Ureteral Occlusion Research Articles

Haemodynamic regulation of renal prostaglandin and renin release.

To examine the relationship between renal release of the prostaglandins E2 (PGE2) and I2 (PGI2) and renin during autoregulatory vasodilation, experiments were performed in anaesthetized dogs with denervated kidneys. Autoregulatory vasodilation was induced by reducing renal arterial pressure (RAP) or by raising ureteral pressure in steps. During progressive renal arterial constriction, PGE2 and PGI2 release reached maximal values (10.6 +/- 1.7 for PGE2 and 6.6 +/- 1.1 pmol min-1 for PGI2 release) at RAP of 70-80 mmHg, associated with almost no increase in renin release. By further reduction of RAP, prostaglandin release was not significantly altered, whereas renin release reached maximal values (18.7 +/- 2.4 micrograms AI min-1) when autoregulatory vasodilation was complete at RAP below 55-60 mmHg. During progressive elevation of ureteral pressure, the release of PGE2, PGI2 and renin increased in concert in a curvilinear fashion, reaching maximal values at a ureteral pressure of 85 mmHg. There was no further increase during ureteral occlusion and the plateau values averaged 23.6 +/- 3.7 pmol min-1 for PGE2, 8.0 +/- 1.6 pmol min-1 for PGI2 and 16.6 +/- 3.4 micrograms AI min-1 for renin. We conclude that vascular dilation enhances both prostaglandin and renin release. During reduction of RAP, preglomerular arteries are dilated at higher RAP than are afferent arterioles. Release of prostaglandins synthetized in arteries consequently occurs at higher RAP than release of renin, which is not enhanced until afferent arterioles ultimately dilate at RAP approaching 60 mmHg. In contrast, elevation of ureteral pressure provides nearly uniform enhancement of prostaglandin and renin release, indicating a more uniform dilation of the whole preglomerular vascular tree.

Effects of ureteral occlusion and ethacrynic acid infusion on renal prostaglandin degradation in the dog

The two major renal prostaglandins PGE2 and PGI2 are partly metabolized during a single passage of the kidney. To examine whether stopping glomerular filtration affected the renal degradation, PGE2 and PGI2 were infused into the suprarenal aorta of dogs during ureteral occlusion. Prostaglandin synthesis was blocked by indomethacin, 10 mg kg-1 b.w. i.v. About 20% of PGI2 and 80-90% of PGE2 were metabolized during one passage through the kidney. Prostaglandin degradation and arterial input were proportional (r greater than 0.95). Compared to control conditions at free urine flow, PGI2 degradation was not changed, whereas the degradation of PGE2 was slightly increased by ureteral occlusion. Ethacrynic acid might reduce degradation of PGE2 by inhibiting two degradation enzymes. To examine the influence of ethacrynic acid, PGE2 was infused in different doses into the suprarenal aorta of dogs before and after administration of ethacrynic acid 3 mg kg-1 b.w. i.v. At all dose levels of PGE2, 75-80% was degraded by one passage through the kidney, whether ethacrynic acid was administered or not. However, although ethacrynic acid did not alter the total renal output, the urinary fraction was reduced from 20-30% to 10-15%. We conclude that degradation of both PGE2 and PGI2 is mainly confined to the blood vessels, and that ethacrynic acid in conventional doses does not prevent degradation of PGE2, but redistributes PGE2 output from urine to renal venous blood.

Percutaneous Management of Ureteral Fistulas

Ureteral occlusion with proximal urinary diversion is often required when treating patients with ureteral fistulas secondary to advanced neoplastic disease. Recent endourologic advancements have stemmed from the high morbidity and mortality associated with formal surgical reconstruction in this population. Endourologic management may be accomplished by a transrenal or retroperitoneal approach. To date, no study has clearly demonstrated the superiority of any one approach because of the small numbers of patients and the uniformly short-term follow-up.

