scholarly journals Risk factors for acute kidney injury following orthotopic liver transplantation: the impact of changes in renal function while patients await transplantation

2010 ◽  
Vol 11 (1) ◽  
Author(s):  
Jose I Iglesias ◽  
John A DePalma ◽  
Jerrold S Levine
2017 ◽  
Vol 37 (6) ◽  
pp. 861-863 ◽  
Author(s):  
Zhi-qiang Zhou ◽  
Long-chang Fan ◽  
Xu Zhao ◽  
Wei Xia ◽  
Ai-lin Luo ◽  
...  

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Thorsten Feldkamp ◽  
Anja Bienholz ◽  
Andreas Paul ◽  
Fuat H. Saner

Abstract Background: Patients following liver transplantation are at risk to develop acute kidney injury (AKI). The aim of our study was to assess risk factors for the development of AKI and the impact of AKI on the outcome of patients after liver transplantation (OLT). Patients and methods: In this retrospective study, we analyzed 149 patients undergoing OLT from 1/2004 to 12/2007. AKI was defined according to the KDIGO definition representing the AKIN and the RIFLE classification, and according to the need for renal replacement therapy (RRT). Results: According to the AKIN criteria alone 14 patients, according to the RIFLE criteria alone no patient and according to both definitions 30 patients developed AKI. RRT was required in 54 patients experiencing AKI, whereas 51 patients did not develop AKI. Pre OLT serum creatinine (SCr) significantly predicted the development of AKI requiring RRT, but not AKI without RRT requirement. Survival rate was significantly inferior after 28 days, one or three years in patients with AKI requiring RRT (70.4, 46.4, 44.4% vs. 100, 92.2, 90.2%, P < 0.001). There was no difference in survival between patients experiencing AKI according to the RIFLE or AKIN criteria without RRT requirement and patients without AKI. Conclusion: Pre OLT renal dysfunction assessed by SCr was the most important risk factor predicting severe forms of AKI, but not milder forms of AKI. AKI requiring RRT had a detrimental impact on patients’ survival, whereas milder forms of AKI were not associated with a worse outcome.


BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Maurice J. D. L. van der Vorst ◽  
Elisabeth C. W. Neefjes ◽  
Elisa C. Toffoli ◽  
Jolanda E. W. Oosterling-Jansen ◽  
Marije R. Vergeer ◽  
...  

Abstract Background Three-weekly high-dose cisplatin (100 mg/m2) is considered the standard systemic regimen given concurrently with postoperative or definitive radiotherapy in locally advanced squamous cell carcinoma of the head and neck (LA-SCCHN). Concurrent chemoradiation (CRT) with high-dose cisplatin is associated with significant acute and late toxicities, including acute kidney injury (AKI). The aims of this study were to investigate the incidence of AKI in patients with LA-SCCHN during and after treatment with high-dose cisplatin-based CRT, to identify risk factors for cisplatin-induced AKI, and to describe the impact of AKI on long-term renal function and treatment outcomes. Methods This is a retrospective cohort study with measurements of renal function before CRT, weekly during CRT, every 1 or 2 days during hospitalizations, and 3 and 12 months after CRT in patients with LA-SCCHN. AKI was defined as increase in serum creatinine (sCr) of ≥1.5 times baseline or by ≥0.3 mg/dL (≥26.5 μmol/L) using the Kidney Disease Improving Global Outcomes (KDIGO) classification. Logistic regression models were estimated to analyze renal function over time and to identify predictors for AKI. Results One hundred twenty-four patients completed all measurements. AKI was reported in 85 patients (69%) with 112 episodes of AKI. Sixty of 85 patients experienced 1 AKI episode; 20 patients experienced ≥2 AKI episodes. Ninety-three (83%) AKI episodes were stage 1, 13 (12%) were stage 2, and 6 (5%) AKI episodes were stage 3. Median follow-up time was 29 months (Interquartile Range, IQR 22–33). Hypertension (Odds Ratio, OR 2.7, 95% Confidence Interval, CI 1.1–6.6; p = 0.03), and chemotherapy-induced nausea and vomiting (CINV; OR 4.3, 95% CI 1.6–11.3; p = 0.003) were associated with AKI. In patients with AKI, renal function was significantly more impaired at 3 and 12 months post-treatment compared to patients without AKI. AKI did not have a negative impact on treatment outcomes. Conclusion AKI occurred in 69% of patients with LA-SCCHN undergoing CRT with high-dose cisplatin. Long-term renal function was significantly more impaired in patients with AKI. Hypertension and CINV are significant risk factors. Optimizing prevention strategies for CINV are urgently needed.


