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Query: UMLS:C0403608 (ureter)
9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injury to the renal microvasculature may be a major factor contributing to the progression of renal disease. Although severe disruption of peritubular capillaries (PTC) could lead to marked tubulointerstitial scarring, elucidation of that process remains incomplete. This study investigated the morphologic changes in PTC and their likely regulation by vascular endothelial growth factor (VEGF) during the progression of tubulointerstitial injuries. Unilateral ureteral obstruction was induced in Wistar rats by ligation of the left ureter, and the kidneys were then collected at selected times. PTC lumina and the expression of VEGF and its receptor Flk-1 were immunohistochemically detected. Morphologic changes in PTC endothelial cells were examined by using Ki67 staining, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling, and electron-microscopic studies. In the first week of the disease period, immunohistochemical labeling of tubular VEGF intensified, with accompanying deformation and dilation of adjacent thrombomodulin (TM)-positive PTC lumina; an angiogenic response of endothelial cells was demonstrated with Ki67 and TM double-staining. During the subsequent 2 wk, tubular VEGF labeling decreased until it was virtually absent, an effect confirmed by Western blotting. Concomitantly, labeling of the VEGF receptor Flk-1 in PTC endothelial cells decreased and PTC lumina began to regress, demonstrating endothelial cell apoptosis (as detected in terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling and electron-microscopic studies). By the end of week 4, the numbers of TM-positive PTC lumina were significantly decreased in areas of marked tubulointerstitial scarring. These results suggest that PTC regression, involving an early, unsustained, angiogenic response followed by progressive endothelial cell apoptosis, could be a potential factor contributing to tubulointerstitial scarring in this unilateral ureteral obstruction model.
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PMID:Peritubular capillary regression during the progression of experimental obstructive nephropathy. 1208 75

Children who develop end-stage renal disease (ESRD) as a result of obstructive uropathies require evaluation and treatment of associated bladder dysfunction to ensure a good outcome following renal transplantation. Bladder dynamics can often be optimized medically, although surgical intervention is occasionally necessary. For those patients who require bladder augmentation, the use of a dilated native ureter (ureterocystoplasty) is preferred to the more commonly used intestine or stomach (enterocystoplasty), which carry a higher risk of complications. Unfortunately, most patients do not have a suitable anatomy for ureterocystoplasty and, by necessity, intestine or stomach has to be utilized. Herein, we describe the successful application of ureterocystoplasty in the presence of ESRD and a solitary kidney prior to renal transplantation. We believe that owing to the many advantages of native urothelium, every effort should be made to use ureter and avoid the use of intestine.
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PMID:Ureterocystoplasty (bladder augmentation) with a solitary kidney. 1210 May 10

The diminishing risk of acute renal scarring with urine infections (reflux nephropathy) after infancy is unexplained, but might reflect kidney maturation. The mechanisms of reflux nephropathy scarring are best explained by a piglet model in which vesicoureteric reflux allows infected urine to enter those segments of renal parenchyme that are drained by compound papillae. We carried out a similar study in adult pigs to determine whether protective maturation occurs. Adult pigs were exposed to urine infection after surgery to produce unilateral vesicoureteric reflux. The intravesical portion of one ureter was deroofed in six female adult Gottingen mini-pigs and the bladder and the ureteric mucosae stitched around the perimeter of the new orifice. One week later Escherichia coli was injected into the urinary bladder to produce cystitis. Three weeks later the animals were killed humanely and the urinary tracts were examined. The animals sustained persistent urine infections; the untreated ureters and kidneys remained normal. However, on the operated side, the ureters were thickened and dilated, vesicoureteric reflux was shown in four cases, and the kidneys had one or more flattened area overlying a renal segment, which showed severe inflammatory changes and early scar formation. The risk of reflux nephropathy scarring is not eliminated by maturation of the kidney in pigs. It is unlikely that the much-reduced risk of initiating scarring that is seen in older children with urine infections is due to a protective maturation of the human kidney. A possible explanation is that most children born with risk factors for developing scarring will have already sustained scars when very young.
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PMID:Renal scarring caused by vesicoureteric reflux and urinary infection: a study in pigs. 1217 58

