Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Unilateral hydronephrosis and urinary incontinence, secondary to a ureterovaginal fistula, were corrected in a cat after surgical excision of the fistula and implantation of the affected ureter into the bladder. Salvage of the kidney was attempted because underlying chronic bilateral renal disease was suspected. Renal scintigraphy was used to monitor improvement in the function of the previously obstructed kidney after surgery.
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PMID:Postoperative evaluation of renal function after surgical correction of a ureterovaginal fistula in a cat. 842 Aug 93

Ochratoxin A (OTA) is a ubiquitous nephrotoxic mycotoxin which was shown to be carcinogenic to laboratory animals and may be responsible for kidney pelvis, ureter and urinary bladder tumors associated with Balkan endemic nephropathy in man. Previous evidence from this laboratory demonstrated that OTA exposure results in adduct formation on kidney, testicles, liver and spleen DNA. We show in this study that after a single oral administration of OTA to mice (2 mg/kg body weight) a high level of DNA adducts (150 per 10(9) nucleotides) is also detected in the urinary bladder. The metabolic pathway of OTA leading to genotoxic compounds is not yet known. We demonstrate here that two inhibitors of the prostaglandin H synthase, indomethacin and aspirin, administered to mice before OTA treatment, dramatically reduce the amounts of DNA adducts, particularly in the urinary bladder and kidney. This suggests a role of protaglandin H synthase in the metabolism of OTA leading to active metabolites which react with DNA.
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PMID:Protection by indomethacin and aspirin against genotoxicity of ochratoxin A, particularly in the urinary bladder and kidney. 882 84

At this point in time, endopyelotomy is first-line therapy for both primary and secondary adult ureteropelvic junction obstruction (UPJO) in many medical centers. However, the potential, albeit small, for significant bleeding with any endoincision of the UPJ has sparked interest in the simple, less morbid technique of endoballoon rupture. To date, no comparative data are available on the effectiveness of these two techniques. Thirty female minipigs were randomized to cutting balloon (Acucise) endopyelotomy (AEP) (N = 13), endoballoon rupture (EBR) (N = 13), or a control arm (N = 4). Following baseline retrograde pyelogram (RPG) and diuretic renogram (DRG), a secondary proximal ureteral stricture was created by laparoscopic ligation of the UPJ. After 8 weeks, AEP or EBR was performed in each of the study pigs. In 16 pigs (8 AEP, 8 EBR), a 7F 22-cm ureteral stent was placed (chronic arm). After 6 weeks, the stent was removed, and a second RPG and DRG were performed. Three months post-treatment, after RPG and DRG, the renal units were harvested, and histologic sections of the affected UPJ, contralateral normal ureter, and ipsilateral kidney were examined. Ten pigs (5 AEP, 5 EBR) underwent harvest immediately after treatment (acute arm). The four control animals remained untreated. At 8 weeks, all minipigs had obstructive findings on RPG and DRG. All UPJs could be treated but one, which had an impassable stricture; there were no perioperative complications. In the acute arm, all UPJs were patent. All five AEP ureters had evidence of an uneven cut and cautery effect. Of the EBR ureters, two had smooth tears and three had ragged tears, and none had evidence of cautery effect. In the chronic arm, 3 months after either AEP or EBR, all minipigs had a patent UPJ, yet only 5 of 16 had an improved 1 1/2 by DRG. Histologic sections of the affected UPJs from 20 minipigs in the chronic arm (8 AEP, 8 EBR, 4 controls) were indistinguishable among the three groups; each revealed significant periureteral fibrosis and chronic inflammation with a mainly unremarkable muscular layer. However, histologic sections of 25 treated kidneys, including both acute and chronic animals (13 AEP, 12 EBR), revealed endstage renal disease (N = 10), chronic inflammatory changes (N = 7), or normal tissue (N = 8). Again, there was no trend favoring either AEP and EBR. In summary, in this laboratory study, we could detect no difference in outcome between an incisional endopyelotomy and an endoballoon rupture for treating secondary UPJO.
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PMID:Comparison of acucise endopyelotomy and endoballoon rupture for management of secondary proximal ureteral stricture in the porcine model. 887 26

