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PubMed2004

Management of ureteral obstruction.

The most common cause of ureteral obstruction in dogs and cats is ureteral calculi. Common clinical signs associated with ureteral obstruction include abnormalities in urination, persistent urinary tract infection, abdominal pain, vomiting, anorexia, weight loss,and depression or lethargy. Medical management of ureteral obstruction includes fluid diuresis, muscle relaxants, and treatment of azotemia using nephrostomy tubes or hemodialysis. Surgical techniques used to restore patency to the ureter include ureterotomy,partial ureterectomy and ureteroneocystostomy, and ureteral resection and anastomosis. Lithotripsy has been used in dogs to remove ureteral calculi. Renal function can be preserved if complete ureteral obstruction is relieved within several days of onset.

Animals↗
PubMed1990

[Percutaneous dissolution of uric acid and cystine stones causing acute ureteral obstruction].

Four cases with ureteral obstruction due to uric acid or cystine stones were treated successfully by percutaneous irrigation with sodium bicarbonate or tromethamine-E. These cases underwent percutaneous nephrostomy for the reason of prolonged complete obstruction (case 1), sustained pyelonephritis (case 2) or decreased renal function (case 3 and 4). Two catheters were placed through the nephrostomy tract before irrigation, 6 Fr. ureteral catheter just above the ureteral stone and 10 Fr. pigtail or 12 Fr. Malecot catheter in the renal pelvis. The ureteral stones were markedly reduced in size and passed spontaneously after 6-11 days' duration of irrigation in three cases. In case 2, the remaining stone was removed transurethrally after 14 days' duration of irrigation, and was found to be composed of organic matrix. Percutaneous dissolution is considered to be a safe and reliable method and may be an alternative way of treating uric acid or cystine stone causing acute ureteral obstruction.

Acute Disease↗
PubMedDate not supplied

Enalapril accelerates remodeling of the renal interstitium after release of unilateral ureteral obstruction in rats.

Complete ureteral obstruction in rats rapidly leads to renal interstitial expansion and fibrosis and this process is ameliorated by concomitant angiotensin converting enzyme inhibition (ACEI). However, models of intervention initiated after unilateral ureteral obstruction (UUO) release may be more analogous to human obstructive renal disease where treatment could more reasonably follow the discovery of obstructive uropathy as compared to models where treatment is initiated at the time of experimentally induced obstruction. We studied interstitial changes in rats before and after release of UUO and examined the effect of ACEI with 200mg/L of enalapril (E) in the drinking water on these changes. Rats were sacrificed after 10 (n=10) and 20 (n=10) days (D) of UUO or 10D after release of 10D of UUO (n=18). Eleven rats received E for 10D after UUO release. Cortical interstitial volume fraction [Vv(I/C)] measured by point counting was increased at 10D (0.32 +/- 0.05) and 20D (0.41 +/- 0.05) of UUO compared to contralateral and sham-operated kidneys (both 0.05 +/- 0.01, ANOVA, p <0.001). Vv(I/C) 10D after release from 10D of UUO (0.26 +/- 0.04) was lower than that of 10D of UUO (p<0.05) and much lower than those with 20D of UUO (p<0.001). However, rats treated with E from the time of UUO release had lower Vv(I/C) (0.21 +/- 0.07) than UUO released E untreated rats (p<0.05). Release of UUO initiates regression of interstitial expansion in rats. ACEI with enalapril significantly accelerates reversal of interstitial expansion after UUO release. This could have important implications for treatment of obstructive nephropathy in humans.

Analysis of Variance↗
PubMedDate not supplied

[Acute ureteral obstruction (renal colic)].

Acute ureteral obstruction is always associated with high intrapelvic hydrostatic pressure. Objective diagnosis of renal colic can be made by direct measurement of intrapelvic pressure (IPP). We propose a very simple device for estimation of IPP consisting of ureteral catheter and polyethylene tube 150 cm long. The device gives intrapelvic pressure in centimeters of urinary column. The figures obtained corresponded to those in measurement of IPP in cm of water column. In normal 187 examinees IPP ranged from 0.5 to 14.2 cm urinary column. Mean normal IPP in females was higher than in males. In 187 patients with renal colic IPP varied from 55 to 150 cm of urinary column. Mean IPP at the height of renal colic was in females and males 97.4 +/- 3.0 and 89.8 +/- 2.5 cm of urinary column, respectively. Thus, IPP in health and renal colic is higher in females than in males. In bilateral renal colic and colic in solitary kidney catheterization of the ureter is mandatory because of anuria. Ureteral catheterization is also indicated in cases of renal colic combination with attack of acute pyelonephritis. If ureteral catheterization is indicated, IPP pressure should be measured. This is important for diagnosis of both acute ureteral obstruction and pathogenesis of anuria.

