scholarly journals Patency period of a metallic ureteral stent and its determinants in patients with malignant ureteral obstruction: a prospective review

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Yasuyuki Kobayashi ◽  
Hiroki Arai ◽  
Masahito Honda

Abstract Background Malignant ureteral obstruction caused by extrinsic compression of a primary malignant tumour or by metastatic disease is an indicator of poor prognosis with a median life expectancy of about one year. We examined clinical outcomes following Resonance Metallic Ureteral Stent (Cook Medical, Bloomington, IN) placement in patients with malignant ureteral obstruction. Methods This was a prospective study of patients with malignant ureteral obstruction who underwent Resonance Metallic Ureteral Stent placement from April 2016 to March 2021. We registered 21 patients (27 collecting systems) with malignant ureteral obstruction and observed them prospectively. The patients first underwent polymer ureteral stent placement followed by replacement with a metallic ureteral stent one month later. Primary outcome was the metallic ureteral stent patency period based on both serum creatinine and the level of hydronephrosis; secondary outcomes were factors affecting patency period and stent-related complications such as symptoms of obstruction (flank pain), bladder irritation, haematuria, and urinary tract infection (presence or absence of fever). Results The study comprised 21 patients (six men, 15 women) with a mean age of 72 years. The median stent patency period in days was not available (NA) (95% CI 210–NA) due to the inability to extract this value from the Kaplan–Meier curve because the event rate did not reach 50%, and the one-year patency rate was 59.2% (95% CI 23.2–82.9). A normal serum creatinine (0.65 to 1.07 mg/dL for men and 0.46 to 0.79 mg/dL for women) one week after polymer ureteral stent placement was a significant factor affecting the long-term metallic ureteral stent patency period. There were no major complications. Conclusion The Resonance Metallic Ureteral Stent was effective and safe for patients with malignant ureteral obstruction. A normal serum creatinine level one week after placement of a polymer ureteral stent may predict a longer patency period of metallic ureteral stents in patients with malignant ureteral obstruction.

2011 ◽  
Vol 22 (7) ◽  
pp. 1012-1016 ◽  
Author(s):  
Hung-Chieh Chen ◽  
Shu-Huei Shen ◽  
Jia-Hwia Wang ◽  
William J.S. Huang ◽  
Hsiou-Shan Tseng ◽  
...  

2018 ◽  
Vol 252 (6) ◽  
pp. 721-731 ◽  
Author(s):  
Philippa R. Pavia ◽  
Allyson C. Berent ◽  
Chick W. Weisse ◽  
Dana Neiman ◽  
Kenneth Lamb ◽  
...  

2010 ◽  
Vol 19 (5) ◽  
pp. 278-286 ◽  
Author(s):  
Alberto Mazza ◽  
Domenico Montemurro ◽  
Antonio Piccoli ◽  
Antonio Pagnan ◽  
Achille Cesare Pessina ◽  
...  

2018 ◽  
Vol 19 (4) ◽  
pp. 606 ◽  
Author(s):  
Jong Woo Kim ◽  
Bumsik Hong ◽  
Ji Hoon Shin ◽  
Jihong Park ◽  
Jin Hyoun Kim ◽  
...  

2008 ◽  
Vol 24 (1) ◽  
pp. 86-92 ◽  
Author(s):  
O. Kenrik Duru ◽  
Roberto B. Vargas ◽  
Dulcie Kermah ◽  
Allen R. Nissenson ◽  
Keith C. Norris

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 1073-1073
Author(s):  
Elizabeth H Phillips ◽  
John Connolly ◽  
John-Paul Westwood ◽  
Siobhan McGuckin ◽  
Daniel P Gale ◽  
...  

