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PubMed1994

Palliative care in bilateral malignant ureteric obstruction.

Bilateral ureteric obstruction is an uncommon complication arising from malignancy and its treatment. There are several effective methods of overcoming the obstruction but the choice of option requires careful consideration of various factors pertaining to each individual. These factors include the patient's age, premorbid health and lifestyle, and the extent and rate of disease. Patient and family expectations, goals and priorities need careful consideration in the context of the patient's prognosis. If measures to relieve the obstruction are not to be undertaken, symptom control then becomes paramount. This paper explores the various options and decision making by focusing on representative patients encountered in the practice of the Central Sydney Area Health Palliative Care Service.

Adult↗
PubMed1995

Regulation of renal growth factors and clusterin by AT1 receptors during neonatal ureteral obstruction.

Unilateral ureteral obstruction (UUO) in the neonate impairs growth of the ipsilateral kidney. Since renal renin expression is increased by UUO, we hypothesized that, by activation of AT1 receptors, angiotensin II (ANG II) regulates expression of transforming growth factor-beta 1 (TGF-beta 1) and epidermal growth factor (EGF) in the obstructed kidney. Sprague-Dawley rats underwent left UUO or sham operation within the first 48 h of life and received losartan, 40 mg.kg-1.day-1, or saline. After 14 days, steady-state renal mRNA was determined for renin, TGF-beta 1, EGF, and clusterin. Losartan reduced the DNA content of the intact kidneys but did not further decrease that of the obstructed kidney. Losartan increased renal renin expression and decreased EGF expression by 80%, regardless of UUO. In contrast, losartan reduced TGF-beta 1 expression by 34% in obstructed kidneys but did not affect TGF-beta 1 in intact kidneys. Losartan increased clusterin expression by 60% in obstructed kidneys and seven-fold in intact kidneys. We conclude that activation of the ANG II AT1 receptor is necessary for normal renal growth and that TGF-beta 1 is regulated by AT1 receptors in the obstructed, but not intact, kidneys. Through AT1 receptors, endogenous ANG II stimulates EGF and inhibits clusterin expression.

Angiotensin II↗
PubMed1995

Sequential changes in renal expression of renin-angiotensin system genes in acute unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) alters the expression of genes encoding for the renin-angiotensin system (RAS). We tested the hypothesis that changes in RAS genes expression occur soon after obstruction. Indeed, measurements during the first 24 hours of UUO showed up-regulation of renin mRNA in the obstructed kidney at 1 hour. UUO also led to increases in PRA and renal renin content, ACE activity and Ang II concentration in the experimental kidney. The obstructed kidney relative abundance of renin mRNA was increased compared to basal at 1, 2, 6, and 24 hours; the contralateral kidney renin mRNA expression was reduced. AT1-R mRNA expression was diminished at 6 and 24 hours in the obstructed kidney compared to contralateral and sham kidneys. ACE activity was up-regulated in the obstructed kidney and transiently down-regulated in the contralateral kidney. These findings show for the first time that activation of the RAS results from as little as 1 hour of UUO and that up-regulation of renin mRNA and ACE activity lead to increase Ang II production which down-regulates AT1-R mRNA as early as 6 hours post-UUO. These studies establish a pattern of sequential, differential regulation of the RAS genes in acute UUO that provide an explanation for the hemodynamic changes in this condition.

Acetylcholinesterase↗
PubMed2000

Osteogenic protein-1 prevents renal fibrogenesis associated with ureteral obstruction.

Unilateral ureteral obstruction (UUO) is a model of renal injury characterized by progressive tubulointerstitial fibrosis and renal damage, while relatively sparing the glomerulus and not producing hypertension or abnormalities in lipid metabolism. Tubulointerstitial fibrosis is a major component of several kidney diseases associated with the progression to end-stage renal failure. Here we report that when a critical renal developmental morphogen, osteogenic protein-1 (OP-1; 100 or 300 microg/kg body wt), is administered at the time of UUO and every other day thereafter, interstitial inflammation and fibrogenesis are prevented, leading to preservation of renal function during the first 5 days after obstruction. Compared with angiotensin-converting enzyme inhibition with enalapril treatment, OP-1 was more effective in preventing tubulointerstitial fibrosis and in preserving renal function. The mechanism of OP-1- induced renal protection was associated with prevention of tubular atrophy, an effect not shared with enalapril, and was related to preservation of tubular epithelial integrity. OP-1 blocked the stimulation of epithelial cell apoptosis produced by UUO, which promoted maintenance of tubular epithelial integrity. OP-1 preserved renal blood flow (RBF) during UUO, but enalapril also stimulated RBF. Thus OP-1 treatment inhibited tubular epithelial disruption stimulated by the renal injury of UUO, preventing tubular atrophy and diminishing the activation of tubulointerstitial inflammation and fibrosis and preserving renal function.