Urinary diversion by using a percutaneous ureteral occlusion device.

Urinary diversion is often necessary to control urinary fistulae and leaks caused by complications of ileal conduits and malignancies. Urinary diversion allows healing of wounds and conduit breakdowns and controls problems of skin breakdown and hygiene. Multiple percutaneous methods have been proposed for temporary or permanent urinary diversion [1 -8]. At our institution, we traditionally have used antegrade or retrograde ureteral stents to bypass the area of breakdown and provide urinary diversion. We evaluated a commercially available percutaneous ureteral occlusion device (Angiomed, Anaheim, CA) that is an olive-shaped silicone device that plugs the ureter, thereby preventing antegrade flow of urine. A nephrostomy catheter is placed in the renal pelvis to provide external urinary drainage. We review our experience with this device.

A renorenal suppression in response to atrial natriuretic peptide in the unilateral ischaemic rat.

1. The present study was carried out to investigate the haemodynamic and natriuretic effects of atrial natriuretic peptide (ANP) in normal rats and in rats with unilateral ischaemia. 2. Twenty-four hour unilateral ureter occlusion gave rise to a marked vasoconstriction in the ipsilateral kidney after its release. Intravenous infusion of ANP doubled p-aminohippurate clearance and inulin clearance and elicited massive natriuresis in the hydronephrotic kidney, while in the contralateral kidney these clearance values were decreased and there was a lack of natriuresis. The responses in the latter kidney were also different from those in the normal rat, in which significant natriuresis was elicited by ANP even though a decrease in p-aminohippurate clearance occurred. 3. After the control kidney in the unilateral hydronephrotic rat was denervated either mechanically or by pretreatment with prazosin, ANP induced a natriuresis in both kidneys. Furthermore, the renal denervation prevented the decrease in inulin clearance in the control kidney after ANP administration. 4. These findings suggest that the renal response to ANP may depend on the vascular tone before administration, and that renal nerve activity may modify the effects of ANP on renal haemodynamics and sodium excretion.

Properties of the macula densa mechanism for renin release in the dog.

To study the macula densa mechanism for renin release, both the macula densa and the haemodynamic mechanisms were activated in anaesthetized dogs with denervated kidneys, either by renal arterial constriction to a renal arterial pressure (RAP) of 52 +/- 2 mmHg or by ureteral occlusion to a ureteral pressure of 95-105 mmHg, 20-25 mmHg below RAP. Renal arterial constriction increased renin release from 0.3 +/- 0.2 to 16 +/- 4 micrograms AI min-1. At low RAP, renin release was subsequently reduced to 7 +/- 3 micrograms AI min-1 when sodium excretion was raised far above control values by plasma volume expansion and acetazolamide infusion. Ethacrynic acid (3 mg kg-1 body wt.) restored renin release to pre-expansion values, and a large dose (25 mg kg-1 body wt.) prevented renin release from falling even after unclamping the artery. During ureteral occlusion with stopped glomerular filtration, plasma volume expansion, acetazolamide and ethacrynic acid infusion did not alter renin release. On the other hand, beta-adrenergic stimulation by isoproterenol raised renin release equally (by 30-40 micrograms AI min-1) before and after plasma volume expansion, during both renal arterial constriction and ureteral occlusion. Indomethacin (10 mg kg-1 body wt.) abolished renin release induced by ethacrynic acid infusion and ureteral occlusion. We conclude that the macula densa mechanism for renin release is inactivated by high NaCl reabsorption during plasma volume expansion and acetazolamide infusion, reactivated by inhibition of NaCl reabsorption with ethacrynic acid and completely inhibited by indomethacin. The degree of activation does not influence the renin release induced by beta-adrenergic stimulation.

Spinoreticular cell responses to renal venous and ureteral occlusion.

