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PubMed1995

Ureteral obstruction due to calculi in the early postoperative period in renal cadaveric transplantation: a case report and discussion of ureteral obstruction in the renal transplant patient.

We report a case of obstruction secondary to multiple ureteral calculi on postoperative day 3 after cadaveric renal transplantation. Treatment consisted of ureterolithotomy with stenting of the ureteroneocystotomy and convalescence was otherwise unremarkable. Obstructive complications of the ureter after renal transplantation are reviewed.

Adult↗
PubMed2005

An unusual cause of ureteral obstruction in a renal transplant recipient: ureteric aspergilloma.

Mycotic infections in various organ transplant recipients represent severe and often fatal complications. Aspergillosis isolated from the urinary tract occurs quite infrequently in renal transplant recipients. Besides, fungus balls are rare causes of ureteral obstruction. We report a 51-year-old patient with the diagnosis of ureteral obstruction caused by aspergillosis in the early post-renal transplant period, who unfortunately died with the clinical picture of disseminated infection and its complications.

Aspergillosis↗
PubMed1985

Danazol in the management of ureteral obstruction secondary to endometriosis.

Ureteral obstruction caused by endometriosis is uncommon. It is, however, an important complication that imposes a 25% chance for permanent loss of renal function on the affected side. The standard management is surgical; however, three cases have been reported in which regression of obstruction followed medical therapy. This case report concerns a patient with long-standing partial ureteric obstruction due to endometriosis who was treated for 2 months with danazol. Clinical response of the endometriosis was excellent, but the obstruction persisted, a retroperitoneal ureteroneocystotomy was therefore performed. The ureter was found to be obstructed by dense fibrous tissue that contained endometrial glands. It seems therefore that a trial of danazol may be attempted in selected cases, but that the drug is unlikely to relieve endometriotic ureteric obstruction once dense fibrosis has occurred.

Adult↗
PubMed1997

Epidermal growth factor suppresses renal tubular apoptosis following ureteral obstruction.

OBJECTIVES: Acute unilateral ureteral obstruction (UUO) results in ipsilateral hydronephrosis characterized by a decrease in epidermal growth factor (EGF) mRNA expression and EGF protein levels in the distal renal tubules. UUO results in programmed cell death with increases in the characteristic markers of apoptosis. To suppress the apoptotic response during UUO, recombinant EGF was administered during renal obstruction and the ensuing molecular and histologic changes were studied. METHODS: Mature Sprague-Dawley rats underwent left ureteral obstruction and the kidneys were harvested at 24, 48, and 72 hours. Markers of apoptosis included DNA laddering pattern on agarose gel electrophoresis, in situ gap labeling of fragmented DNA for quantitative apoptotic body determination, polyadenylated mRNA expression of SGP-2, and in situ hybridization for sulfated glycoprotein-2 (SGP-2) mRNA. Studies were repeated in rats following administration of 10, 20, and 40 micrograms of subcutaneous recombinant EGF on a daily basis after UUO. RESULTS: Subcutaneous injection of EGF into unilaterally obstructed rats promotes renal tubular epithelial cell regeneration, as demonstrated by increased cortical mitotic activity. Systemic EGF supplementation in these unilaterally obstructed rats also resulted in a decrease in the intensity of the DNA laddering pattern associated with renal tubular apoptosis. An in situ labeling procedure to identify apoptotic nuclei in the ureterally obstructed kidneys revealed a 50% reduction in apoptosis after EGF administration. Northern blot analysis and in situ hybridization for SGP-2 mRNA or clustering gene product also revealed a decreased expression in the obstructed and EGF-treated renal parenchyma. CONCLUSIONS: These data suggest that EGF, apart from its known role as a mitogenic substance for renal tubular epithelial cells, is also a critical in vivo renal cell survival factor for the developmentally mature kidney.

Animals↗
PubMed1997

Renal accumulation and distribution of hyaluronan after ureteral obstruction.

In a unilateral ureteral obstruction model, a progressive accumulation of hyaluronan (HA) was observed in the renal papilla during the first 11 days of obstruction, after which the amount of HA decreased until the last day of observation, i.e. day 22. The initial accumulation of HA in the obstructed kidney probably reflects the attempts of the kidney to maintain osmotic balance. Consequently, when filtration ceases, HA synthesis decreases and the concentration of HA falls. In the papilla of the contralateral kidney, that had not been exposed to any mechanical damage, the HA content was found to vary in a similar way to that in the obstructed kidney. The explanation for this could be that the mesenchymal cells within the papilla increase their production of HA in order to meet the requirements of increased function necessary to also shoulder the function of the damaged kidney. In short similar variations in the HA content of the renal papilla was observed in both healthy and obstructed kidneys in a unilateral ureteral obstruction model.