Actins↗
PubMed1988

Differential effect of platelet-activating factor (PAF) receptor antagonists on peptide and PAF-stimulated prostaglandin release in unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) results in increased renal resistance as well as in exaggerated prostaglandin (PG) release from the obstructed hydronephrotic kidney (HNK). We have reported previously that platelet-activating factor (PAF) dose-dependently stimulates the release of PGs from both the HNK and unobstructed contralateral kidney (CLK), with CLK release being 10% that of the HNK. In the present report, we studied the interaction of PAF with its receptor by examining the effects of PAF-receptor antagonists on the release of PGs from the isolated perfused rabbit HNK and CLK stimulated by PAF; angiotensin II (AII), and bradykinin (BK) were also used as agonists. In the HNK, kadsurenone (3 microM) inhibited PAF-stimulated PGE2 and thromboxane B2 (TxB2) release by 28.2 and 62.5% respectively. CV-3988 (20 microM) and triazolam (5 microM) also preferentially diminished PAF-stimulated TxB2 release. In addition, all three drugs significantly diminished BK- and AII-stimulated TxB2 release, while CV-3988 was the only antagonist to affect peptide-stimulated PGE2 release. While effective against agonist-stimulated PG synthesis, these drugs had no direct effect on arachidonic acid metabolism to PGs. Furthermore, in the CLK, CV-3988 had no effect on BK- or AII-stimulated PGE2 release, whereas it totally inhibited PAF-stimulated release of PGE2. These results show that PAF-receptor antagonists in the HNK preferentially inhibit TxB2 release whether stimulated by PAF, AII or BK; in the CLK only PAF-stimulated PG release is affected. This biochemical difference may be of physiological significance and explain some of the functional differences between the HNK and CLK. Therefore, PAF may be an important mediator of some of the biochemical and functional changes associated with UUO.

Angiotensin II↗
PubMed2005

COX-2 inhibition prevents downregulation of key renal water and sodium transport proteins in response to bilateral ureteral obstruction.

Bilateral ureteral obstruction (BUO) is associated with marked changes in the expression of renal aquaporins (AQPs) and sodium transport proteins. To examine the role of prostaglandin in this response, we investigated whether 24-h BUO changed the expression of cyclooxygenases (COX-1 and -2) in the kidney and tested the effect of the selective COX-2 inhibitor parecoxib (5 mg.kg(-1).day(-1) via osmotic minipumps) on AQPs and sodium transport. Sham and BUO kidneys were analyzed by semiquantitative immunoblotting, and a subset of kidneys was perfusion fixed for immunocytochemistry. BUO caused a significant 14-fold induction of inner medullary COX-2 (14.40 +/- 1.8 vs. 1.0 +/- 0.4, n = 6; P < 0.0001) and a reduction in medullary tissue osmolality, whereas COX-1 did not change. Immunohistochemistry confirmed increased COX-2 labeling associated with medullary interstitial cells. COX isoforms did not change in cortex/outer medulla after 24-h BUO. In BUO kidneys, inner medullary AQP2 expression was reduced, and this decrease was prevented by parecoxib. In the inner stripe of outer medulla, the type 3 Na(+)/H(+) exchanger (NHE3) and apical Na(+)-K(+)-2Cl(-) cotransporter (BSC-1) were significantly reduced by BUO, and this decrease was significantly attenuated by parecoxib. Immunohistochemistry for AQP2, NHE3, and BSC-1 confirmed the effect of parecoxib. Parecoxib had no significant effect on the Na-K-ATPase alpha(1)-subunit, type II Na-P(i) cotransporter, or AQP3. In conclusion, acute BUO leads to marked upregulation of COX-2 in inner medulla and selective COX-2 inhibition prevents dysregulation of AQP2, BSC-1, and NHE3 in response to BUO. These data indicate that COX-2 may be an important factor contributing to the impaired renal water and sodium handling in response to BUO.

Animals↗
PubMed1999

Increased oxidative stress in mouse kidneys with unilateral ureteral obstruction.