Responses of 65 thoracolumbar spinoreticular neurons to renal vein or ureteral occlusion were studied in 40 alpha-chloralose-anesthetized cats. Cells were antidromically activated from the medial medullary reticular formation and all responded to somatic stimuli as well as renal nerve stimulation. Renal vein occlusion excited 17 of 40 cells. Activity increased from 6 +/- 1 to 13 +/- 2 spikes/s, with little adaptation. Depressor responses occurred in 9 cats and pressor responses in 12 cats. Pressor responses, but not depressor responses, were abolished by renal denervation. Ureteral occlusion increased activity of 28 of 50 cells. Responses were always rapid in onset but were either nonadapting, slowly adapting, or completely adapting. Activity increased from 7 +/- 1 to a peak of 17 +/- 3 spikes/s. Pressor responses occurred in 22 of 25 cats and tachycardia in 15 cats. Transection of renal nerves abolished cardiovascular responses. Twenty-five cells were tested for responses for both stimuli. Ten were excited by both, six by only ureteral occlusion, and nine failed to respond to either. The responding group of cells had a significantly greater incidence of A delta- and C-fiber renal input compared with nonresponding cells. Nonresponding cells tended to have only A delta-input. The results show that renal and ureteral mechanical stimuli which evoke cardiovascular reflexes excite spinoreticular cells. These cells may be part of supraspinal reflex arcs initiated by renal receptors.

Tubular prostaglandin E2 production and its role in urinary hypotonicity after release of ureteral occlusion in the rat.

1. In order to explore the involvement of endogenous prostaglandin E2 (PGE2) in the urine concentration defect after ureteral occlusion, PGE2 production by isolated collecting ducts in vitro and effects of indomethacin on urine osmolality in vivo were examined. 2. Twenty-four hours ureter obstruction caused increased PGE2 production by the medullary collecting ducts, which was maintained at a high level on the day after release of obstruction (0.8 +/- 0.2 pg/mm normal, 8.1 +/- 0.9 pg/mm 24 h obstruction, and 6.6 +/- 1.0 pg/mm post-obstruction, mean +/- SEM). An enhanced PGE2 production was also observed for papillary collecting duct on the day after release of 24 h ureteral occlusion (3.9 +/- 0.5 pg/mm normal and 7.7 +/- 1.2 pg/mm post-obstruction). 3. Administration of indomethacin to the unilateral post-obstructive rats slightly raised the urine osmolality of the post-obstructed kidney (from 339 +/- 17 to 390 +/- 22 mosmol/kg H2O), while it had a greater effect on the contralateral intact kidney (from 1569 +/- 138 to 2567 +/- 198 mosmol/kg H2O). 4. Our data may indicate that the urine concentration defect after 24 h ureteral occlusion is ascribable mainly to a mechanism other than increased endogenous PGE2.

Percutaneous Ureteral Fulguration: A Nonsurgical Technique for Ureteral Occlusion

Three patients with lower urinary tract fistulas after multiple operations and radiation therapy for pelvic cancer were treated with percutaneous ureteral fulguration and nephrostomy tube drainage. This technique occluded the ureter and allowed for maintenance of a dry fistula site in all 3 patients. There were no complications. The longest followup in these patients was 21 months. The procedure is simple technically and it can be performed with the patient under local anesthesia. The technique of percutaneous ureteral fulguration is described and other techniques for nonoperative occlusion of the ureter are discussed.