Animals↗
PubMed2000

Role of leukocyte adhesion molecules in monocyte/ macrophage infiltration in weanling rats with unilateral ureteral obstruction.

BACKGROUND: Unilateral ureteral obstruction (UUO) of rats is a well-established model for studying obstructive nephropathy. Meanwhile, pathophysiology of pediatric obstructive nephropathy is not well understood. In this report, we studied monocyte/macrophage infiltration and expression of intercellular adhesion molecule 1 (ICAM-1) and macrophage antigen 1 (Mac-1) in weanling rats with UUO. METHODS: Three-week-old male Sprague-Dawley rats underwent left unilateral ureteral ligation. Both obstructed kidneys (OBK) and contralateral kidneys (CLK) were harvested at 3, 6, 12, 24, 72 and 120 h after surgery. Monocyte/macrophage infiltration and expression of ICAM-1 and Mac-1 were evaluated immunohistochemically, and results were compared with those of sham-operated control rats (SOK). RESULTS: Monocyte/macrophage infiltration was observed in the interstitium and perivascular region in the cortex of OBK within 6 h. The CLK and SOK showed slight monocyte/macrophage infiltration. Expression of ICAM-1 was markedly observed in the periarterial and peritubular interstitium and in renal cortical peritubular capillaries 12 h after obstruction. In CLK and SOK, ICAM-1 was slightly expressed in the endothelium of microvessels and parietal linings of Bowman's capsule. Expression of Mac-1 was detected mainly in cells infiltrating the perivascular interstitium in OBK. In CLK and SOK, few Mac-1-positive cells were observed. CONCLUSIONS: Adhesion molecules, ICAM-1 and Mac-1, are expected to recruit monocyte/macrophage infiltration into OBK of weanling rats with UUO.

Animals↗
PubMedDate not supplied

Interference of enalaprilat on glomerular permeability to macromolecules (IgG) in acute unilateral ureteral obstruction in rats.

INTRODUCTION: Unilateral ureteral obstruction breaks out events that cause the transitory increase of glomerular permeability to macromolecules, both in the obstructed kidney and in the contralateral kidney, suggesting the presence of some factor, with a systemic action, liberated as a response to the obstruction. We know that the rennin-angiotensin system is activated by acute ureteral obstruction. We have developed an experiment to assess the role of angiotensin II on the glomerular permeability to IgG due to acute ureteral obstruction, using enalaprilat, an angiotensin enzyme conversion inhibitor, to block the effects of the activation of the rennin-angiotensin system. MATERIALS AND METHODS: We have used 45 adult Wistar female rats, distributed into 3 main groups: a control group with 5 animals and 2 experiment groups each one with 10 animals submitted to unilateral ureteral obstruction and nephrectomy at 60 and 120 minutes. Each experiment group had its simulation correspondent (sham). We have studied both kidneys through the direct immunofluorescence method. RESULTS: We have found positive permeation in animals without enalaprilat in both kidneys and negative permeation in those in which the drug was used. CONCLUSION: We have concluded that enalaprilat interferes in this alteration of permeability, suggesting that angiotensin II is involved in the loss of selectivity of the glomerular membrane.

Acute Disease↗
PubMed2006

Effect of combination therapy with enalapril and the TGF-beta antagonist 1D11 in unilateral ureteral obstruction.

