Nephrostomy in patients with ureteral obstruction secondary to nonurologic malignancy. Obstructive uropathy in malignant disease

1980 ◽  
Vol 140 (4) ◽  
pp. 494-497 ◽  
Author(s):  
T. E. McNamara
2012 ◽  
Vol 140 (1-2) ◽  
pp. 91-93
Author(s):  
Srdjan Babic ◽  
Djordje Radak ◽  
Predrag Matic ◽  
Vladimir Kovacevic ◽  
Dario Jocic

Introduction. The natural course of abdominal aneurysms is progressive expansion, rupture, embolisation, thrombosis and compression of the visceral organs. The majority of papers report that inflammatory aortic and iliac aneurysms are associated with perianeurysmal and retroperitoneal fibrosis that ultimately results in the structural compromise of the urinary tract. Ureteral obstruction occurs in 20% to 71% of cases and approximately one half of these patients will present with obstructive uropathy. Most patients with inflammatory aneurysm are symptomatic, with elevated serum inflammatory markers, and characteristic multislice CT findings including a thickened aortic wall and a mass of periaortic inflammatory tissue. Case Outline. A 70-year-old man was admitted at the Vascular Surgery Clinic ?Dedinje?, Belgrade, because of ultrasonically verified asymptomatic aortoiliac aneurysm. Multisclice CT findings showed left urethral dilatation and hydronephrosis secondary to extrinsic ureteral obstruction due to aortoiliac aneurysm. CT findings, laboratory tests and finally, histopathologic examination showed atherosclerotic aneurysm without inflammation and retroperitoneal fibrosis. The patient was successfully treated with surgical resection of the aneurysm and aortobiiliac reconstruction with ?Y? prosthesis. Conclusion. We present a rare case of ureteral obstruction secondary to atherosclerotic aneurysm which, to our knowledge, has not been previously described in the domestic literature. A successful operative repair was performed. Postoperative course was uneventful and the patient was discharged on the seventh day after the surgery with normal vascular status and renal function.


1997 ◽  
Vol 33 (1) ◽  
pp. 61-68 ◽  
Author(s):  
BJ Rivers ◽  
PA Walter ◽  
DJ Polzin

Fluoroscopically guided, percutaneous antegrade pyelography in canine patients has been described previously in the veterinary literature. This report describes the technique with ultrasonographic guidance and its clinical application in the diagnosis of four cases (two dogs, two cats) of obstructive uropathy. The technique provided successful diagnosis of ureteral obstruction in all four cases. No complications were observed in three cases. In one feline case, ureteral obstruction with a blood clot occurred following the procedure; however, it could not be ascertained whether this event represented a complication of the technique.


2013 ◽  
Vol 305 (5) ◽  
pp. F618-F627 ◽  
Author(s):  
Shenyang Li ◽  
Nithya Mariappan ◽  
Judit Megyesi ◽  
Brian Shank ◽  
Krishnaswamy Kannan ◽  
...  

We examined the effects of increased expression of proximal tubule peroxisome proliferator-activated receptor (PPAR)α in a mouse model of renal fibrosis. After 5 days of unilateral ureteral obstruction (UUO), PPARα expression was significantly reduced in kidney tissue of wild-type mice but this downregulation was attenuated in proximal tubules of PPARα transgenic (Tg) mice. When compared with wild-type mice subjected to UUO, PPARα Tg mice had reduced mRNA and protein expression of proximal tubule transforming growth factor (TGF)-β1, with reduced production of extracellular matrix proteins including collagen 1, fibronectin, α-smooth muscle actin, and reduced tubulointerstitial fibrosis. UUO-mediated increased expression of microRNA 21 in kidney tissue was also reduced in PPARα Tg mice. Overexpression of PPARα in cultured proximal tubular cells by adenoviral transduction reduced aristolochic acid-mediated increased production of TGF-β, demonstrating PPARα signaling reduces epithelial TGF-β production. Flow cytometry studies of dissociated whole kidneys demonstrated reduced macrophage infiltration to kidney tissue in PPARα Tg mice after UUO. Increased expression of proinflammatory cytokines including IL-1β, IL-6, and TNF-α in wild-type mice was also significantly reduced in kidney tissue of PPARα Tg mice. In contrast, the expression of anti-inflammatory cytokines IL-10 and arginase-1 was significantly increased in kidney tissue of PPARα Tg mice when compared with wild-type mice subjected to UUO. Our studies demonstrate several mechanisms by which preserved expression of proximal tubule PPARα reduces tubulointerstitial fibrosis and inflammation associated with obstructive uropathy.