Congenital and acquired renal diseases that can produce renal insufficiency during the neonatal period may be classified according to their ultrasonographic (US) characteristics: increased parenchymal echogenicity (renal parenchymal diseases, angiotensin-converting enzyme inhibitor fetopathy, cortical necrosis), cystic disease (glomerulocystic kidney disease, autosomal recessive polycystic renal disease, multicystic dysplastic kidney, cystic renal dysplasia), obstructive uropathies (ureteropelvic junction obstruction, posterior urethral valves), infections (candidal infections and bezoars), and renal agenesis. High-resolution sector and linear-array transducers allow characterization of the underlying pathologic conditions in many cases. Findings of renal parenchymal disease will vary at Doppler US and, during the acute phase, diastolic flow can be decreased, absent, or reversed. In patients with glomerulocystic kidney disease, US shows bilaterally enlarged kidneys with diffusely increased echogenicity and retention of a reniform contour, loss of corticomedullary differentiation, and cortical cysts. Obstruction of the ureteropelvic junction, the most common cause of hydronephrosis in neonates, can be seen at US as a dilated renal pelvis with dilated and communicating calices, lack of dilatation in the distal portion of the ureter, changes of renal dysplasia with increased echogenicity of the renal parenchyma, and parenchymal cysts, depending on the severity and duration of the obstruction. High-resolution US provides improved characterization of the renal parenchyma and more precise description of renal architecture.
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PMID:US of renal insufficiency in neonates. 1243 13

Unilateral ureteral obstruction (UUO) is a well-established model for the study of interstitial fibrosis in the kidney. It has been shown that the renin-angiotensin system plays a central role in the progression of interstitial fibrosis. Recent studies indicate that endothelin, a powerful vasoconstrictive peptide, may play an important role in some types of renal disease. To investigate the effects of angiotensin II on endothelin and its receptors in the kidney, mice were subjected to UUO and treated with or without enalapril, an orally active angiotensin-converting enzyme inhibitor, in their drinking water (100 mg/l). The animals were killed 5 days later. Using RT coupled with PCR, we measured the levels of endothelin-1, endothelin A, and endothelin B (ET(B)) along with transforming growth factor-beta, TNF-alpha, and collagen type IV mRNA expression in the kidney with UUO and the contralateral kidney along with interstitial expansion in the kidney cortex by a standard point counting method. We found that enalapril administration ameliorated the increased expression of ET-1 mRNA in the obstructed kidney by 44% (P < 0.02). Although the level of endothelin A mRNA expression was significantly increased in the obstructed kidney, it was not affected by enalapril. We found that enalapril treatment increased ET(B) mRNA expression by 115% (P < 0.05) and protein expression (measured by Western blot) in the kidney with an obstructed ureter. Enalapril treatment alone inhibited the expansion of interstitial volume due to UUO by 52%. Cotreatment with enalapril and the ET(B) receptor antagonist BQ-788 inhibited the expression of interstitial volume by only 19%. This study confirms that enalapril inhibits the interstitial fibrosis in UUO kidneys. It also suggests a beneficial and unforeseen effect of enalapril on the obstructed kidney by potentially stimulating the production of nitric oxide through an increased expression of the ET(B) receptor.
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PMID:ACE inhibition increases expression of the ETB receptor in kidneys of mice with unilateral obstruction. 1247 37

Henoch-Schonlein purpura (HSP) is a systemic vasculitic disorder involving both arterioles and capillaries. Although mainly a disease of early childhood, it can occur at any age. HSP is typically recognized as a syndrome with four major components: rash, joint manifestations, abdominal symptoms and renal disease. It is usually a mild condition with a tendency to relapses and generally has a good prognosis. Occasionally, however, it takes on an aggressive course. Gastrointestinal involvement is potentially the most serious complication of HSP. It may mimic an abdominal emergency and in its severest form result in small bowel infarction and/or perforation. Renal manifestations range from asymptomatic haematuria and/or proteinuria through a nephrotic syndrome to progressive glomerulonephritis leading to end stage renal failure. Apart from the major components outlined above, HSP may affect almost every other bodily organ. Vasculitis involving the myocard, lungs (pulmonary haemorrhage), ureter (stenosing ureteritis) and nervous system have been reported. We describe a case of HSP in a 50 year old woman which was complicated by the development of necrotizing crescentic glomerulonephritis and a left hemiparesis due to cerebral vasculitis. Interestingly, this patient had first appeared at the age of 9 years with a nephrotic syndrome and had been diagnosed by renal biopsy at the age of 31 as IgA nephropathy (IgAN). On her current admission, steroid and immunosuppressive therapy resulted in an improvement of renal function and an almost complete disappearance of her neurologic deficit.
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PMID:[Crescentic glomerulonephritis and cerebral vasculitis in the course of Henoch-Schonlein purpura]. 1247 29