In unilateral ureteral obstruction (UUO), the kidney is characterized by increased fibrosis and apoptosis. Both transforming growth factor-beta (TGF-beta) and ANG II have been implicated, and ANG II may mediate its effects through TGF-beta. Previous studies demonstrated amelioration of renal damage when either TGF-beta or ANG II has been individually targeted. In this study, we sought to determine whether combining 1D11 (monoclonal antibody to TGF-beta) and an ACE inhibitor, enalapril, would be more effective in UUO than either individual treatment, as has been shown in diabetic and glomerulonephritic models. Rats underwent UUO and were given either control monoclonal antibody, 1D11 or enalapril, or 1D11/enalapril combination, for 14 days. Kidneys were harvested and examined for fibrosis [trichrome; collagen (real-time PCR, Sircol assay) and fibroblast-specific protein expression (immunohistochemistry), apoptosis (TUNEL), macrophage infiltration (immunohistochemistry), and TGF-beta expression (real-time PCR and tubular localization with immunohistochemistry)]. UUO was found to induce fibrosis, apoptosis, macrophage infiltration, and TGF-beta expression in the obstructed kidney. Administration of either 1D11 or enalapril individually significantly decreased all these changes; when 1D11 and enalapril were combined, there was little additive effect, and the combination did not provide full protection against damage. The results demonstrate that, for the most part, combination therapy is not additive in UUO. This could be due to the continued presence of a physical obstruction or to biochemical differences between UUO and other renal disease models. Furthermore, it suggests that other targets may be amenable to pharmacological manipulation in UUO.

Animals↗
PubMed1997

Regulation of angiotensin II AT1 and AT2 receptors in neonatal ureteral obstruction.

Chronic unilateral ureteral obstruction (UUO) in early development activates the intrarenal renin-angiotensin system and leads to profound renal vasoconstriction, renal growth arrest, and interstitial fibrosis. To investigate the response of the AT1 and AT2 subtypes of the angiotensin II (ANG II) receptors to UUO, Sprague-Dawley rats underwent UUO or control sham operation in the first 48 h of life and were studied 1-28 days later. Renal mRNA for renin, AT1 and AT2 receptor, and receptor binding and distribution were determined. In contrast to controls, renin mRNA increased from 14 to 28 days in the obstructed kidney. After ipsilateral UUO, AT1 mRNA was suppressed at 1 day, but had increased compared with controls at 28 days. AT2 receptor mRNA fell rapidly in all kidneys from 1 to 3 days of age, after which it remained undetectable. Compared with the intact opposite kidney, AT2 mRNA was suppressed in the obstructed kidney 1 day after UUO. Compared with controls, AT1 and AT2 receptor binding was decreased by ipsilateral UUO at 1 day, whereas AT1 binding was increased at 28 days. Renal ANG II content was increased in the obstructed compared with the intact opposite kidney 28 days after UUO. In view of the increase in renal renin and angiotensin II production resulting from UUO, increased renal AT1 mRNA and receptor binding are likely to contribute to the vasoconstriction and interstitial fibrosis of the neonatal kidney after prolonged UUO.

Angiotensin II↗
PubMed1991

Renal nerves modulate renin gene expression in the developing rat kidney with ureteral obstruction.

Chronic unilateral ureteral obstruction (UUO) in newborn rats activates renin gene expression in the obstructed kidney, and increases renin distribution along afferent glomerular arterioles in both kidneys. To investigate the role of the renal nerves in this response, 2-d-old Sprague-Dawley rats were subjected to UUO or sham operation. Chemical sympathectomy was performed by injection of guanethidine, whereas, control groups received saline vehicle. At 4-5 wk, renal renin distribution was determined by immunocytochemistry, and renin mRNA levels were determined by Northern blot hybridization. Compared to the saline-treated rats with UUO, renin remained localized to the juxtaglomerular region in both kidneys of rats with UUO receiving guanethidine (P less than 0.05). Moreover, renin mRNA levels were eightfold lower in obstructed kidneys of rats receiving guanethidine than in those receiving saline. Additional groups of rats with UUO were subjected to unilateral mechanical renal denervation: renin gene expression in the obstructed kidney was suppressed by ipsilateral but not by contralateral renal denervation. These findings indicate that either chemical or mechanical denervation suppressed the increase in renin gene expression of the neonatal kidney with ipsilateral UUO. We conclude that the renal sympathetic nerves modulate renin gene expression in the developing kidney with chronic UUO.

Animals↗
PubMed2000

Antibody to transforming growth factor-beta ameliorates tubular apoptosis in unilateral ureteral obstruction.