Acute Disease↗
PubMed1991

Cellular distribution of H(+)-ATPase following acute unilateral ureteral obstruction in rats.

Unilateral ureteral obstruction for 24 h produces an acidification defect in the rat kidney that closely resembles the human disorder. We examined the role of renal vacuolar H(+)-ATPase distribution and content in the generation of the postobstructive abnormality in distal hydrogen ion secretion. Rats were subjected to unilateral ureteral obstruction for 24 h, and the obstructed and contralateral kidneys were removed at 3 h, 5 days, and 10 days after release of the obstruction. The postobstructed and contralateral kidneys and kidneys from sham-operated rats were analyzed for intercalated cell number and subtype and for the cellular distribution of ATPase staining by means of a monoclonal antibody specific for the 31-kDa subunit of the vacuolar H(+)-ATPase. No change in the number or distribution of subtypes was detected in the cortex nor in the outer or inner stripe of the outer medulla. Immunoreactive H(+)-ATPase increased in both the cortex and medulla at 3 h after obstruction, and thereafter it declined to control values. The major morphological changes in H(+)-ATPase staining detected were an alteration in the intracellular distribution of the enzyme, which we refer to as discontinuity of (or "gaps" in) apical staining, and a decrease in the percent of intercalated cells showing a rim (or plasma membrane) staining pattern in the inner medulla. The changes observed may be a morphological representation of the physiological abnormalities underlying the postobstructive acidification defect.

Animals↗
PubMed2007

COX-2 activity transiently contributes to increased water and NaCl excretion in the polyuric phase after release of ureteral obstruction.

Release of bilateral ureteral obstruction (BUO) is associated with reduced expression of renal aquaporins (AQPs), polyuria, and impairment of urine-concentrating capacity. Recently, we demonstrated that 24 h of BUO is associated with increased cyclooxygenase (COX)-2 expression in the inner medulla (IM) and that selective COX-2 inhibition prevents downregulation of AQP2. In the present study, we tested the hypothesis that COX-2 activity increases in the postobstructive phase and that this increase in COX-2 activity contributes to polyuria and impaired urine-concentrating capacity. We examined the effect of the selective COX-2 inhibitor parecoxib (5 mg.kg(-1).day(-1) via osmotic minipumps) on renal functions and protein abundance of AQP2, AQP3, Na-K-2Cl cotransporter type 2 (NKCC2), and Na-K-ATPase 3 days after release of BUO. At 3 days after release of BUO, rats exhibited polyuria, dehydration and urine and IM tissue osmolality were decreased. There were inverse changes of COX-1 and COX-2 in the IM: COX-2 mRNA, protein, and activity increased, while COX-1 mRNA and protein decreased. Parecoxib reduced urine output 1 day after release of BUO, but sodium excretion and glomerular filtration rate were unchanged. Parecoxib normalized urinary PGE(2) and PGI(2) excretion and attenuated downregulation of AQP2 and AQP3, while phosphorylated AQP2 and NKCC2 remained suppressed. Parecoxib did not improve urine-concentrating capacity in response to 24 h of water deprivation. We conclude that decreased NKCC2 and collapse of the IM osmotic gradient, together with suppressed phosphorylated AQP2, are likely causes for the impaired urine-concentrating capacity and that COX-2 activity is not likely to mediate these changes in the chronic postobstructive phase after ureteral obstruction.

Animals↗
PubMed2006

Case report: bilateral ureteral obstruction secondary to Aspergillus bezoar.

