the status of renal injury and repair. Furthermore, increased cilium length following renal injury has implications for the specification of epithelial phenotype during repair of the renal tubule and duct. [source]

    Renal sonography in the diagnosis of renal obstruction or hydronephrosis in patients with cervical cancer

    JOURNAL OF CLINICAL ULTRASOUND, Issue 7 2002
    Verna Vanderpuye MBCHB
    Abstract Purpose The aim of this prospective study was to evaluate the role of renal sonography and its use as an alternative to intravenous urography in detecting ureteral obstruction or hydronephrosis in patients with cervical cancer. Materials and Methods Patients with biopsy-confirmed carcinoma of the cervix who were referred to the radiotherapy center from February 6, 2001, through July 20, 2001, were enrolled in this trial. All patients had previously undergone clinical staging by physical examination and either intravenous urography or CT scanning as the standard tests for diagnosing ureteral obstruction or hydronephrosis. All patients underwent renal sonography as an alternative diagnostic tool for diagnosing ureteral obstruction or hydronephrosis. Results Forty patients were enrolled. Their mean age was 46 years (range, 26,65 years). According to the FIGO staging system, 12% of the patients had clinical stages 1B2 and 2A disease, 20% had stage 2B, 8% had stage 3A, 50% had stage 3B, and 10% had a postoperative recurrence of cervical cancer. Thirty-four patients had had intravenous urography and 6 had had CT scans of the abdomen and pelvis. Sensitivity, specificity, positive and negative predictive values and overall accuracy rates for renal sonography were 76.5% (13/17), 100% (23/23), 100% (13/13), 85% (23/27), and 90% (36/40), respectively. Seventy-five percent (3/4) of the false-negative results occurred in patients with pelvic sidewall thickening on physical examination. Conclusions Renal sonography may be used as an effective and relatively low-cost means of diagnosing ureteral obstruction in patients with cervical cancer without clinically evident pelvic sidewall thickening. © 2002 Wiley Periodicals, Inc. J Clin Ultrasound 30:424,427, 2002 [source]

    Rosiglitazone treatment attenuates renal tissue inflammation generated by urinary tract obstruction

    NEPHROLOGY, Issue 2 2009
    SHAI EFRATI
    SUMMARY Aim: Peroxisome proliferator-activated receptor (PPAR)-, activation by rosiglitazone decreases manifestation of intrarenal inflammatory hallmarks. Inflammation significantly aggravates renal injury following urinary tract obstruction. The effect of rosiglitazone on renal inflammation following unilateral ureteral obstruction was investigated. Methods: Ninety-six Srague,Dawley rats were subjected to unilateral ureteral ligation, or to sham operation. Half of each group received rosiglitazone, 5 mg/kg bodyweight per day. The animals were killed and their kidneys allocated following 1 h, 24 h or 2 weeks, for pathological examination or for intrarenal transforming growth factor (TGF)-,, interleukin (IL)-4, IL-6, IL-10 and nitric oxide (NO) assessment by specific enzyme-linked immunosorbent assays. Apoptosis rates, extracellular matrix deposition, PPAR-,, ,-smooth muscle actin (,-SMA) expression and macrophage infiltration were assessed by specific immunohistological stainings. Results: PPAR-, receptor expression was downregulated, and infiltration of macrophages decreased, in all rosiglitazone-treated kidneys. Rosiglitazone significantly decreased apoptosis, TGF-,, IL-6, ,-SMA expression and NO availability in obstructed kidneys. Synthesis of IL-10 was unaltered, while IL-4 augmented by Rosiglitazone. Rosiglitazone also affected NO and IL-4 production in sham-operated controls. Conclusion: (i) Rosiglitazone attenuates profibrotic and pro-inflammatory responses in a rat model of ureteral obstruction-induced renal inflammation; (ii) rosiglitazone stimulates counteractive anti-inflammatory responses in the damaged kidneys; (iii) in part, rosiglitazone exerts comparable anti-inflammatory effects on obstructed kidneys and unobstructed healthy controls. Taken together, this ascertains the importance of the anti-inflammatory role of rosiglitazone treatment in amelioration of ureteral obstruction-induced renal damage. [source]

    Apoptosis of circulating lymphocyte in rats with unilateral ureteral obstruction: Role of angiotensin II