2017 ◽  
Vol 41 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Hakan K. Atalan ◽  
Bulent Gucyetmez ◽  
Serdar Aslan ◽  
Serafettin Yazar ◽  
Kamil Y. Polat

Purpose: There are many risk factors for postoperative acute kidney injury in liver transplantation. The aim of this study is to investigate the risk factors for postoperative acute kidney injury in living donor liver transplantation recipients. Methods: 220 living donor liver transplantation recipients were retrospectively evaluated in the study. According to the Kidney Disease Improving Global Outcomes Guidelines, acute kidney injury in postoperative day 7 was investigated for all patients. The patient’s demographic data, preoperative and intraoperative parameters, and outcomes were recorded. Results: Acute kidney injury was found in 27 (12.3%) recipients. In recipients with acute kidney injury, female population, model for end-stage liver disease score, norepinephrine requirement, duration of mean arterial pressure less than 60 mmHg, the usage of gelatin and erythrocyte suspension and blood loss were significantly higher than recipients with nonacute kidney injury (for all p<0.05). In multivariate analyses, the likelihood of acute kidney injury on postoperative day 7 were increased 2.8-fold (1.1-7.0), 2.7-fold (1.02-7.3), 3.4-fold (1.2-9.9) and 5.1-fold (1.7-15.0) by postoperative day 7, serum tacrolimus level ≥10.2 ng dL−1, intraoperative blood loss ≥14.5 mL kg−1, the usage of gelatin >5 mL kg−1 and duration of MAP less than 60 mmHg ≥5.5 minutes respectively (for all p<0.05). Conclusions: In living donor liver transplantation recipients, serum tacrolimus levels, intraoperative blood loss, hypotension period and the usage of gelatin may be risk factors for acute kidney injury in the early postoperative period.


2015 ◽  
Vol 122 (1) ◽  
pp. 72-86 ◽  
Author(s):  
Chenfang Luo ◽  
Dongdong Yuan ◽  
Xiaoyun Li ◽  
Weifeng Yao ◽  
Gangjian Luo ◽  
...  

Abstract Background: Postliver transplantation acute kidney injury (AKI) severely affects patient survival, whereas the mechanism is unclear and effective therapy is lacking. The authors postulated that reperfusion induced enhancement of connexin32 (Cx32) gap junction plays a critical role in mediating postliver transplantation AKI and that pretreatment/precondition with the anesthetic propofol, known to inhibit gap junction, can confer effective protection. Methods: Male Sprague–Dawley rats underwent autologous orthotopic liver transplantation (AOLT) in the absence or presence of treatments with the selective Cx32 inhibitor, 2-aminoethoxydiphenyl borate or propofol (50 mg/kg) (n = 8 per group). Also, kidney tubular epithelial (NRK-52E) cells were subjected to hypoxia–reoxygenation and the function of Cx32 was manipulated by three distinct mechanisms: cell culture in different density; pretreatment with Cx32 inhibitors or enhancer; Cx32 gene knock-down (n = 4 to 5). Results: AOLT resulted in significant increases of renal Cx32 protein expression and gap junction, which were coincident with increases in oxidative stress and impairment in renal function and tissue injury as compared to sham group. Similarly, hypoxia–reoxygenation resulted in significant cellular injury manifested as reduced cell growth and increased lactate dehydrogenase release, which was significantly attenuated by Cx32 gene knock-down but exacerbated by Cx32 enhancement. Propofol inhibited Cx32 function and attenuated post-AOLT AKI. In NRK-52E cells, propofol reduced posthypoxic reactive oxygen species production and attenuated cellular injury, and the cellular protective effects of propofol were reinforced by Cx32 inhibition but cancelled by Cx32 enhancement. Conclusion: Cx32 plays a critical role in AOLT-induced AKI and that inhibition of Cx32 function may represent a new and major mechanism whereby propofol reduces oxidative stress and subsequently attenuates post-AOLT AKI.


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