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At least 19 recordsLinked to original sources
PubMed2006

Initial experience with full-length metal stent to relieve malignant ureteral obstruction.

Ureteral obstruction caused by extrinsic compression by a malignancy generally can be overcome initially with a ureteral stent. However, the long-term failure rate is high, usually necessitating placement of a nephrostomy tube. Herein, we present the initial case, in this country, of intractable ureteral obstruction managed successfully with the newly developed all-metal Resonance stent (Cook Ireland Ltd., Limerick, Ireland) constructed of MP35N alloy, a composite of nonmagnetic nickel-cobalt-chromium-molybdenum. The patient is a 64-year-old woman with metastatic breast cancer causing retroperitoneal fibrosis and ureteral obstruction diagnosed laparoscopically. The obstruction failed to respond to placement of a single 7F double-J stent and then of two 6F double-J stents in the left ureter. As a last resort, in order to avoid nephrostomy-tube placement, the 6F metal stent was placed; this provided unobstructed flow of urine, as documented on a subsequent Whitaker test and, most recently, on a renal scan, 4 months after initial stent placement.

Alloys↗
PubMed2006

Evidence that inhibition of tubular cell apoptosis protects against renal damage and development of fibrosis following ureteric obstruction.

Ureteric obstruction is frequently encountered in primary care urology and can lead to damage to the ipsilateral kidney. Relief of all types of obstruction generally leads to the normalization of any deterioration in renal function noted at diagnosis. However, some evidence from animal models suggests that obstruction can cause progressive deleterious effects on renal function and blood pressure control, especially in the presence of preexisting pathologies such as essential hypertension. The last 10 years have seen a proliferation of studies in rodents wherein complete unilateral ureteric obstruction has been used as a model of renal fibrosis. However, the relevance of the findings to human obstructive uropathy has, in many cases, not been the primary aim. In this review, we outline the major events linking damage to the renal parenchyma and cell death to the evolution of fibrosis following obstruction. Special focus is given to the role of apoptosis as a major cause of cell death during and post-complete ureteric obstruction. Several interventions that reduce tubular apoptosis are discussed in terms of their ability to prevent subsequent progression to end-organ damage and fibrosis.

Animals↗
PubMed1990

Atrial natriuretic peptide-induced changes in renal prostacyclin production in ureteral obstruction.

Ureteral obstruction is characterized by a marked reduction in renal hemodynamic function that is mediated in part by increased production of the vasoconstrictor eicosanoid thromboxane. However, animals with bilateral ureteral obstruction (BUO) sustain less renal functional impairment than unilaterally obstructed (UUO) animals. Recent evidence suggests that atrial natriuretic peptide (ANP) may be important in maintaining these differences. We therefore investigated the possibility that ANP-induced changes in renal arachidonic acid metabolism may be linked to and important in maintaining the differences between BUO and UUO animals. We measured renal function, renal eicosanoid production, and plasma ANP levels in BUO and UUO animals after the release of 24 h of ureteral obstruction. Renal function was reduced in both groups of obstructed animals compared with sham-operated controls. Inulin and p-aminohippurate clearance were significantly increased in BUO compared with UUO animals. Renal 6-ketoprostaglandin F1 alpha production by BUO kidneys was also significantly increased compared with kidneys from the UUO group or the sham-operated controls. In contrast, thromboxane B2 production by BUO kidneys was significantly reduced compared with UUO kidneys and was not significantly different from controls. Plasma ANP levels of BUO animals were significantly greater than those of UUO or sham-operated animals. When ANP was administered to in situ perfused UUO or BUO kidneys, renal vascular resistance fell significantly, and ANP induced a dramatic increase in 6-ketoprostaglandin F1 alpha production without affecting production of thromboxane B2. Indomethacin blunted the reduction in renal vascular resistance to ANP by 35-50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The use of corticosteroids in the management of bilateral malignant ureteric obstruction.

Ureteric obstruction is not an uncommon complication of malignant disease or its treatment. We describe the effectiveness of a corticosteroid in a patient with bilateral ureteric obstruction from metastatic colon cancer causing acute renal failure. We presume that the effectiveness was because of its activity in reducing edema related to the tumor. Other modalities of treatment are discussed but each case requires individualization of treatment with due ethical consideration.