BACKGROUND: Unilateral ureteral obstruction (UUO) is a well-established experimental model of renal injury leading to interstitial fibrosis. The molecular and cellular mechanism(s) of interstitial fibrosis in UUO kidney is beginning to be elucidated. Oxidative stress has been implicated in the pathogenesis of various forms of renal injury; however, little is known about its involvement in the setting of ureteral obstruction. METHODS: To investigate the possible involvement of oxidative stress in the obstructive nephropathy, we studied the occurrence and distribution of Nepsilon-carboxymethyl-lysine (CML) in the kidneys after ureteral obstruction. CML is an integrative biomarker of the cumulative protein damage induced by glycoxidation. Heme oxygenase-1 (HO-1) mRNA and protein expression, which is a sensitive and reliable indicator of oxidative stress, were also examined. RESULTS: CML immunoreactivity was found in the interstitium of UUO kidneys 10 days after the onset ureteral obstruction. HO-1 mRNA was up-regulated as early as 12 hours after ureteral obstruction. HO-1 immunoreactivity was observed in the periglomerular and peritubular interstitium two days after ureteral obstruction. CONCLUSIONS: These results strongly suggested the presence of increased oxidative stress in the interstitium of UUO kidneys. The oxidative stress and the formation of various kind of biological active oxidative products in the interstitium are supposed to play significant roles in UUO kidney.

Animals↗
PubMed1998

Up-regulation of HSP47 in the mouse kidneys with unilateral ureteral obstruction.

BACKGROUND: Unilateral ureteral obstruction (UUO) is a well established experimental model of renal injury leading to interstitial fibrosis. The molecular and cellular mechanism(s) of interstitial fibrosis in UUO are beginning to be elucidated. In the progression of interstitial fibrosis in UUO, up-regulation of collagen synthesis is commonly observed. HSP47 is a collagen-binding stress protein and is thought to be a collagen-specific molecular chaperone, which plays a pivotal role during the biosynthesis and secretion of collagen molecules in the endoplasmic reticulum. The synthesis of HSP47 has been demonstrated to always parallel that of collagen in physiological and pathophysiological conditions. It is well recognized that renin-angiotensin system (RAS) is enhanced in the setting of UUO and that enhanced RAS has been implicated in the pathogenesis of interstitial fibrosis in the obstructed kidneys. METHODS: To investigate the role of HSP47 in the progression of interstitial fibrosis in mouse UUO, the expression of HSP47 was examined by Northern blotting, immunohistochemistry and in situ hybridization in the obstructed kidneys. To test the possible involvement of enhanced RAS on the HSP47 expression, we examined the effects of lisinopril, an angiotensin converting enzyme inhibitor, on interstitial fibrosis. HSP47 and type I collagen mRNA expression. RESULTS: By Northern blot analysis, HSP47 mRNA was significantly up-regulated at 12 hours (about twice that of sham operated kidneys) after the onset of ureteral obstruction, further increased and stayed at the increased level until seven days (about 8 times that of sham operated kidneys). HSP47 mRNA and protein expression were observed in the periglomerular and peritubular interstitial regions of the obstructed kidneys. Distribution of smooth muscle alpha actin and type I collagen immunoreactivity were similar to the HSP47 distribution pattern, suggesting that HSP47 was up-regulated in the myofibroblasts. Lisinopril ameliorated the expansion of cortical interstitium in the obstructed kidneys at four and seven days after ureteral obstruction. HSP47 mRNA expression was suppressed at four and seven days, whereas type I collagen mRNA was suppressed only at seven days after the onset of ureteral obstruction. CONCLUSIONS: These results demonstrate the early and persistent up-regulation of HSP47 during the progression of interstitial fibrosis in mouse UUO kidneys, and further suggest the potential role of HSP47 in the pathogenesis of interstitial fibrosis in the obstructed kidneys. Partial suppression of HSP47 mRNA expression by lisinopril at day 4 and day 7 after ureteral obstruction suggests that there are other immediate trigger(s) that induce the HSP47 mRNA expression. Identification of the molecular mechanism of HSP47 induction during UUO may give an insight into the novel aspects of the molecular pathophysiology of interstitial fibrosis in obstructive nephropathy.

Actins↗
PubMed1999

Recovery of distal nephron enzyme activity after release of unilateral ureteral obstruction.