Vesicoureteral reflux (VUR) is common in children with urinary tract infections (UTI) and may result in renal scarring or reflux nephropathy. To date, the primary diagnostic tool has been voiding cystourethrography (VCUG). A new technique for evaluation of grade 1 and 2 VUR is described using color Doppler imaging-mode cystography (CDIMC): 77 children, aged 7 months to 14 years, were examined for VUR by CDIMC and standard VCUG. According to the established reflux sonography (US) using a real-time mode, all patients selected for this study had a normal urinary tract on conventional gray-scale US. We studied 154 ureters, and a total of 31 were found to be refluxing on CDIMC and 30 on VCUG. A positive sonogram was defined as visualization of Doppler signals from the bladder to the ureter during the course of bladder filling. Taking VCUG as the gold standard, we had ten false-positive findings. The false-positive rate of 18.5% may have been due to the shorter observation time of fluoroscopy. Comparison of the two methods shows CDIMC to be 70% sensitive with a specificity of 92% in the detection of VUR grade 1 and 2. To evaluate the incidence of asymptomatic low-grade VUR in a non-infected population, a second series of 38 children (19 males, 19 females) aged 3 to 15 years (mean 8.8 years) with normal urologic status and urine cultures were studied by color Doppler imaging mode (CDIM) for detection of asymptomatic low-grade VUR. Four children were found to have a unilateral refluxing ureter. The incidence of VUR in children with a normal urinary tract and no prior UTI was 10.5%. In conclusion, CDIMC can be used as a possible alternative to standard VCUG for the screening and follow-up of low-grade VUR. In addition, our study indicates that asymptomatic grade 1 and 2 reflux might be a physiological condition.
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PMID:Detection of low-grade vesicoureteral reflux in children by color Doppler imaging mode. 903 8

Recently, we reported that aristolochic acid (AA) a naturally occurring nephrotoxin and carcinogen is implicated in a unique type of renal fibrosis, designated Chinese herbs nephropathy (CHN). Indeed, we identified the principal aristolochic acid-DNA adduct in the kidney of five such patients. We now extend these observations and demonstrate the presence of additional AA-DNA adducts by the 32P-post-labelling method not only in the kidneys, but also in a ureter obtained after renal transplantation. Using the nuclease P1 version of the assay not only the major DNA adduct of aristolochic acid, 7-(deoxyadenosin-N6-yl)-aristolactam I (dA-AAI), but also the minor adducts, 7-(deoxyguanosin-N2-yl)-aristolactam I (dG-AAI) and 7-(deoxyadenosin-N6-yl)-aristolactam II (dA-AAII) were detected, and identified by cochromatographic analyses with TLC and HPLC. Quantitative analyses of six kidneys revealed relative adduct levels from 0.7 to 5.3/10(7) for dA-AAI, from 0.02 to 0.12/10(7) for dG-AAI and 0.06 to 0.24/ 10(7) nucleotides for dA-AAII. The detection of the dA-AAII adduct is consistent with the occurrence of aristolochic acid II (AAII) in the herb powder imported under the name of Stephania tetrandra and confirms that the patients had indeed ingested the natural mixture of AAI and AAII. 32P-post-labelling analyses of further biopsy samples of one patient showed the known adduct pattern of AA exposure not only in the kidney, but also in the ureter, whereas in skin and muscle tissue no adduct spots were detectable. In an attempt to explain the higher level of the dA-AAI adduct compared to the dG-AAI adduct level in renal tissue even 44 months after the end of regimen, the persistence of these two purine adducts was investigated in the kidney of rats given a single oral dose of pure AAI. In contrast to the dG-AAI adduct, the dA-AAI adduct exhibited a lifelong persistence in the kidney of rats. Our data demonstrate that AA forms DNA adducts in human tissue by the same activation mechanism(s) reported from animal studies. Thus, the carcinogenic/mutagenic activity of AA observed in animals could also be responsible for the urothelial cancers observed in two of the CHN patients.
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PMID:32P-post-labelling analysis of DNA adducts formed by aristolochic acid in tissues from patients with Chinese herbs nephropathy. 916 97