Acute Kidney Injury↗
PubMed1979

Adenocarcinoma of gallbladder producing unilateral ureteral obstruction.

Ureteral obstruction is a common problem facing the urologist. Tumors, either primary in the urinary tract or metastases from other organs, may be the causal agent. Herein we present the first case reported of ureteral obstruction caused by metastases from adenocarcinoma of the gallbladder.

Adenocarcinoma↗
PubMed1985

Hydraulic water permeability and transepithelial voltage in the isolated perfused rabbit cortical collecting tubule following acute unilateral ureteral obstruction.

Ureteral obstruction affects the kidney's ability to conserve water and sodium. Using the isolated perfused tubule technique, we studied cortical collecting tubules (CCT) taken from rabbits subjected to a sham operation or to 4 h of unilateral ureteral obstruction (UUO). Tubules were perfused in the presence of an osmotic gradient directed to promote water movement from lumen to bath, and volume flux (Jv), hydraulic water permeability (Lp), and transepithelial voltage (V1) were determined. In tubules from sham-operated and UUO animals, basal (before exposure to vasopressin) J, and Lp were not different from zero. After addition of 200 microU . ml-1 of arginine vasopressin (aVP) to the bath, Jv and Lp increased to 1.64 +/- 0.23 nl . mm-1 . min-1 and 127.9 +/- 19.8 cm . s-1 . atm-1 x 10(7), respectively, in tubules from sham-operated animals, but not only 0.27 +/- 0.09 nl . mm-1 . min-1 an 18.8 +/- 6.2 cm . s-1 . atm-1 . 10(7) in tubules from UUO animals. Pretreatment with desoxycorticosterone acetate (DOCA) or indomethacin in vivo did not prevent the blunted vasopressin response seen in tubules taken from UUO animals. The Jv and Lp responses to the cyclic AMP (cAMP) analogue, 8-Br-cAMP, were also diminished in tubules taken from UUO animals compared with shams. V1, measured during the basal period, was diminished in tubules from UUO kidneys (-5.0 +/- 2.1 mV) compared with shams (-21.9 +/- 4.1 mV), and pretreatment with DOCA did no prevent the effects of UUO on V1. In contrast, tubules taken from animals that received indomethacin prior to UUO developed voltages not different from voltages in tubules taken from sham-operated animals (-17.3 +/- 1.7 mV). We conclude that, although CCT from UUO animals can maintain osmotic gradients, their ability to respond to vasopressin by increasing Lp is impaired by an intrinsic defect located at a step beyond the generation of cAMP, and that prostaglandin inhibition or DOCA pretreatment do not reverse the decreased responsiveness of Lp to aVP. UUO also diminished V1, and this abnormality was prevented by previous treatment with indomethacin, suggesting that prostaglandins may mediate the effect of UUO on V1.

Adrenal Cortex Hormones↗
PubMed1985

Periappendicular abscess as a cause of ureteral obstruction.

Ureteral obstruction due to appendicitis is a rarity. A twenty-five year old man with no previous abdominal symptoms showed right-sided hydronephrosis and hydroureter on intravenous urography. At operation the cause for this was found to be a ureteral kink due to adhesions caused by a healed periappendicular abscess.

Abscess↗
PubMed1993

The pathophysiology of ureteral obstruction.

Ureteral obstruction can have a variety of causes intrinsic or extrinsic to the kidney. The effects of obstruction are examined from the perspectives of duration, severity, totality, and the presence of complicating factors. There is a difference in the postobstructive pathophysiology depending on whether one or both ureters were obstructed. Atrial natriuretic peptide may be important in postobstructive diuresis, and preliminary evidence suggests a role for it as protection against nephron ischemia in acute obstruction. The potential for recovery of renal function after relief of obstruction depends on the duration and degree of obstruction, the condition of the contralateral kidney, and the presence or absence of infection. Ability to acidify the urine to pH < 6.0 preoperatively may be a good predictor of the recovery potential of an obstructed kidney. Urine concentrations of lysosomal enzymes such as N-acetylglucosaminidase also may be useful for this purpose, as may measurement of creatinine clearance in urine obtained from a nephrostomy tube.