PURPOSE: Unilateral ureteral obstruction (UUO) for 24 hours results in a severe compromise of distal tubular function. The acidification defect is believed to be localized in the collecting duct. To characterize distal tubular function recovery one month after junction release, clearance studies in whole animals and enzyme studies in microdissected segments were performed in an experimental model of unilateral ureteral obstruction. MATERIALS AND METHODS: Following release of ureteral obstruction of 24 hours duration, a significant decrease of whole kidney glomerular filtration rate was observed in the postobstructed kidney (POK) with a marked increase in urinary pH, fractional excretion of bicarbonate (FEHCO3-) and decrease in urinary osmolality. By orthograde stop flow experiment, bicarbonate excretion rate (Fr:Ff HCO3-/Fr:Ff Inutest) increased in the first and second urine fractions of 120 microl. corresponding to the collecting segment in the POK, one day after release. Decrease in U-P pCO2 (p<0.01) suggested an impaired H+ secretion on distal nephron in POK. Recovery of inulin clearance and values of urinary pH, FEHCO3- and urinary osmolality near contralateral and control kidneys were observed thirty days following ureteral release. The decline in enzyme activity in the distal nephron due to structural damage from high intratubular pressure was evaluated. Bafilomycin sensitive H+ -ATPase activity measurement in the medullary collecting duct segments of the POK showed an important decrease (68%), with lightly reduced activity (20%) in the cortical collecting duct, 24 hours after obstruction release. Localized in the connecting tubule cells and secreted into the tubular fluid in the late distal nephron, renal kallikrein has been involved in bicarbonate transport at cortical collecting duct segments. The renal kallikrein-like activity was reduced in POK (p<0.01). RESULTS: Recovery of enzyme activity was shown thirty days after unilateral ureteral obstruction. Our results show severe functional damage of the collecting duct after 24 hours of unilateral ureteral obstruction. H+ -ATPase activity was markedly decreased on medullary collecting duct segments. CONCLUSIONS: A correlation between the functional impairment of distal H+ secretion and decreased distal nephron enzyme activity has been shown. Recovery of both the functional and the enzyme activity at the distal nephron was demonstrated thirty days after obstruction release.

Adenosine Triphosphatases↗
PubMed1989

Gene expression in response to acute unilateral ureteral obstruction.

Acute unilateral ureteral obstruction results in differential growth characteristics of both the ipsilateral and contralateral kidney. The obstructed kidney undergoes cellular atrophy following an initial phase of interstitial proliferation while the contralateral kidney hypertrophies. To evaluate the molecular events occurring in both kidneys after obstruction, we examined the expression of growth related (c-fos, c-myc, cH-ras, HSP 70), cell maintenance (beta-actin), and cellular damage (TRPM-2) genes at the mRNA level. In the contralateral kidney an early and transitory induction of c-fos and c-myc expression occurred while a bimodal induction was noted in the obstructed kidney. The patterns of cH-ras, HSP 70 and actin expression also differed in both kidneys. Induction of TRPM-2 was noted only in the obstructed kidney. Rapid gene activation is evident in both the contralateral and obstructed kidney following unilateral ureteral obstruction. The patterns of expression are distinct and may reflect the cellular response to stress (cell death and stromal proliferation) in the obstructed kidney versus a response to a systemic stimulus resulting in cellular hypertrophy in the contralateral kidney.

Acute Disease↗
PubMed1997

Two distinct epithelial responses may compensate for the ureteral obstruction in early and late phase of unilateral ureteral obstruction-treated rat: cellular proliferation in acute phase and osteopontin expression in chronic phase.

In order to clarify cellular responses in dilated renal tubules in the acute and chronic phase of ureteral obstruction, we investigated the expression of proliferating cell nuclear antigen and osteopontin (OPN) in unilateral ureteral obstruction (UUO)-treated rat kidneys. The results showed that renal epithelial cells proliferate in association with tubular dilatation to compensate for the ureteral obstruction in the acute phase of UUO while the proliferative activity decreases in the chronic phase. In the chronic phase, however, the expression of OPN was up-regulated in various tubules but not associated with the tubular dilatation. Taken together with its chemoattractant activity for macrophage, OPN may be involved in the interstitial fibrosis as another compensatory mechanism in the chronic phase of ureteral obstruction. Therefore, these results suggest that two distinct epithelial responses may compensate for the ureteral obstruction in the acute and chronic phase of UUO-treated rat, respectively.

Acute Disease↗
PubMedDate not supplied

How can we predict ureteral obstruction after gynecological surgery? The changes in Doppler resistive index and plasma creatinine and magnesium concentrations after surgical, unilateral ureteral obstruction in a rabbit model.