BACKGROUND: Unilateral ureteral obstruction (UUO) is characterized by progressive renal atrophy, renal interstitial fibrosis, an increase in renal transforming growth factor-beta (TGF-beta), and renal tubular apoptosis. The present study was undertaken to determine the effect of a monoclonal antibody to TGF-beta (1D11) in UUO. METHODS: Mechanical stretch was applied to tubular epithelial cells (NRK-52E) by a computer-assisted system. Three doses of 1D11 (either 0.5, 2, or 4 mg/rat) were administered to rats one day prior to UUO and every two days thereafter, and kidneys were harvested at day 13. Fibrosis was assessed by measuring tissue hydroxyproline and mRNA for collagen and fibronectin. Apoptosis was assessed with the terminal deoxy transferase uridine triphosphate nick end-labeling assay. TGF-beta levels were determined by bioassay. Western blot and immunostaining were used to identify proliferating cell nuclear antigen (PCNA), p53, bcl-2, and inducible nitric oxide synthase (iNOS). RESULTS: Stretch significantly induced apoptosis in NRK-52E cells, which was accompanied by an increased release of TGF-beta; 1D11 (10 microg/mL) totally inhibited stretch-induced apoptosis. Control obstructed kidney contained 20-fold higher TGF-beta as compared with its unobstructed kidney; 1D11 neutralized tissue TGF-beta of the obstructed kidney. Control obstructed kidney exhibited significantly more fibrosis and tubular apoptosis than its unobstructed counterpart, which was blunted by 1D11. In contrast, 1D11 significantly increased tubular proliferation. p53 immunostaining was localized to renal tubular nuclei of control obstructed kidney and was diminished by 1D11. In contrast, bcl-2 was up-regulated in the 1D11-treated obstructed kidney. Total NOS activity and iNOS activity of the obstructed kidney were increased by 1D11 treatment. CONCLUSION: The present study strongly suggests that an antibody to TGF-beta is a promising agent to prevent renal tubular fibrosis and apoptosis in UUO.

Animals↗
PubMed2001

Regional expression of inducible nitric oxide synthase in the kidney in dogs with unilateral ureteral obstruction.

PURPOSE: In the early stage of unilateral ureteral obstruction total renal blood flow increases but medullary blood flow decreases, exacerbating medullary tissue hypoxia. We examined the expression of inducible nitric oxide synthase, a product of a hypoxia sensitive gene, in the cortex and medulla in dogs with unilateral ureteral obstruction for 21 hours. MATERIALS AND METHODS: Hemodynamic and clearance experiments were performed after release of ureteral obstruction in 6 dogs with unilateral ureteral obstruction, followed by Western blot analysis of nitric oxide synthase and immunohistochemistry. RESULTS: Ureteral obstruction raised mean ureteral pressure plus or minus standard error to 35.0 +/- 7.2 mm. Hg. In dogs with unilateral ureteral obstruction mean renal blood flow was 116 +/- 10 ml. per minute, lower than the 213 +/- 22 ml. per minute in sham operated dogs (p <0.01). After unilateral ureteral obstruction release the mean glomerular filtration rate was 9.5 +/- 2.1 ml. per minute, lower than the 27.3 +/- 1.8 ml. per minute in the contralateral unobstructed kidney (p <0.01). Western blot analysis showed that mean nitric oxide synthase/beta-actin in the cortex of the obstructed kidney was 0.04 +/- 0.01 densitometry units, lower than 0.11 +/- 0.02 densitometry units in the unobstructed contralateral kidney (p <0.05). In contrast, mean nitric oxide synthase/beta-actin in the medulla of the obstructed kidney was 1.29 +/- 0.33 densitometry units, greater than the 0.34 +/- 0.03 densitometry units in the unobstructed kidney (p <0.05). Immunohistochemistry revealed that the increased expression of nitric oxide synthase protein was localized to the endothelium of the vasa recta. CONCLUSIONS: Unilateral ureteral obstruction enhances nitric oxide synthase expression in the medulla but not in the cortex. This increased expression in the medulla may be the result of increased medullary hypoxia in unilateral ureteral obstruction, possibly contributing to medullary hyperemia after unilateral ureteral obstruction release.

Animals↗
PubMed2005

Altered expression of rat renal cortical OAT1 and OAT3 in response to bilateral ureteral obstruction.