2016 ◽  
Vol 19 (11) ◽  
pp. 1132-1133 ◽  
Author(s):  
Benoît Vogt ◽  
François-Noël Desfemmes ◽  
Arnaud Desgrippes

2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Jeong In Choi ◽  
Jee Geun Yoo ◽  
Sa Jin Kim ◽  
Hae Nam Lee ◽  
Min Jeong Kim

Ureteral involvement by endometriosis is a rare and often silent disease but capable of producing significant morbidity and leading to hydronephrosis and to renal failure. Surgery is the treatment of choice to remove endometriotic lesions and relieve ureteral obstruction if the kidney is still functional or a nephrectomy is performed if there is a complete loss of renal function. We report a case of acute renal failure induced ureteral endometriosis managed with laparoscopic unilateral nephrectomy and endometrioma cystectomy. Differential diagnosis is important to confirm diagnosis for patients with ureteral obstruction presenting nonspecific symptoms.


1982 ◽  
Vol 73 (9) ◽  
pp. 1139-1147
Author(s):  
Makoto Hata ◽  
Masaki Tachibana ◽  
Nobuhiro Deguchi ◽  
Hiroshi Tazaki

1994 ◽  
Vol 4 (8) ◽  
pp. 1516-1521
Author(s):  
L M Rich ◽  
W F Piering

The ureter is an unusual location for lesions of Wegener's granulomatosis (WG). A patient in whom recurrence of WG after kidney transplantation was manifested by obstructive uropathy due to granulomatous vasculitis (WG) at the ureterovesicle anastomosis, as well as nasal and lung involvement, is reported. The occurrence of WG in the ureter in relation to the processes causing ureteral obstruction and the recurrences of WG after kidney transplantation and its treatment are briefly reviewed.


2013 ◽  
Vol 304 (5) ◽  
pp. F481-F490 ◽  
Author(s):  
Carolina I. Galarreta ◽  
Barbara A. Thornhill ◽  
Michael S. Forbes ◽  
Lauren N. Simpkins ◽  
Dae-Kee Kim ◽  
...  

Unilateral ureteral obstruction (UUO), a widely used model of chronic kidney disease and congenital obstructive uropathy, causes proximal tubular injury and formation of atubular glomeruli. Because transforming growth factor-β1(TGF-β1) is a central regulator of renal injury, neonatal and adult mice were subjected to complete UUO while under general anesthesia and treated with vehicle or ALK5 TGF-β1receptor inhibitor (IN-1130, 30 mg·kg−1·day−1). After 14 days, glomerulotubular integrity and proximal tubular mass were determined by morphometry of Lotus tetragonolobus lectin distribution, and the fraction of atubular glomeruli was determined by serial section analysis of randomly selected individual glomeruli. Glomerular area, macrophage infiltration, fibronectin distribution, and interstitial collagen were measured by morphometry. Compared with placebo, inhibition of TGF-β1by IN-1130 decreased apoptosis and formation of atubular glomeruli, prevented parenchymal loss, increased glomerular area and glomerulotubular integrity, and increased proximal tubule fraction of the adult obstructed kidney parenchyma from 17 to 30% ( P < 0.05, respectively). IN-1130 decreased macrophage infiltration and fibronectin and collagen deposition in the adult obstructed kidney by ∼50% ( P < 0.05, respectively). In contrast to these salutary effects in the adult, IN-1130 caused widespread necrosis in obstructed neonatal kidneys. We conclude that whereas IN-1130 reduces obstructive injury in adult kidneys through preservation of glomerulotubular integrity and proximal tubular mass, TGF-β1inhibition aggravates obstructive injury in neonates. These results indicate that while caution is necessary in treating congenital uropathies, ALK5 inhibitors may prevent nephron loss due to adult kidney disease.


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