Tubuloglomerular feedback in animals with unilateral, partial ureteral occlusion

Previous experiments have shown that the sensitivity of the tubuloglomerular feedback system (TGF) is reduced by volume expansion in normal rats. This reduction in sensitivity is probably mediated by changes in the renal interstitial pressure. The present study was designed to investigate the TGF control system during volume expansion in rats with chronic, partial ureteral occlusion--hydronephrosis. Hydronephrosis was induced on the left or right side according to the method described by Ulm and Miller, in weanling Sprague-Dawley rats three weeks old. Three to six weeks later the rats were prepared for whole kidney and micropuncture experiments. Sham-operated animals were used as controls. Net interstitial pressure (that is, interstitial hydrostatic pressure minus interstitial oncotic pressure) was higher in the hydronephrotic, volume expanded animals than in the volume expanded controls. From findings in earlier investigations this increase in interstitial pressure would have been expected to reduce TGF sensitivity but this sensitivity was increased in the hydronephrotic kidneys, as indicated by a reduction in the turning point, the tubular flow rate at which 50% of the maximal stop-flow pressure response was observed (14.4 nl/min, sham-operated control 33.4 nl/min). Strong activity of the TGF mechanism was also indicated by a large proximal-distal difference in the single-nephron glomerular filtration rate (11.9 nl/min versus 3.3 nl/min in sham-operated controls) in the hydronephrotic kidney during volume expansion. Thus, in hydronephrotic kidneys in the latter condition the TGF mechanism was highly sensitive and activated to reduce the glomerular filtration rate. This mechanism may protect the diseased kidney from high intrapelvic pressures which otherwise could damage the kidney during saline volume expansion.

Management of Ureteroscopic Injuries

Ureteroscopy is an important technique in the management of calculous disease and ureteral lesions but it appears to have a greater potential for injury than percutaneous nephroscopy. In 2 years 4 patients with severe ureteroscopic injuries were treated. In 3 patients complete obstruction of the ureter occurred, and 1 had a major ureteral tear, prolonged urinary extravasation and infection. Even in the presence of total ureteral occlusion patients with short strictures were managed successfully percutaneously but the 2 patients with longer strictures were not. Previous surgery on the ureter or pelvic surgery and radiation therapy appear to be negative factors that affect adversely the ureteral blood supply, and potentiate poor healing and scarring. Nephrostomy tube drainage and ureteral stenting after ureteral dilation appear to be important steps in the percutaneous management of these patients.

Kidney Function in Domestic Fowl with Chronic Occlusion of the Ureter and Caudal Renal Vein

A previously published technique for producing renal insufficiency in chicks involves ligating the caudal renal vein together with the ureter near the midpoint of the kidney. This ligation occludes the normal route (caudal renal vein) by which blood exits the medial and posterior kidney divisions. The present study was conducted to evaluate kidney function following chronic caudal renal vein and ureter occlusion. The ureters and caudal renal veins of 2 to 3-week-old chicks were clamped with hemostatic clips (Clamp Group), and kidney function evaluations were conducted when the birds reached 14 weeks of age. Plasma values [osmolality, Na, K, Ca, inorganic P (Pi)] of control, sham, and clamp groups did not differ significantly. Plasma uric acid concentrations did not differ when the control and clamp groups were compared. Clamping the ureter near the midpoint of the kidney caused a significant reduction in the number of filtering glomeruli per kidney, but due to compensatory hypertrophy the kidney weights of the groups did not differ significantly. Kidney function comparisons (urine flow rates, glomerular filtration rates, renal plasma flow rates, urine pH, fractional excretion of Na, K, Ca, Pi, and uric acid) revealed a significant reduction in Na and K excretion by the clamp group, but other renal function parameters did not differ significantly. These experiments demonstrate that chickens have a remarkable capacity to survive significant reductions in renal mass and to adapt to major disruptions of blood flow patterns.

Chronic incomplete obstruction of the ureter: a new experimental model.

To produce a chronic moderate hydronephrosis in dog, a method of partial ureteral occlusion using a specially designed polypropylene obturator was developed. In 11 of 14 dogs undergoing this procedure, excretory urography constantly revealed a moderate degree of hydronephrosis persisting for 7 weeks. Combination of this method in one ureter with the vaginal-cuff cutaneous ureterostomy, previously reported, in the contralateral ureter is a useful model for split renal function study of unilateral chronic hydronephrosis or obstructive nephropathy analogous to that of clinical case.