BACKGROUND: Bilateral ureteral obstruction (BUO) is characterized by the development of hemodynamic and tubular lesions. However, little is known about the expression of organic anion renal transporters. The objective of this work was to study the renal excretion of p-aminohippurate (PAH) and the cortical renal expression of the organic anion transporter 1 (OAT1) and organic anion transporter 3 (OAT3) in BUO rats. METHODS: Male Wistar rats underwent bilateral obstruction of the proximal ureters for 24 hours (BUO) or sham operation. After 24 hours of ureteral releasing, the following studies were performed: PAH renal excretion employing conventional clearance techniques and OAT1 and OAT3 abundance (homogenates, intracellular and basolateral plasma membrane fractions from renal cortex) using immunoblotting and immunocytochemical techniques (light microscopic and confocal immunofluorescence microscopic analysis). RESULTS: BUO rats showed a lower renal excretion of PAH. In obstructed kidneys, immunoblotting revealed a significant decrease in the abundance of both OAT1 and OAT3 in basolateral plasma membranes from renal cortex. An increase of OAT1 expression was observed in homogenates and in intracellular membrane fractions in kidneys from BUO rats compared with sham-operated ones, indicating an internalization of this carrier. Immunocytochemical techniques confirmed these results. On the contrary, OAT3 expression was reduced both in homogenates and in intracellular membrane fractions in obstructed kidneys. CONCLUSION: BUO was associated with down-regulation of OAT1 and OAT3 in basolateral plasma membranes from proximal tubule cells, thus these carriers may play important roles in the impaired organic anion excretion displayed in the obstructed kidney.

Animals↗
PubMed2005

Result of endoscopic ureteroureterostomy with holmium:YAG laser for complete ureteral obstruction.

BACKGROUND AND PURPOSE: Complete ureteral obstruction after pelvic surgery is traditionally managed by open repair. Recent advances in endoscopic instruments and techniques have improved the efficacy with which these conditions are treated. Here, we describe our experiences with a holmium:YAG laser in the endoscopic management of complete ureteral obstruction. PATIENTS AND METHODS: Retrograde endoscopic ureteroureterostomy using a Ho:YAG laser was performed on five patients with complete ureteral obstruction having a mean length of 0.9 +/- 0.2 cm after gynecologic surgery. The obliterated segment was incised with a 550-microm fiber through a rigid ureteroscope and under fluoroscopic guidance. Afterward, balloon dilatation was performed. A 7F/14F endopyelotomy stent was maintained for a mean time of 7 weeks, and follow-up was conducted via radiologic imaging. RESULTS: Recanalization was possible in all five patients immediately. One month after the initial operation, one patient exhibited a normal ureteral passage, and three other patients exhibited partial ureteral stricture. The remaining patient was lost to follow-up. Of the three patients with partial strictures, two evidenced no stricture after additional endoscopic treatment(s), and the remaining patient eventually underwent open repair. Overall, three of four (75%) patients exhibited normal excretory function without any open surgery and were symptom free with a mean follow-up time of 45 months (range 23-67 months). CONCLUSIONS: Although the number of patients in this study was small, it appears that endoscopic ureteroureterostomy with a Ho:YAG laser may constitute a valuable option for the treatment of complete short ureteral obstructions.

Adult↗
PubMed1978

Prostaglandin-mediated hyperemia and renin-mediated hypertension during acute ureteral obstruction.

Acute elevation of ureteral pressure to 100 mm Hg in anesthetized dogs (n=7) resulted in an increase (P less than 0.005) in systemic blood pressure form 151 +/- 7 to 163 +/- 7 mm Hg, a transient (approximately 15 min) increase (P less than 0.05) in renal blood flow from 413 +/- 27 to 465 +/- 27 ml/min and a rise (P less than 0.05) in plasma renin activity from 6.0 +/- 1.6 to 10.3 +/- 2.1 ng/ml/hr. Pretreatment with a competitive inhibitor of angiotensin II, i.e. sar1gly8AII, abolished the hypertensive response to acute ureteral obstruction, and pretreatment with 2 mg/kg of either indomethacin (n=6) or meclofenamate (n=3), 15 min before obstruction, prevented the hyperemic response. These results suggest that acute ureteral obstruction leads to hypertension via activation of the renin-angiotensin system and hyperemia via a prostaglandin-initiated mechanism.

Acute Disease↗
PubMed1994

Nephrogenic diabetes insipidus associated with bilateral ureteral obstruction.

Nephrogenic diabetes insipidus associated with ureteral obstruction is rare. We report a case of nephrogenic diabetes insipidus associated with ureteral obstruction caused by ileal leiomyosarcoma in a 32-year-old man. The treatment with trichlorothiazide and diclofenac sodium reduced urine output from 8 L/day to 4 L/day. Six months after nephrostomy, urine output decreased to 2.5 L/day without any drug administration. This case suggests that ureteral obstruction may cause an increase in urine output to 8 L/day and that surgical treatment for ureteral obstruction is effective in reducing urine output in nephrogenic diabetes insipidus patients with ureteral obstruction.

Adult↗