Vesicoureteric reflux (VUR) is a common childhood condition characterised by regurgitation of urine from the bladder to the kidney. It is the commonest cause of end stage renal failure in children and an important cause in adults. Primary VUR is often familial, suggesting that genetic factors play an important role in its aetiology. Recently, VUR was observed as part of a syndrome, involving optic nerve colobomas and renal anomalies, caused by mutations of the PAX2 gene. PAX2 is a member of the paired box family of genes and is expressed in the ureteric bud and differentiating nephrogenic mesenchyme of the developing kidney. PAX2 has been shown to play a critical role in the development of both the kidney and the ureter. The occurrence of VUR in one family with the PAX2 mutation, and the expression pattern of PAX2 in developing ureteric bud, strongly suggested that PAX2 could be the cause of primary familial VUR. Single strand conformational polymorphism (SSCP) analysis of 23 affected subjects in eight families with primary familial VUR showed no alterations in exons 2-5 of the PAX2 gene. In addition, a polymorphic dinucleotide repeat marker located within the PAX2 gene segregated independently of the disease trait in one large family who primarily had VUR or reflux nephropathy. These results suggest that PAX2 is not a major cause of primary familial reflux.
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PMID:Absence of PAX2 gene mutations in patients with primary familial vesicoureteric reflux. 959 33

Aetiology remains the main unanswered problem in Balkan endemic nephropathy (BEN) despite investigations into the roles of genetic factors, environmental agents and immune mechanisms. Evidence has accumulated that BEN is an environmentally-induced disease. Weathering of low-rank coals near to the villages where BEN is endemic produces water-soluble polycyclic aromatic hydrocarbons and aromatic amines, similar to metabolic products of acetaminophen that cause analgesic nephropathy. Many of these compounds are known to be carcinogenic and could also cause urothelial cancer. Genetic studies have supported genetic predisposition to BEN. The candidate genes have been localized to a region between 3q25 and 3q26, the 3q BEN marker being detected in both BEN patients and in some healthy relatives with initial morphological changes peculiar to BEN. Three bands with increased frequencies of spontaneous and induced aberrations contain oncogenes. The frequent association of BEN and urinary tract tumours (UTT) can be explained by the chromosomal hypothesis of oncogenesis. The results of molecular biological investigations will allow the identification of genetic markers of BEN, permitting early detection of BEN-predisposing mutations and identification of susceptible individuals who may be at risk of exposure to the environmental agents. An increased incidence of tumours of renal pelvis and ureter in patients with BEN and in population from endemic settlements has been observed. Familial clustering of the UTT was also reported. The frequency of urinary bladder tumours in BEN-endemic settlements is also increased compared with the non-endemic villages and cities. The geographic correlation between BEN and UTT supports the speculation that these diseases share a common aetiology.
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PMID:Balkan endemic nephropathy: a need for novel aetiological approaches. 979 28

Therapy for obstructive uropathy is largely determined by whether the obstruction involves one or both kidneys, and by the age of the patient. In the infant and child, obstructive uropathy is almost always due to a congenital malformation of the ureter, bladder, or urethra. Ultrasonographic prenatal diagnosis has permitted early detection and even fetal intervention for posterior urethral valves, although this form of treatment must be considered experimental at present. More important to the affected infant than optimal renal development is the prevention of pulmonary hypoplasia, which is a consequence of fetal oliguria and oligohydramnios. Congenital ureteropelvic junction (UPJ) obstruction is generally unilateral, and although there is controversy regarding the timing of surgical correction, current evidence favors early pyeloplasty. In the adult, obstructive nephropathy is often acquired, with ureteral obstruction usually a consequence of nephrolithiasis. Removal of the stone can be accomplished surgically or by lithotripsy. Bladder outlet obstruction is usually secondary to prostatic hyperplasia, which may progress slowly, allowing a delay in surgical intervention. Neurogenic bladder may require intermittent catheterization or cholinergic therapy; those with hypertonic bladder may benefit from anticholinergics. Regardless of the patient's age, prompt and accurate diagnosis is essential to planning an optimal strategy for the management of obstructive uropathy.
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PMID:Therapeutic approaches in obstructive uropathy. 981 56