Therapeutic Ureteral Occlusion in Advanced Pelvic Malignant Tumors

A technique for ureteral occlusion, combining insertion of nylon plugs with injection of polidocanol, is described. The method was used in 15 patients with vesicovaginal fistulas after operation and irradiation for advanced gynecological malignancy, or with severe malfunction and fibrosis of the bladder after radiotherapy for bladder carcinoma. The urinary leakage ceased in 11 patients, was greatly diminished in 2 and was unchanged in 2. Migration of plugs to the renal pelvis was the most serious complication and may have been the cause of pyelonephritis in 1 case. The technique is recommended for patients with a short life expectancy and uncontrolled, distressing leakage of urine.

Dissociation between renal prostaglandin E2 and renin release. Effects of glucagon, dopamine and cyclic AMP in dogs.

To examine the relationship between prostaglandin E2 (PGE2) and renin release, glucagon, dopamine and dibutyryl cyclic AMP (DB-cAMP) were infused into dog kidneys during autoregulatory dilation of preglomerular vessels. Autoregulatory vasodilation, which enhances PGE2 and renin release, was induced by renal arterial constriction or ureteral occlusion. Glucagon infusion increased both PGE2 and renin release during autoregulatory vasodilation, and renin release was almost abolished after inhibiting PGE2 release by indomethacin. In contrast, dopamine and DB-cAMP infused during autoregulatory vasodilation increased renin release without significantly changing PGE2 release. Stimulation of renin release was not dependent on vasodilatory effects, which for all drugs were greatly diminished during autoregulatory vasodilation. Hence, glucagon stimulates both PGE2 and renin release. Most of the increase in renin release during glucagon infusion is prostaglandin-dependent since indomethacin greatly reduced the stimulatory effect. In contrast, dopamine and DB-cAMP stimulate renin release without increasing PGE2 release as previously found for beta-adrenergic stimulation.

Renal vasodilation with ureteral occlusion and prostaglandins: attenuation by histamine H1 antagonists.

We evaluated the effects of histamine receptor antagonists on the renal vasodilatory responses to ureteral occlusion (UO), to the intrarenal infusion of prostaglandins E2, I2, A2, D2 and E1, and to bradykinin. We also determined the effects of meclofenamic acid, a cyclooxygenase inhibitor, on histamine-induced renal vasodilation and the effects of 2-methylhistamine (2-MeH), and H1 agonist, on glomerular filtration rate (GFR) and renal blood flow (RBF). Experiments were performed on adult mongrel dogs anesthetized with pentobarbital sodium. RBF was measured with an electromagnetic flow probe. Neither UO-induced nor prostaglandin- (PG) induced renal vasodilation was affected by infusion of the histamine H2 receptor antagonist cimetidine into the renal artery at 10(-5) M/min. On the other hand, renal artery infusion of the H1 receptor antagonist chlorpheniramine (CP) at 10(-5) M/min blocked UO-induced renal vasodilation [RBF increased 34 +/- 4% (SE) prior to but only 2 +/- 2% during infusion of CP) and markedly attenuated PGI2-, PGA2-, and PGE2-induced increases in RBF (CP inhibited 64 +/- 9% of the PGE2-induced renal vasodilation). CP had less effect on the renal vasodilation associated with infusion of PGD2 or PGE1 and had no effect on the vasodilation induced by bradykinin. Infusion of exogenous histamine (1 micrograms X kg-1 X min-1) into the renal artery prior to ureteral occlusion resulted in a typical H1 + H2-mediated vasodilatory response (RBF increased 53 +/- 7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Renal glutathione and mercury uptake by kidney