    NEPHROLOGY, Issue 5 2005
    SOMCHIT EIAM-ONG
    SUMMARY: Background: Unilateral ureteral obstruction (UUO) could induce increased renal angiotensin II (ANG II), which enhances apoptosis of renal tubular cells and renal tissue loss. Systemic ANG II is also increased in UUO. There are no data available about whether UUO can induce apoptosis of circulating lymphocytes or not. Methods: UUO or sham-operated male Wistar rats (n = 8 in each group) were fed a drinking solution containing water, angiotensin II receptor type 1 antagonist (ARA; losartan, 500 mg/L) or angiotensin-converting enzyme inhibitor (ACEI; enalapril: 200 mg/L) for 1 day or 7 days. Blood samples were collected and circulating lymphocyte cells were separated. The apoptotic cells were detected by in situ terminal deoxynucleotidyl transferase (TdT assay)-mediated digoxigenin/antidigoxigenin conjugated fluorescein method and counted under a fluorescence microscope. The apoptotic index was calculated. Results: UUO caused marked increases in the apoptotic index of circulating lymphocytes in UUO rats at both 1 day and 7 days when compared with the respective sham groups (P < 0.001). Neither ARA nor ACEI treatment had an effect on the apoptotic index values in the UUO rats at 1 day. In the UUO rats at 7 days, the apoptosis of circulating lymphocytes was markedly decreased from 29.2 ± 2.7% to 11.9 ± 2.7% (P < 0.01) in the ARA-treated rats and to 7.6 ± 2.7% (P < 0.001) in the ACEI-treated rats. Conclusion: UUO, via stimulation of ANG II, could promptly enhance apoptosis of circulating lymphocytes. The apoptosis persisted throughout the 7 days of the study. Prolonged UUO would impair lymphocyte cell immunity and the host defense mechanism. Continuous treatment with either ARA or ACEI could abrogate ANG II-stimulated circulating lymphocyte apoptosis. [source]

    Upregulation of heparin-binding epidermal growth factor-like growth factor and osteopontin in experimental hydronephrosis

    NEPHROLOGY, Issue 3 2000
    M Katerelos
    SUMMARY This study examined the expression of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and osteopontin in unilateral ureteral obstruction (UUO) in the rat, a model of obstructive uropathy. HB-EGF mRNA was upregulated 5.5-fold at 4 h post-obstruction (P < 0.05) and 4.5-fold after 12 h (P < 0.05). Immunohistochemical staining for HB-EGF demonstrated an increase in protein in the distended tubules. To determine what effects increased HB-EGF might have in the obstructed kidney, we attempted to determine whether HB-EGF upregulates osteopontin and ,-smooth muscle actin (,-SMA) in the tubular line NRK-52E. Both of these molecules are increased in UUO. Osteopontin mRNA was upregulated in NRK-52E cells after 24, 48 and 72 h HB-EGF stimulation. In contrast, HB-EGF caused a downregulation of ,-SMA protein by Western blot in NRK-52E cells. When a blocking mAb against secreted HB-EGF was administered, however, there was no effect on osteopontin mRNA levels or immunohistochemical staining for ,-smooth muscle actin. These data suggest that the action of HB-EGF in UUO may be to increase osteopontin and reduce ,-smooth muscle actin expression by tubular epithelial cells by an autocrine or intracrine mechanism. By reducing ,-SMA expression, HB-EGF may also act to maintain epithelial cell morphology in this model. [source]

    Causal link between neonatal hydronephrosis and later development of hypertension

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2 2010
    Mattias Carlström
    Summary 1. Although congenital ureteral obstruction is a common disorder in infants, its pathophysiology remains poorly understood and its clinical management continues to be debated. During the past decade, the surgical management of non-symptomatic hydronephrosis in children has become more conservative, but the long-term physiological consequences of this new policy are unclear. 2. In experimental models with complete ureteral obstruction, tubular atrophy and interstitial inflammation occur rapidly. Although this type of obstruction is very rare in clinical practice, it is often referred to in clinical discussions. New studies, using a model with chronic partial ureteral obstruction, have demonstrated that hydronephrosis is associated with renal injuries and is causally related to hypertension. 3. The mechanisms underlying the development of hypertension in experimental hydronephrosis are complex and involve changes in both the renin,angiotensin system and renal sympathetic nerve activity. Furthermore, oxidative stress and nitric oxide deficiency in the diseased kidney, with consequent resetting of the tubuloglomerular feedback mechanism, appear to play a pivotal role in the development and maintenance of hyper-tension. 4. In view of the new knowledge regarding the long-term effects of partial ureteral obstruction, today's non-operative management of hydronephrosis should be reconsidered to prevent obstructive nephropathy and hypertension in later life. [source]