Acute Disease↗
PubMed1979

Abdominal aortic aneurysms and ureteric obstruction.

Ureteric obstruction is rarely encountered in abdominal aortic aneurysms and is due to perianeurysmal fibrosis. 3 cases are described in which aortic aneurysm and retroperitoneal fibrosis are found. Excision of the aneurysm and ureterolysis with intraperitonization of the ureter is the most appropriate surgical procedure but treatment must be individualized according to the patient's condition and the operative discoveries.

Aged↗
PubMed1998

Zinc deficiency aggravates tubulointerstitial nephropathy caused by ureteral obstruction.

Ureteral ligation causes tubulointerstitial nephropathy characterized by the tubular dilatation, the interstitial expansion, and a leukocyte infiltration into the tubulointerstitium. The present study was designed to explore whether zinc (Zn) deficiency affects the development of unilateral ureteral obstruction (UUO)-induced tubulointerstitial nephropathy. Compared to rats fed a standard diet, rats fed a Zn-deficient diet exhibited a greater influx of leukocytes into the tubulointerstitium of the cortex of the obstructed kidney 3 d following UUO. Furthermore, rats fed a Zn-deficient diet showed a slight invasion of leukocytes into the tubulointerstitium of the cortex of the contralateral nonobstructed kidney (CLK), although there was no infiltration of leukocytes into the CLK of rats fed a standard diet. These histological changes, however, were ameliorated by administration of enalapril, an angiotensin (ANG) I-converting enzyme inhibitor. Thus, it is suggested that Zn deficiency aggravates UUO-induced tubulointerstitial nephropathy via an increase in the action of ANG II.

Animals↗
PubMed1991

Ureteral obstruction and ureteral fistulas after aortofemoral or aortoiliac bypass surgery.

Ureteral injury after aortofemoral or aortoiliac bypass surgery has seldom been described in the literature considering the large number of bypass operations performed. Some causative factors, such as the position of the bypass, are obvious while others are less clear. However, no attempt has been made to unify criteria to establish a management protocol. Of 154 cases of ureteral units with ectasia reviewed ureteral fistulas were present in 19. Radiological ureteral obstruction appears to precede fistula formation. Symptoms, time of diagnosis and treatment according to the predominant etiology have been discussed. Etiological (in varying degrees of importance), clinical and diagnostic criteria, together with a management and therapeutic protocol in which early and late lesions are clearly differentiated were established, while bearing in mind that not all radiological obstruction patterns correspond to true ureteral lesions.

Aorta, Abdominal↗
PubMed1982

Transient ureteral obstruction after ureteral stenting.

Transient distal ureteral edema and obstruction have been recognized complications of retrograde ureteral catheterization for years. Similar changes in the proximal ureter may be induced by antegrade (percutaneous) ureteral intubation and are being more widely recognized as radiologists become more involved in upper urinary tract percutaneous manipulative procedures. Marked mucosal edema of the ureter was observed in four patients who had percutaneously placed, in-dwelling stent catheters. This was severe enough to produce transient ureteral obstruction after stent removal in two. Some degree of mucosal edema may be seen in most patients with in-dwelling stents. These ureteral changes may be secondary to the pressure effect of large diameter catheters on the proximal and midureter. Temporary proximal urinary diversion should be maintained until the edematous changes improve or subside, usually within 5-8 days.

Adult↗
PubMed2004

Suppression of 15-hydroxyprostaglandin dehydrogenase messenger RNA concentration, protein expression, and enzymatic activity during human ureteral obstruction.