Although ultrasonography is regarded as the gold standard in the diagnosis of obstructive nephropathy, dilatation is sometimes not observed by ultrasonography. We report upon a case of minimally dilated obstructive nephropathy due to an ureter stone in a kidney donor with volume depletion. A 54-year-old man was admitted due to anuria and abdominal pain of 2 days duration. Ten years previously, his right kidney was donated for transplantation, and one month before admission, he abstained from all food except water and salt, for 30 days for religious reasons. He had lost 8 kg of body weight. On admission, he had clinical signs of volume depletion, i.e., a dehydrated tongue and decreased skin turgor. Laboratory data confirmed severe renal failure, his blood urea nitrogen level was 107.3 mg/dL, and his serum creatinine 16.5 mg/dL. The plain X-ray was unremarkable and ultrasonography showed only minimal dilatation of the renal collecting system. On follow-up ultrasonography, performed on the 5th hospital day, the dilatation of the collecting system had slightly progressed and a small stone was found at ureter orifice by cystoscopy. Removal of stone initiated dramatic diuresis with a rapid return of renal function to normal by the third day.
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PMID:Minimally dilated obstructive nephropathy initially suspected as pre-renal azotemia in a kidney donor with volume depletion. 1471 34

Congenital obstructive nephropathy is the principal cause of renal failure in infants and children. The underlying molecular and cellular mechanisms of this disease, however, remain largely undetermined. We generated a mouse model of congenital obstructive nephropathy that resembles ureteropelvic junction obstruction in humans. In these mice, calcineurin function is removed by the selective deletion of Cnb1 in the mesenchyme of the developing urinary tract using the Cre/lox system. This deletion results in reduced proliferation in the smooth muscle cells and other mesenchymal cells in the developing urinary tract. Compromised cell proliferation causes abnormal development of the renal pelvis and ureter, leading to defective pyeloureteral peristalsis, progressive renal obstruction, and, eventually, fatal renal failure. Our study demonstrates that calcineurin is an essential signaling molecule in urinary tract development and is required for normal proliferation of the urinary tract mesenchymal cells in a cell-autonomous manner. These studies also emphasize the importance of functional obstruction, resulting from developmental abnormality, in causing congenital obstructive nephropathy.
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PMID:Calcineurin is required in urinary tract mesenchyme for the development of the pyeloureteral peristaltic machinery. 1505

A 54-year old man received a cadaveric renal allograf for end-stage renal disease due to membranous nephropathy. The patient developed scrotal oedema, 14 days after renal transplantation. The biochemical analysis of scrotal fluid after surgical drainage demostrated urine. Helical computed tomography was performed and it showed contrast leaks in medial, distal ureter and bladder. The urinary fistula was treated with surgical repairment and catheter endoluminal of ureter which was retired in four weeks. The incidence of urinary fistula ranged from 3 to 9%. The scrotal or perineal oedema is unusual clinical presentation of urinary leaks. The diagnosis of urinary fistula may be difficult and depends on a high degree of clinical suspicion. The helical computed tomography is a technique which allows a high resolution three-dimensional reconstruction and it can be used to make the diagnosis of urinary fistula.
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PMID:[Scrotal oedema in a kidney graft recipient]. 1521 95

Late renal graft failure is in most cases due to a chronic allograft nephropathy. In this report, we present a case in which a surgical complication led to ureteral stenosis more than 10 years after transplantation. The patient developed slowly deteriorating renal function and ultimately progressive hydronephrosis. At surgical exploration, the ureter was found to perforate the wall of the small bowel before entering the bladder. We successfully performed ureter reimplantation to restore the outflow of the kidney.
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PMID:Rare cause of ureteral stenosis more than 10 years after kidney transplantation. 1583 43


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