When perfusion pressure to the kidney falls, e.g., as a result of dehydration or mechanical hindrance to the renal arterial blood flow, the release of renin, hence angiotensin (Ang), surges. This feedback regulation is geared to preservation of renal hemodynamic environment by raising systemic blood pressure. We are aware that a surge of renin-angiotensin release also occurs when there is a mechanical hindrance to urine outflow. This phenomenon of ureteral pressure-sensitive activation of renin-angiotensin has been heretofore viewed as an error of nature. We have obtained evidence which challenges this traditional view when we examined strains of mutant mice which are completely devoid of either angiotensin type 1 (AT1) receptor gene (Agtr1-) or angiotensin type 2 (AT2) receptor gene (Agtr2-) as a result of genetic manipulation of these animals. These strains of mice display varying degrees of urinary tract obstruction. In Agtr2- mice obstructions develop during early kidney ontogenesis in ureto, and, in Agtr1- mice, during late ontogenesis ex utero. One may recall that, throughout its normal ontogenesis, the kidney is twice at risk for obstruction of urine outflow. Thus, in utero the ureter is transiently obliterated. This transient obliteration is believed to protect the kidney from the high pressure from the cloaca when urine is not yet formed. During this period, the ureter is surrounded by dense layers of undifferentiated mesenchymal cells. Subsequent expansive growth that the ureter must achieve, therefore, in concert with a timely disappearance of the surrounding mesenchymal cells. The study in Agtr2- embryos indicated that Ang, through the Agtr2 receptor, promotes disappearance of these mesenchymal cells, and that inactivation of this receptor results in congenital obstructive nephropathy. Our additional studies in human specimens indeed indicate that many infants with congenital anomalies of the kidney and urinary tract have a significant mutation within the AT2 gene. Once animals are born, the kidney comes to be of primary importance for preservation of body fluid homeostasis, and urinary output increases dramatically. The large volume of urine predisposes the kidney to obstructive nephropathy due to the high resistance offered to the urine by the downstream ureter. Normally, a special device develops within the urinary tract in a timely fashion, which enables the kidney to collect a bulk of urine, and then to expel it downward periodically without imposing positive pressure upon the renal parenchyma. This special device is the renal pelvis. In the studies on Agtr1 null mutant mice, we learned that Ang, through the AT1 receptor, promotes development of the pelvis shortly after birth, so that inactivation of this receptor in Agtr1- mice leads to absence of development of the pelvis, hence to obstructive nephropathy. Collectively, Agtr1 or Agtr2 null mutant mice suffer from urinary tract obstruction. Given that urinary tract obstruction per se is a potent stimulus for Ang generation, Ang is essential for the kidney to escape from obstructive injury.
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PMID:Role of angiotensin in the development of the kidney and urinary tract. 985 80

Cellular and molecular events contributing to tubulointerstitial fibrosis of the kidney during obstructive nephropathy are driven in large part through increased angiotensin II levels in the obstructed kidney. Angiotensin converting enzyme inhibition or AT1 receptor antagonism have been shown to ameliorate the fibrosis of the kidney due to obstruction of the ureter. In this investigation, we determine the effects of the AT2 receptor antagonist PD-123319 on pathophysiological events within the kidneys of rats with unilateral ureteral obstruction. Treatment with PD-123319 was found to exacerbate the increase in interstitial volume and collagen IV matrix score of the ureteral obstructed kidney. Monocyte/macrophage infiltration of the injured kidney was no different between treated and untreated animals. The AT2 receptor antagonist did, however, inhibit apoptosis of tubular cells, alpha-smooth muscle actin expression within the interstitium, and p53 expression in the ureteral obstructed kidney. These results suggest that angiotensin II operating through the AT2 receptor exerts an antifibrotic effect on the kidney during obstructive nephropathy in opposition to the profibrotic effects of angiotensin II operating through the AT1 receptor.
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PMID:Effect of AT2 receptor blockade on the pathogenesis of renal fibrosis. 988 78


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