The kidney is well documented as the target organ for mercuric ion. Mechanisms by which this ion accumulates in renal tissue, however, are less well understood. Sulfhydryl groups in renal tissue might well bind this metal and serve as a sink for its accumulation. Various studies have indicated that both methyl mercury as well as mercuric ion are accumulated less by renal tissue after depletion of nonprotein sulfhydryl groups. A similar reduction in hepatic accumulation of mercuric ion or methyl mercury does not occur after nonprotein sulfhydryl depletion. This observation may relate to the higher tissue content of nonprotein sulfhydryls in liver than kidney or to a fundamentally different mechanism of metal uptake. Mercuric ion accumulation by renal tissue also can be reduced by ureteral occlusion, a reduction that is less than that for inulin in comparable experiments. These data are complex and do not clearly establish a role for filtration in the delivery of mercury to the kidney. Inhibition of the renal enzyme γ-glutamyl transpeptidase (γ-GT) results in a marked increase in the excretion of both glutathione and mercury in the urine. Although there is a tendency for kidneys of the γ-GT-inhibited animals to contain less mercury than controls, the change in renal content was not significant. These observations suggest that γ-GT may have a role in the reabsorption of mercury from the tubular lumen. Interestingly, both mercuric chloride-induced mortality and effects on renal slice accumulation of organic ions were enhanced in the presence of nonprotein sulfhydryl depletion caused both by immediate depletion of the glutathione pool and by inhibition of its synthesis.

Follow-up results of embolization therapy for palliation of incurable bladder carcinoma

Embolization therapy of the renal artery (N=10), hypogastric arteries (N=18) and ureter (N=24) was performed in 41 patients with incurable bladder carcinoma for palliation of gross hematuria and severe dysuria. Careful follow-up of the patients until death gave a mean survival time of 12.3 months after embolization; 6 patients are still alive. The results show that embolization therapy is justified for management of bleeding and dysuric complaints. Ureteral occlusion alone has almost no effect on hematuria. Combined embolization procedures yield better results than occlusion of the vessels or the ureter. Ureteral occlusion with a detachable balloon is superior to embolization with tissue adhesive.

Use of retrograde occlusion balloon catheters in percutaneous removal of renal calculi

The best results in percutaneous renal calculus removal are in patients with solitary pelvic stones and dilated collecting systems. Calyceal andlor infundibular calculi and ureteral calculi constitute more complex problems and are less successfully removed. Placement failure of the nephrostomy tube, and inability to gain access to calyceal calculi, and to engage impacted stones are the usual causes for unsuccessful procedures. To try to improve overall success we inserted occlusion balloon catheters prior to nephrostomy insertion in 60 of 71 patients. In a select group of 23 patients with a small renal pelvis and large calculi or infundibular calculi or patients with ureteral calculi, overnight application of 20 cm of hydrostatic pressure through the ureteric catheter led to marked dilatation in all instances. In all other patients the occlusion balloon catheter was placed immediately prior to the definitive nephrostolithotomy procedure. These ureteral catheters allow for better opacification and for dilatation of a small collecting system thereby facilitating the placement of the nephrostomy tube. They permit manipulation of calyceal and especially ureteral calculi. Placement of ureteral occlusion catheters is a safe adjunct to nephrostolithotomies and, in our experience, resulted in increased overall success.

Experience with Pyeloureterostomy Associated with Simple Ligation of Native Ureter without Ipsilateral Nephrectomy in Renal Transplantation

Ureteroneocystostomy was used as the primary method of urinary tract reconstruction in 282 allograft renal transplants at our center since 1965. A nonrefluxing anastomosis was incorporated whenever possible. Seven patients who suffered major urological complications involving the ureteroneocystostomy required pyeloureterostomy as the method of repair using the patient’s distal native ureter. No ipsilateral nephrectomy was performed and simple ligation of the native ureter with nonabsorbable suture was accomplished. Of the 7 patients 3 suffered hydronephrosis of the native kidney. None of these patients had signs or symptoms secondary to acute and chronic ureteral occlusion. Our experience suggests that intentional ligation of the native ureter during pyeloureterostomy does not result in increased morbidity to the transplant patient, and that the need for ipsilateral nephrectomy with its own added morbidity may not be necessary.