Ureteral obstruction as a result of a primary aspergillus infection is rare. Early clinical suspicion in immunosuppressed patients is essential to diagnosis. We report a case of a 50-year-old diabetic woman presenting with acute renal failure, sepsis, and bilateral ureteral obstruction. Initial management included bilateral percutaneous nephrostomy tubes. Urine culture from both the left and right renal pelvis grew Aspergillus flavus. The left-sided obstruction resolved with antifungal therapy. However, her right ureteral obstruction persisted and was managed with ureteroscopy and removal of the fungal bezoar.

Aspergillosis↗
PubMed1983

The renal response to ureteral obstruction.

The renal pathophysiology during ureteral obstruction was investigated in rat experiments, especially designed to study the role of the tubuloglomerular feedback (TGF) control mechanism. This mechanism, operating by sensing the distal delivery of fluid to the macula densa site, regulates the glomerular capillary pressure (PGC) and the glomerular filtration rate (GFR). Interstitial pressure conditions are known to influence the sensitivity of this control mechanism. Micropuncture experiments were performed to investigate the TGF activity before, during and after release of 2 h unilateral ureteral obstruction (UUO) and after 24 h UUO and bilateral ureteral obstruction (BUO). Renal interstitial hydrostatic and oncotic pressure, proximal stop-flow pressure (PSF) and GFR were also determined. In other experiments, the effects of indomethacin on renal pelvic pressure and PGC, estimated from PSF, were studied during the initial vasodilatory phase of UUO. Cortical and regional medullary blood flow was measured using a combination of labelled microspheres and the 86-Rb extraction method. The present results indicate that the initial vasodilatation, demonstrated by an increased PGC and accompanied by an elevated renal pelvic pressure, was caused by prostaglandin release. These pressures could be reduced by injection of indomethacin. Blood flow measurements revealed that the initial vasodilatation seems to occur both in the cortex and in the medulla, but after a few hours progressive vasoconstriction took place in all regions of the kidney. Two hours of UUO caused increased interstitial hydrostatic and decreased oncotic pressure and the TGF response was abolished. This phenomenon participated in the vasodilatory process at this stage of UUO. After release of 2 h UUO, GFR was reduced, indicating vasoconstriction, probably caused by activation of the highly sensitized TGF control mechanism seen in this situation. At 24 h of UUO there was a normal hydrostatic and high oncotic pressure and high TGF sensitivity. These findings contrast to those at 24 h of BUO, with normal interstitial pressure conditions and a slight decrease in TGF sensitivity. These differences between animals with UUO and BUO might be of importance for the absence of post-obstructive diuresis in UUO and the presence of this phenomenon in BUO animals.

Animals↗
PubMed1993

Electrical properties of the rabbit cortical collecting duct from obstructed and contralateral kidneys after unilateral ureteral obstruction.

Electrophysiological techniques were used to determine the electrical properties of the collecting duct (CD) cell in the isolated cortical collecting duct from obstructed (UUOOK) and contralateral (UUOCK) kidneys in rabbits 24 h after unilateral ureteral obstruction (UUO); results were compared with those from sham-operated kidneys. The lumen-negative transepithelial voltage and the basolateral membrane voltage (VB) were decreased in the UUOOK, and increased in the UUOCK. The transepithelial conductance (GT) was decreased in parallel with an increase in the fractional apical membrane resistance (fRA) and a decrease in apical membrane conductance in the UUOOK. By contrast, the GT was increased in parallel with increases in apical and basolateral membrane conductances in the UUOCK. The amiloride-sensitive changes in apical membrane voltage (VA), GT and fRA were lower in the UUOOK, but greater in the UUOCK. The changes in VA and GT upon raising the perfusate K+ concentration and upon addition of luminal Ba2+ were decreased in the UUOOK, and increased in the UUOCK. Addition of ouabain to the bath resulted in a smaller depolarization of VB in the UUOOK, but in a greater depolarization in the UUOCK. Upon lowering bath Cl-, the change in basolateral membrane electromotive force (delta EMF) was increased in the UUOOK, and decreased in the UUOCK. Reversely, upon raising bath K+, the delta EMF was decreased in the UUOOK, and increased in the UUOCK. We conclude: (a) the conductances of Na+ and K+ in the apical membrane, and active Na(+)-K+ pump activity and relative K+ conductance in the basolateral membrane are decreased in the UUOOK, and increased in the UUOCK; (b) the relative basolateral membrane Cl- conductance was increased in the UUOOK, and decreased in the UUOCK.