Prostanoids produce significant effects in the ureter, particularly in response to obstruction. Ureteral obstruction is associated with increased prostanoid synthesis via cyclooxygenase induction; however, prostaglandin degradation mediated by 15-hydroxyprostaglandin dehydrogenase (PGDH) has not been evaluated in the ureter. The purpose of this study was to determine whether PGDH steady-state mRNA, protein, and enzyme activity are altered in the human ureter during obstruction. Human ureteral segments from patients undergoing donor nephrectomy (normal segments) or ureteral stricture repair (obstructed segments) were obtained with proper informed consent. We evaluated PGDH steady-state mRNA relative to ribosomal protein S26 reference gene by reverse transcription-polymerase chain reaction and Vistra Green fluoroimaging. We determined PGDH protein content relative to glyceraldehyde-3-phosphate dehydrogenase by immunoblotting and PGDH localization by immunohistochemistry. PGDH enzymatic activity was determined by measurement of conversion of 15-hydroxy- to 15-keto-prostaglandin using thin layer chromatography separation. We found that PGDH mRNA and protein were decreased 4- to 6-fold, and enzyme activity was decreased >3-fold in obstructed human ureter relative to normal controls. PGDH was localized to the urothelial cells, with little or no expression in smooth muscle. Our results indicate that PGDH mRNA, protein, and enzyme activity are suppressed in the human ureter during obstruction. Increased concentrations of prostanoids subsequent to ureteral obstruction seem to be due to decreased degradation as well as increased synthesis. Modulation of prostanoid degradation may have therapeutic relevance in obstructive disorders of the ureter.

Gene Expression Regulation, Enzymologic↗
PubMed1982

The ureteral "J" sign: radiographic demonstration of iatrogenic distal ureteral obstruction after ureteral reimplantation.

Progressive caliceal and ureteral dilatation in postoperative patients is assumed to be secondary to either postoperative distal ureteral stricture or ureteral atony. Any study used to differentiate obstruction from atony must be done with an awareness of the effect of a full bladder on the upper tracts, since it can by itself produce varying degrees of ureteral dilatation. We describe 2 patients who had virtually complete distal ureteral obstruction on anterograde pyelography with a "J" shaped distal ureteral segment. The striking observation was that the deformity and associated distal ureteral obstruction could be made to appear and disappear at will, merely by distending or emptying the bladder. We believe that this is an important factor in the progressive dilatation, as well as in the observed deterioration of renal function, and it is properly regarded as an iatrogenic complication.

Child↗
PubMed2005

Elevated plasma concentrations of transforming growth factor-beta 1 in patients with unilateral ureteral obstruction.

We measured plasma concentrations of TGF-beta 1 in patients with obstructive ureteral calculi and compared them with the plasma concentrations of healthy volunteers. The present study was a prospective study containing a homogenous group of patients with unilateral ureteral obstruction (UUO). The study consisted of patients with ureteral stones less than 7 mm in diameter that caused mild to moderate obstruction. All patients were referred by the emergency department of our hospital and examined between April 2003 and April 2004. The presence and characteristics of both stone and obstruction were determined by plain abdominal x-ray and gray-scale ultrasonography (US). Blood samples were collected from both patients and control individuals on admission and 1 week after conservative follow-up. The plasma TGF-beta 1 concentration was determined using a quantitative sandwich enzyme immunoassay specific for TGF-beta 1. There were 35 patients with 20 women and 15 men (average age 26.8+/-5.9 years), and 15 volunteers in the control group, with nine women and six men (average age 24.2+/-4.5 years). Average stone size was 5.6 mm+/-1.2 mm (range 3.5-7) for the patient group. US showed the presence of mild hydronephrosis in 24 and moderate hydronephrosis in 11 patients. Plasma concentrations of TGF-beta 1 in patients with ureteral obstruction (1,117+/-5.8 ng/ml, range 36-2,442 ng/ml) were significantly higher than those in the healthy control group (32+/-4 ng/ml) on admission (P<0.001). There was a significant increase in TGF-beta 1 plasma concentrations in the patient group (33,525+/-6.8 ng/ml, range 1,107-73,288 ng/ml) after 1 week follow-up (P<0.001). Ureteral obstruction increases plasma TGF-beta 1 concentrations in patients with ureteral stones as in UUO models in animal studies. A concomitant treatment with an anti-fibrotic agent may reduce the incidence of renal injury during obstruction.

Adult↗