Bilateral renal obstruction is a rare critical condition, requiring a prompt diagnostic approach and treatment to restore the renal function. The most commonly observed obstructive uropathy in children is congenital malformation, such as posterior urethral valves and bilateral ureteropelvic junction obstruction. Malignant pelvic masses obstructing the ureter are widely reported in adults but are rarely observed in children. The treatment of ureteral obstruction related to pelvic malignancy is a therapeutic challenge with a median survival duration of 3-7 months in adults; however, pediatric patients with pelvic malignancy leading to ureteral obstruction had better outcomes, with a reported 5-year mortality rate of 20%, than the adult patients. Here, we report a rare case of bilateral ureteral obstruction associated with pelvic rhabdomyosarcoma presenting with acute kidney injury treated by ureteral diversion with double J stent, and concommittent emergency hemodialysis, leading to restoration of good renal function. We suggest that bilateral ureteral obstruction should be released as soon as possible using surgical or interventional approach to minimize the obstruction period, and subsequential chemotherapy may contribute to improvement of survival and recovery of renal function.
The aim of this study was to evaluate double-pigtail ureteral stent fixation in cats. Medical records of 19 cats (23 ureters) with complete ureteral obstruction that double-pigtail ureteral stent placement were carried out were retrospectively reviewed. The cats were randomly classified into two groups; 13 cats (16 ureters) with double-pigtail ureteral stent fixed to urinary bladder (SF group) and 6 cats (7 ureters) with not fixed to urinary bladder (SNF group). The average age and weight of the cats was 7.4 years and 3.73 kg, respectively. Postoperative complications included chronic renal failure (n = 11), lower urinary track diseases (cystitis, hematuria, pollakiuria) (n = 7), stent migration (n = 6), anemia (n = 5), ascites (n = 2), hyperthermia (n = 1), enteritis (n = 1), oliguria (n = 1), hypotension (n = 1), ureteritis (n = 1), and pyelonephritis (n = 1). Stent migration did not occur in the 16 ureters of the cats in SF group but did occur in 4 out of 7 ureters of the cats in SNF group. The prevention of stent migration by stent fixation was significant (P = 0.04). Among the 13 cats in SF group, only 2 cats developed lower urinary track diseases, while 4 of the 6 cats in SNF group showed symptoms of lower urinary track disease. Thus, the cats that underwent double-pigtail ureteral stent fixation to the urinary bladder developed significantly fewer lower urinary diseases (P = 0.046). In conclusion, double-pigtail ureteral stent fixation to the urinary bladder for treatment of complete ureteral obstruction in cats can effectively prevent stent migration, which is common complication of stent placement.
Ureteral obstruction causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Although increased renal prostaglandin production is responsible for the former, it is not clear whether or not it is also responsible for the latter. Therefore, we investigated the role which prostaglandins play in the autoregulation of RBF during an ureteral pressure elevation (40 $cmH_2O$). Since the major mechanism of RBF autoregulation is the tubuloglomerular feedback, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. To pursue the purpose, six anesthetized dogs were prepared for the measurements of RBF, mean sytemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from $170{\pm}8 ml{\cdot}min^{-1}\;to\;189{\pm}8$, and the systemic arterial pressure didn't change significantly. During spontaneous urine flow, RBF autoregulation was abolished when RAP was reduced to $59{\pm}3$ mmHg. On the other hand, during the ureteral pressure elevation, the autoregulation curves shifted upward and rightward from control, and the pressure when RBF autoregulation was abolished was $74{\pm}3$ mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulaion during both control ($63{\pm}5$ mmHg) and the elevated ureteral pressure ($77{\pm}5$ mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during partial ureteral obstruction. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at spontaneous RAP and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.
