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      Spontaneous perirenal urinoma induced by NSAID-associated acute interstitial nephritis

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          Abstract

          Urinoma, defined as the urine leakage beyond the urinary tract, is commonly induced by blunt trauma or urinary tract obstruction by stone, intra-abdominal malignancy, or retroperitoneal fibrosis. Spontaneous urinoma is rare and parenchymal pathologic change is rarely mentioned when urinoma is found. We present a case of a 28-year-old woman with bilateral flank pain induced by spontaneous urinoma. The lady received chronic analgesics because of migraine. After intravenous ketorolac injection, bilateral perirenal urinoma developed. Renal biopsy showed acute interstitial nephritis associated with nonsteroid anti-inflammatory drug (NSAID). After discontinuing the medication, urinoma subsided, and the patient was discharged with normal serum creatinine. This was the first case of urinoma induced by NSAID-related interstitial nephritis, and pathophysiology and management of spontaneous urinoma are discussed.

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          Most cited references 13

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          Association of Individual Non-Steroidal Anti-Inflammatory Drugs and Chronic Kidney Disease: A Population-Based Case Control Study

          Background Non-steroidal anti-inflammatory agents (NSAIDs) are known to be associated with renal damage. No clear evidence exists regarding differential risk of chronic kidney disease (CKD), specifically, across various NSAIDs. Aim The aim of this population-based case-control study was to evaluate the association between use of individual NSAIDs and risk of CKD in a general population of Southern Italy. Methods A nested case-control study was carried out using the general practice Arianna database, identifying incident CKD patients as cases and matched controls from 2006 to 2011. The date of first CKD diagnosis was defined as the index date (ID). Conditional logistic regressions were performed to estimate the risk of CKD associated with NSAIDs by class and individual drugs as compared to non-use during different time windows (within one year, six or three months prior to ID), with the latter being defined as current users. Among current users, the effect of cumulative exposure to these drugs was evaluated. Results Overall, 1,989 CKD cases and 7,906 matched controls were identified. A statistically significant increase in the risk of CKD was found for current users of oxicams (adjusted OR: 1.68; 95% CI: 1.15-2.44) and concerning individual compounds, for ketorolac (adj. OR: 2.54; 95% CI: 1.45-4.44), meloxicam (adj. OR: 1.98; 95% CI: 1.01-3.87) and piroxicam (adj. OR: 1.95; 95% CI: 1.19-3.21). Conclusions The risk of CKD varies across individual NSAIDs. Increased risk has been found for ketorolac, which may precipitate subclinical CKD through acute renal damage, and long-term exposure to oxicams, especially meloxicam and piroxicam.
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            The role of lymphatics in renal inflammation.

            Progressive renal diseases are characterized by tubulointerstitial inflammatory cell recruitment, tubular atrophy and fibrosis. Various aspects of the recruitment of leukocytes have been extensively studied, but the exit routes (i.e. the lymphatic vessels and their biology) have only recently found attention. Similar to the recruitment of inflammatory cells, the exit is coordinated by an orchestrated interaction of chemotactic cytokines and adhesion molecules. During inflammatory injury, new routes are created by the de novo formation of lymphatic vessels, i.e. neolymphangiogenesis. These newly formed lymphatic vessels help to cope with the increase in interstitial fluid related to inflammation. Here, we review some aspects of lymphatic biology and the current knowledge about lymphatic vessels in renal inflammation.
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              Impact of acetylsalicylic acid on tumor angiogenesis and lymphangiogenesis through inhibition of VEGF signaling in a murine sarcoma model.

              Aspirin is a salicylate drug that is widely used, and recently it has been shown to influence the development of various types of cancers. Our previous study revealed that aspirin had an inhibitory effect on the growth of S180 sarcoma and 3AO human ovarian cancer cells. The present study utilized a murine S180 sarcoma model to investigate the molecular mechanisms involved in aspirin-induced tumor growth inhibition. Tumor-bearing mice were randomly divided into five groups with 10 mice in each group: i) control; ii) 5-fluorouracil (5-FU); iii) high-dose aspirin (250 mg/kg); iv) low-dose aspirin (50 mg/kg); and v) combination of 5-FU and aspirin (50 mg/kg). The effect of aspirin on tumor growth was observed by measuring tumor volume and evaluating the antitumor effect. Tumor histology and immunohistochemistry were performed to detect the microvessel density (MVD), lymphatic vessel density (LVD), and the expression levels of vascular endothelial growth factor A (VEGF-A) and VEGF-C. The expression of VEGF-A and VEGF-C was also confirmed and quantified by western blotting. We discovered significant growth delay in murine S180 sarcoma as a result of aspirin treatment. The inhibition rate of tumor growth induced by high-dose and low-dose aspirin was 33.5 and 22.2%, respectively (P<0.05). The expression of VEGF-A and VEGF-C in tumor tissues inhibited by aspirin was demonstrated by immunohistochemistry, and the MVD was decreased in a dose-dependent manner (p<0.05). Reduced LVD was particularly apparent in the high-dose aspirin group (p<0.05). Western blot data showed that the expression of both VEGF-A and VEGF-C was reduced after treatment with aspirin. In conclusion, the impact of aspirin-induced tumor growth delay of murine S180 sarcoma may correlate with the inhibition of angiogenesis and lymphangiogenesis by reducing VEGF-A and VEGF-C expression in tumor tissues.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2018
                23 March 2018
                : 14
                : 595-599
                Affiliations
                [1 ]Department of Internal Medicine, Cardinal Tien Hospital, School of Medicine, Fu-Jen Catholic University, Xin-dian District, New Taipei City, Taiwan, Republic of China
                [2 ]Division of Urology, Department of Surgery, Cardinal Tien Hospital, New Taipei City, Taiwan, Republic of China
                [3 ]Department of Internal Medicine, Cardinal Tien Hospital An-Kang Branch, School of Medicine, Fu-Jen Catholic University, Xin-dian District, New Taipei City, Taiwan, Republic of China
                Author notes
                Correspondence: Ying-Lan Tseng, Department of Internal Medicine, Cardinal Tien Hospital, School of Medicine, Fu-Jen Catholic University, 362 Chung-Cheng Road, Xin-dian District, New Taipei City 23148, Taiwan, Republic of China, Tel +886 22 219 3391, Email switch50@ 123456gmail.com
                Yi-Chou Hou, Department of Internal Medicine, Cardinal Tien Hospital An-Kang Branch, School of Medicine, Fu-Jen Catholic University, 15 Chezi Road, Xin-dian District, New Taipei City 23155, Taiwan, Republic of China, Tel +886 22 212 3066, Email athletics910@ 123456gmail.com
                Article
                tcrm-14-595
                10.2147/TCRM.S155978
                5870632
                © 2018 Chang et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Case Report

                Medicine

                acute kidney injury, ketorolac, interstitial nephritis, spontaneous urinoma, nsaid

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