Abstract Increasing understanding of abnormalities within the alternative complement pathway in atypical hemolytic uremic syndrome (aHUS) is changing the way the disease is both diagnosed and treated. It is rarely possible to definitively diagnose aHUS at the time of initial acute presentation and treatment, with plasma exchange, is initiated on clinical grounds. With the risk of further acute episodes and increasing availability of terminal complement inhibitors accurate molecular diagnosis is imperative. Aim to determine the clinical phenotype and nature of complement abnormalities within a cohort of aHUS patients referred to a large thrombotic thrombocytopenic purpura (TTP) referral centre. Patients and methods Data from 14 patients with a clinical diagnosis of aHUS was retrospectively analysed. 13 patients were referred with thrombotic microangiopathy not initially requiring renal replacement therapy (RRT). 1 patient presented to another institution requiring urgent RRT and was subsequently transferred to our care following recovery of renal function. All patients had ADAMTS13 levels above 30% and negative anti-ADAMTS13 antibody levels at presentation to exclude a diagnosis of TTP. 3 patients had diarrhoea at presentation; all were enterotoxin negative. Patients were subsequently assessed for mutations within complement factors H (CFH), I (CFI), B (CFB), C3 and membrane cofactor protein (MCP), at risk haplotypes and CFH antibodies. A control group of 14 acute acquired TTP patients with confirmed ADAMTS13 levels <5% were assessed for the same abnormalities within complement regulatory proteins. Results In the aHUS cohort, the median age of presentation was 25.5 years (11 months to 72 years). The median serum creatinine was 275 µmol/l (range 79-1812 µmol/l), platelet count 27 x109/l (10-115) and LDH was 2016 IU (342-4621). In the TTP group, presenting creatinine was 106 µmol/l (61-353) µmol/l, platelets 13 x109/l (5-74) and LDH 1954 IU (756-3518). aHUS precipitants at initial presentation or relapse included pregnancy (n=2), upper respiratory tract infection (n=6), vaccination (n=1), abdominal sepsis (n=4). In 3 cases, there was no identified trigger. Headache was a common presenting symptom; only one hypertensive patient (72 years) had a transient ischemic attack; no other neurological events were documented in the aHUS group. In 57% (8/14 patients) variants of the alternative complement pathway were identified; 5 with MCP mutations, encoding p.R59X, p.C157Y (present in 2 brothers), p.C64F and c.286+2T>C/c.286+2T>G (both present in the same patient); 2 with CFH mutations, encoding c.3134-5T>C and p.R1215X; and 1 with a CFB mutation (p.D371G). All of the mutations identified, except CFH c.3134-5T>C, are of clear functional significance. 2 of the patients with MCP mutations had a normal serum creatinine at presentation. C3/4 levels were low in 3/8 patients. In the control group of TTP patients with ADAMTS13 <5% no complement mutations were identified. 13/14 aHUS patients were treated initially with plasma exchange; 1 received eculizumab subsequently. 3 patients required temporary RRT and 1 died within 24 hours of presentation with progressive cardiorespiratory failure. At follow-up, all patients had platelet counts >150 x109/l and 12/13 had normal serum creatinine levels; one patient had a creatinine of 122 µmol/l. 5/13 patients had recurrent episodes, 4 of whom had confirmed complement pathway abnormalities (3 MCP mutated, 1 CFB mutated). None required long-term RRT or progressed to end-stage renal failure (ESRD) at a median follow-up of 2 years (range 0.25-28 years). Conclusions This aHUS cohort, without ESRD, demonstrates the difficulty in clinically differentiating TTP from complement mediated TMAs. We demonstrate that diagnostic differentiation based on platelet count, renal function and serum C3/C4 levels is insufficient to predict an underlying complement mutation. This distinction is increasingly important with the proven efficacy of complement inhibitor therapy in targeting complement activation in aHUS. Specifically, we demonstrate a very high frequency of functionally significant MCP mutations which mimic relapsing/remitting TTP. An ADAMTS13 activity >5% in a patient with a TMA should necessitate genetic screening for complement gene mutations prior to consideration of complement inhibitor therapy. Disclosures: No relevant conflicts of interest to declare.


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