Yoon, Ji Hyung;Park, Sejun;Park, Sungchan;Moon, Kyung Hyun;Cheon, Sang Hyeon;Kwon, Taekmin
Investigative and Clinical Urology
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제59권6호
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pp.376-382
/
2018
Purpose: The authors performed this study to investigate the risk factors for predicting stent failure and to evaluate its impact on prognosis. Materials and Methods: Between January 2002 and March 2017, we retrospectively reviewed 117 consecutive patients who underwent retrograde ureteral stenting and exchanging at least once every 3 months for malignant ureteral obstruction. The patients were classified according to their pre-stenting chronic kidney disease (CKD) stage. The factors affecting stent failure were analyzed using a logistic regression model. Overall survival (OS) was estimated, and the prognostic significance of each variable was estimated using Cox proportional-hazards regression modeling. Results: Before stenting, 91 patients were CKD stages 1-3 and 26 patients were CKD stages 4-5. These two groups differed significantly only in pre-stenting estimated glomerular filtration rate (eGFR), bilateral obstruction, and pre-stenting pyuria. Among the 117 patients, stent failure occurred in 30 patients (25.6%), and there were no differences between the groups. Pre-stenting pyuria and post-stenting complications were significant predictors of stent failure. There were 79 deaths in total, including 56 in the CKD stages 1-3 group and 23 in the CKD stages 4-5 group. In the multivariate analysis predicting patient OS, pre-stenting eGFR and post-stenting disease progression were significant factors. Conclusions: Internal ureteral stenting was effective for maintaining renal function in malignant ureteral obstruction. However, it did not restore renal function, which is related to the prognosis of the patients. Therefore, to improve patients' renal function and prognosis, patients who require stenting must be quickly recognized and treated.
The present study was designed to investigate the effects renin-angiotensin-aldosterone system (RAAS), endothelin (ET) and local natriuretic peptide (NP) system for glomerulopathy induced in the experimental bilateral ureteral obstructive rats. Sprague-Dawley male rats ($200{\sim}220g$ body weight) were bilaterally obstructed by ligation of the proximal ureters for 24 hours. Control rats were treated in the same ways, except that no ligature was made. The glomeruli were isolated from cortex by graded sieve methods, and the mRNA expressions of local renin-angiotensin system (RAS), aldosterone synthase (CYP11B2), endothelin-1 (ET-1) and NP system were determined by real-time polymerase chain reaction. Following the bilateral ureteral obstruction, the mRNA expressions of renin, angiotensin converting enzyme 1 as well as ET-1 were increased, while that of angiotensin converting enzyme 2 was not changed. The expressions of CYP11B2 and angiotensin II receptors were not changed. C-type natriuretic peptide (CNP) expression was increased, while its receptors (natriuretic peptide receptor-B) were not changed. We suggest that the upregulation of local RAS and ET playa role in the progressive glomerular injury, and that the enhanced CNP activity also plays a compensatory role in obstructive uropathy in the glomerulus.
Changes in handling of $Li^+$ by contralateral kidney during acute $Li^+$ loading were investigated immediately after unilateral ureteral obstruction. Carotid artery, jugular vein, renal vein and ureter of experimental animal were catheterized and renal venous flow was shunted to .external jugular vein. In experimental group right ureter was ligated. One to two hours after operation a single shot of LiCl solution (2 mEq/kg) was intravenously injected and then .arterial, renal venous blood and urine samples were taken sequentially for 1 to $1{\frac{1}{2}}$ hours. Urine volume, plasma and urinary concentrations of $Li^+$, $Na^+$ and $K^+$ were measured and urinary excretion of them were calculated. Results obtained were as follows: 1) In experimental group urine volume, urinary excretion of $Na^+$, and $K^+$ by contralateral kidney after unilateral ureteral obstruction were slightly larger than mean value of both kidney in control group. 2) During acute $Li^+$ loading contralateral kidney in experimental group showed limited $K^+$ excretion, but urinary flow and $Na^+$ excretion were comparable to mean value of both kidney in control group. 3) Urinary osmolar concentration in experimental group was much lower than that in control group, and it was maintained at low level even after Li loading. 4) In experimental group plasma$Li^+$ concentration decreased more slowly than in control group after a single shot of LiCl solution. 5) Urinary excretion of $Li^+$ in experimental group was markedly decreased, even lesseer than mean of both kidney in control group. 6) From the above results it was concluded that immediately after unilateral ureteral obstruction contralateral kidney showed normal water and $Na^+$ diuretic response to Li load but urinay $Li^+$ excretion was decreased and reclaimed $Li^+$ to systemic circulation.