The aim of this study is to evaluate the changes in Doppler resistive index (RI) and plasma creatinine and magnesium concentrations after unilateral ureteral obstruction in a rabbit model. Fourteen adult female rabbits were used in this study. In seven rabbits, the left ureter was ligated with silk suture, and the control group was sham operated. Before surgery and on the second and seventh days after surgery, blood samples were obtained to measure plasma creatinine and magnesium concentrations. Doppler RIs of both kidneys were also measured before surgery and on the second and seventh days after the surgical procedure. With regard to magnesium levels, there was a significant within-subjects sessions difference [F(2, 20) = 15.21, P= 0.001] indicating a decrease through sessions. Magnesium concentrations decreased significantly at the postoperative second and seventh days compared to preoperative baseline levels (P= 0.003 and P= 0.001, respectively). Multifactorial analysis of variance was applied for each session separately with laterality, and groups as factors. The Doppler RI and the creatinine level did not show any significant differences or interactions for all sessions (P > 0.05). The decreasing plasma magnesium concentration after surgery may indicate ureteral injury; however, Doppler studies and creatinine levels may not be useful as well.

Analysis of Variance↗
PubMed1997

Downregulation of aquaporin-2 parallels changes in renal water excretion in unilateral ureteral obstruction.

In bilateral ureteral obstruction, both aquaporin-2 (AQP2) levels and urinary concentrating capacity are markedly reduced. However, the mechanisms involved in AQP2 downregulation are unknown. In rats with unilateral ureteral obstruction (UUO) the relative role of intrarenal and systemic factors can be evaluated. Semiquantitative immunoblotting revealed a marked decrease in AQP2 in obstructed kidneys to 23 +/- 7% (n = 9) of sham levels. This downregulation persisted 24 h after release of UUO. Furthermore, there was a significant but less extensive downregulation of AQP2 in the nonobstructed kidneys to 75 +/- 7% (n = 9) of sham levels. Consistent with impairment of collecting duct water reabsorption, free water clearance was greatly elevated in the obstructed kidneys (-2 +/- 1 microliter-min-1.kg-1, determined immediately after release) and only moderately elevated in nonobstructed kidneys (-44 +/- 5 microliters.min-1.kg-1) compared with sham-operated controls (-59 +/- 3 microliters.min-1.kg-1). Also AQP2 mRNA levels were reduced in obstructed kidneys. Immunocytochemistry confirmed the marked decrease in AQP2 expression in obstructed kidneys. In nonobstructed kidneys AQP2 was predominantly found in intracellular vesicles, which together with the reduced expression and elevated free water clearance strongly suggests a role of AQP2 in the observed compensatory diuresis from nonobstructed kidneys. The much lower AQP2 protein and mRNA levels in obstructed vs. nonobstructed kidneys are consistent with intrarenal factors playing a major role for downregulation of AQP2.

Animals↗
PubMed1988

Response of the renin-angiotensin system to relief of neonatal ureteral obstruction.

Chronic partial ureteral obstruction (CPUO) causes an increase in renal vascular resistance (RVR) that can be prevented by angiotensin II (ANG II)-converting enzyme inhibition. To assess the early effects of CPUO, guinea pigs subjected to neonatal left ureteral obstruction were anesthetized at 11-13 days of age for measurement of cardiac output and renal blood flow (RBF) using radioactive microspheres. Although RBF of the hydronephrotic kidney was not decreased at this age, that of the intact kidney more than doubled (P less than 0.01). To evaluate the hemodynamic response to relief of 5 or 10 days of neonatal left CPUO, animals were studied at 19-28 days of age. Although chronic enalapril maleate administration (30 mg.kg-1.day-1) did not further reduce the ratio of RVR to total vascular resistance (TVR) of the postobstructed kidney, it lowered RVR/TVR of the intact contralateral kidney by 40% (P less than 0.05). Renal renin content [RRC, pg angiotensin I (ANG I).mg protein-1.h-1] was twofold higher in both kidneys of animals with unilateral CPUO compared with those of sham-operated guinea pigs (P less than 0.03), and relief of obstruction normalized RRC. The rise in RVR/TVR resulting from ANG II infusion was not different in left kidneys of sham, CPUO, and CPUO-relief groups. However, for the intact kidney of animals with contralateral relief of CPUO, the increase was greater than in remaining groups (P less than 0.05). We conclude that by reducing intrarenal renin, relief of neonatal unilateral CPUO decreased ANG-mediated vasoconstriction of the postobstructed kidney and increased the vasoconstrictor response of the intact kidney to ANG II.

Aging↗
PubMed1978

Thin needle biopsy in the diagnosis of ureteral obstruction with malignancy.

Ureteral obstruction after treatment for abdominal cancers is a common situation in which the thin needle biopsy presents an attractive low morbidity alternative to laparotomy for the diagnosis of malignant disease. A negative biopsy is still nonconclusive, although helpful in determining the next step in the patient's management. In our own series, biopsy in the region of ureteral obstruction revealed tumor rather than benign disease in four of five patients. No morbidity was encountered.

Abdominal Neoplasms↗