Amiloride↗
PubMed2005

Rare cause of ureteral obstruction.

This report presents bilateral ureteral obstruction due to possible ureteritis in a bone marrow transplant patient with resurgence of BK virus after hemorrhagic cystitis. This is believed to be the first description of this type of ureteral obstruction. The presented case includes the management plan.

Adult↗
PubMed2003

Endothelin in unilateral ureteral obstruction: vascular and cellular effects.

PURPOSE: Unilateral ureteral obstruction results in decreased blood flow and tissue loss in the obstructed kidney. This condition is compensated by increased perfusion and trophic changes in the contralateral kidney. Vascular mediators' effects are central to these changes and of these mediators endothelin is the most potent vasoconstrictor known. We explored the role of endothelin and the effects of endothelin receptor blockade in unilateral ureteral obstruction. MATERIALS AND METHODS: Rats were subjected to unilateral ureteral obstruction for 24 hours. Endothelin-1 mRNA expression was determined in kidney extracts from control, obstructed and contralateral (nonobstructed) kidneys. Cortical and medullary blood flow was determined in control and obstructed kidneys, and after endothelin receptor blockade with bosentan. Apoptotic rates were determined in control and obstructed kidneys after treatment with bosentan using the terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end technique. RESULTS After 24 hours of unilateral ureteral obstruction endothelin-1 mRNA expression was increased in the obstructed kidney and decreased in the contralateral kidney. Obstruction was associated with a decrease in renal blood flow, which was reversed by endothelin receptor blockade. Unilateral ureteral obstruction also increased apoptosis, which was blocked by endothelin inhibition. CONCLUSIONS: Endothelin expression increases in the obstructed kidney. Inhibition of its action protects against vascular and cellular changes. Decreased endothelin expression in the contralateral kidney may facilitate trophic changes and compensatory increased blood flow.

Animals↗
PubMed1991

Evidence for two distinct and functionally important sites of enhanced thromboxane production after bilateral ureteral obstruction in the rat.

1. After bilateral ureteral obstruction there is an enhanced production of thromboxane A2 by the kidney which contributes to a decline in renal function. An acute interstitial macrophage infiltrate also occurs. 2. The relative contribution of infiltrating cells and intrinsic renal cells to the enhanced production of thromboxane A2 by the hydronephrotic kidney were determined. The effects of both irradiation and subsequent administration of the thromboxane synthesis inhibitor OKY-046 on both thromboxane B2 excretion and renal function were examined in rats with 24 h bilateral ureteral obstruction. 3. Irradiation effectively prevented the leucocyte infiltrate after bilateral ureteral obstruction (1.2 +/- 0.8 x 10(5) versus 27.1 +/- 0.1 x 10(5) cells/g of cortex, n = 4 in each group), resulted in a significantly higher inulin clearance (2.78 +/- 0.27 versus 1.49 +/- 0.17 ml min-1 kg-1 body weight, n = 7 and n = 8, respectively, P less than 0.001) and reduced thromboxane B2 excretion to 39% of non-irradiated values. Subsequent administration of OKY-046 to previously irradiated animals further reduced thromboxane B2 excretion to 20% of the value in non-irradiated rats with bilateral obstruction and further increased inulin clearance to 3.34 +/- 0.26 ml min-1 kg-1 body weight. 4. Glomerular macrophage numbers were decreased after bilateral ureteral obstruction (in contrast to the interstitium). However, glomeruli isolated from rats with 24 h bilateral ureteral obstruction exhibited enhanced production of thromboxane B2 compared with sham-operated control rats (855.6 +/- 31.1 versus 392.2 +/- 25.5 pg 60 min-1 mg-1 of protein, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Ureteral obstruction of renal transplant due to ureteral candidiasis.

In a diabetic renal transplant recipient a nephrocutaneous fistula developed after percutaneous renal graft biopsy, and ureteral obstruction due to Candida albicans fungus balls was demonstrated. Local irrigation with amphotericin B, systemic antifungal therapy, and rigid blood sugar control led to rapid clearing of the fungal infections. This cause of renal transplant insufficiency should be considered prior to renal biopsy in diabetic patients with yeast forms in the urine.

Adult↗