Kim, Jee In;Noh, Mi Ra;Yoon, Ga-Eun;Jang, Hee-Seong;Kong, Min Jung;Park, Kwon Moo
The Korean Journal of Physiology and Pharmacology
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제25권2호
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pp.139-146
/
2021
Mitochondrial NADP+-dependent isocitrate dehydrogenase 2 (IDH2) produces NADPH, which is known to inhibit mitochondrial oxidative stress. Ureteral obstruction induces kidney inflammation and fibrosis via oxidative stress. Here, we investigated the role and underlying mechanism of IDH2 in unilateral ureteral obstruction (UUO)-induced kidney inflammation using IDH2 gene deleted mice (IDH2-/-). Eight- to 10-week-old female IDH2-/- mice and wild type (IDH2+/+) littermates were subjected to UUO and kidneys were harvested 5 days after UUO. IDH2 was not detected in the kidneys of IDH2-/- mice, while UUO decreased IDH2 in IDH2+/+ mice. UUO increased the expressions of markers of oxidative stress in both IDH2+/+ and IDH2-/- mice, and these changes were greater in IDH2-/- mice compared to IDH2+/+ mice. Bone marrow-derived macrophages of IDH2-/- mice showed a more migrating phenotype with greater ruffle formation and Rac1 distribution than that of IDH2+/+ mice. Correspondently, UUO-induced infiltration of monocytes/macrophages was greater in IDH2-/- mice compared to IDH2+/+ mice. Taken together, these data demonstrate that IDH2 plays a protective role against UUO-induced inflammation through inhibition of oxidative stress and macrophage infiltration.
Kim, Mi Young;Im, Young Jae;Hyun, Hye Sun;Kang, Hee Gyung;Ha, Il Soo;Cheong, Hae Il;Park, Eujin
Childhood Kidney Diseases
/
제22권1호
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pp.28-31
/
2018
Ureteropelvic junction obstruction is one of the common causes of hydronephrosis in infancy and childhood. Most cases of ureteropelvic junction obstruction are diagnosed prenatally and are usually asymptomatic. Although less common, older children can experience ureteropelvic junction obstruction that presents with symptoms including flank or abdominal pain. Here, we present the case of a nine-year-old healthy girl who had repeated flank pain and abdominal symptoms, with mild left hydronephrosis, for several months. Computed tomography that was performed during the period of acute flank pain revealed aggravated hydronephrosis on her left kidney, which was secondary to an ureteropelvic junction obstruction. She underwent laparoscopic pyeloplasty, and a crossing vessel that passed the ureteropelvic junction was identified. In addition, we reviewed the current literature of this rare entity.
Lin28a has diverse functions including regulation of cancer, reprogramming and regeneration, but whether it promotes injury or is a protective reaction to renal injury is unknown. We studied how Lin28a acts in unilateral ureteral obstruction (UUO)-induced renal fibrosis following unilateral ureteral obstruction, in a mouse model. We further defined the role of Lin28a in transforming growth factor (TGF)-signaling pathways in renal fibrosis through in vitro study using human tubular epithelium-like HK-2 cells. In the mouse unilateral ureteral obstruction model, obstruction markedly decreased the expression of Lin28a, increased the expression of renal fibrotic markers such as type I collagen, α-SMA, vimentin and fibronectin. In TGF-β-stimulated HK-2 cells, the expression of Lin28a was reduced and the expression of renal fibrotic markers such as type I collagen, α-SMA, vimentin and fibronectin was increased. Adenovirus-mediated overexpression of Lin28a inhibited the expression of TGF-β-stimulated type I collagen, α-SMA, vimentin and fibronectin. Lin28a inhibited TGF-β-stimulated SMAD3 activity, via inhibition of SMAD3 phosphorylation, but not the MAPK pathway ERK, JNK or p38. Lin28a attenuates renal fibrosis in obstructive nephropathy, making its mechanism a possible therapeutic target for chronic kidney disease.
Objectives: The objective of this study is to develop a new animal model with Kidney-hypofunction for Sasang Constitutional Medicine, especially for partial Soyangin(one of four constitution which has good digestive function and poor renal function) by Unilateral Ureteral Obstruction, and to estimate the factor related to obesity, dyslipidemia, and metabolic syndrome. Methods: The C57BL/6J mice were divided into 3 groups : normal group, high fat diet(HFD) control group, and HFD group with Unilateral Ureteral Obstruction(UUO). Then, the HFD control group and the experimental group were fed with high fat diet for 6 weeks. Food intake and body weight were measured at regular time by week. After the final experiment, blood was gathered for bloodchemical examination and organs(liver, fatty tissue) were remoed, weighted, and mRNA was analyzed with real-time PCR. Results: The weight growth rate with High fat diet went down by 8.35% in experimental group and had similar FER with the normal group, while HFD control group had higher weight growth rate and FER than any other groups. Also The experimental group had lower triglyceride and LDL cholesterol rate and higher glucose rate in serum. and in mRNA expression, GLUT-9, the protein related to excretion of uric acid and metabolic syndrome, expressed lower rate than that of HFD control group. and IL-6, a kind of cytokine related to obesity and metabolic syndrome, expressed more than HFD control group. Conclusions: It was found that Kidney-hypofunction animal-experimental model is susceptible to metabolic syndrome.
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