scholarly journals Biomarkers of Renal Injury in Cirrhosis: Association with Acute Kidney Injury and Recovery after Liver Transplantation

Nephron ◽  
2017 ◽  
Vol 138 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Ashwani K. Singal ◽  
Bradford Jackson ◽  
Glauber B. Pereira ◽  
Kirk B. Russ ◽  
Paul Stephen Fitzmorris ◽  
...  
2017 ◽  
Vol 152 (5) ◽  
pp. S1132
Author(s):  
Ashwani K. Singal ◽  
Bradford Jackson ◽  
Glauber B. Pereira ◽  
Kirk B. Russ ◽  
Paul S. Fitzmorris ◽  
...  

Biomedicines ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 572
Author(s):  
Jung-Yeon Kim ◽  
Jungmin Jo ◽  
Jaechan Leem ◽  
Kwan-Kyu Park

Cisplatin is an effective chemotherapeutic agent, but its clinical use is frequently limited by its nephrotoxicity. The pathogenesis of cisplatin-induced acute kidney injury (AKI) remains incompletely understood, but oxidative stress, tubular cell death, and inflammation are considered important contributors to cisplatin-induced renal injury. Kahweol is a natural diterpene extracted from coffee beans and has been shown to possess anti-oxidative and anti-inflammatory properties. However, its role in cisplatin-induced nephrotoxicity remains undetermined. Therefore, we investigated whether kahweol exerts a protective effect against cisplatin-induced renal injury. Additionally, its mechanisms were also examined. Administration of kahweol attenuated renal dysfunction and histopathological damage together with inhibition of oxidative stress in cisplatin-injected mice. Increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and decreased expression of manganese superoxide dismutase and catalase after cisplatin treatment were significantly reversed by kahweol. Moreover, kahweol inhibited cisplatin-induced apoptosis and necroptosis in the kidneys. Finally, kahweol reduced inflammatory cytokine production and immune cell accumulation together with suppression of nuclear factor kappa-B pathway and downregulation of vascular adhesion molecules. Together, these results suggest that kahweol ameliorates cisplatin-induced renal injury via its pleiotropic effects and might be a potential preventive option against cisplatin-induced nephrotoxicity.


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.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Antoine Dewitte ◽  
Mylène Defaye ◽  
Anissa Dahmi ◽  
Alexandre Ouattara ◽  
Olivier Joannes-Boyau ◽  
...  

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Boby Pratama Putra ◽  
Felix Nugraha Putra

Abstract Background and Aims Orthotopic liver transplantation (OLT) procedure is increased as incremental end-stage liver disease patients’ prevalence. Acute kidney injury (AKI) is one of most common post-OLT complications that is associated with poor renal outcomes and increased mortality risk although the results are still inconclusive. This study aims to measure the risk of deterioration of renal outcomes and mortality risk due to AKI incidence in post-OLT patients. Method We did comprehensive searching using predefined terms in online databases of Pubmed, EMBASE, ScienceDirect, and The Cochrane Library, to include all relevant studies from 2000-2020. We included all cohort studies that reported AKI incidence in post-OLT patients and accessed the risk of 3-month renal replacement therapy (RRT) need, 1-year chronic kidney disease (CKD) progression, and 1-year mortality rate. We used The Newcastle-Ottawa Scale for cohort study for accessing bias risk. We conducted analysis to pooled risk ratio (RR) with 95% confidence interval (CI) using random-effect heterogeneity test. Results We included 10 cohort studies met our inclusion criteria. The AKI incidence significantly both increases the need of RRT in post-OLT patients (pooled RR = 8.41. 95% CI = 2.82 to 25.09, p = 0.0001, I2 = 0%) then leads the CKD progression in one year (pooled RR = 6.76. 95% CI = 2.03 to 22.51, p = 0.002, I2 = 84%). The post-OLT patients who suffered from AKI has significant incremental 1-year mortality risk (pooled RR = 7.27. 95% CI = 4.34 to 12.18, p&lt;0.00001, I2 = 5%). Conclusion The incidence of AKI in post-OLT patients significantly increase the deterioration of renal outcomes and mortality risks. However, further trials are needed to establish the causalities.


2015 ◽  
Vol 6 (1) ◽  
pp. 25-36 ◽  
Author(s):  
Maciej T. Wybraniec ◽  
Katarzyna Mizia-Stec

Background: Contrast-induced acute kidney injury (CI-AKI) remains one of the crucial issues related to the development of invasive cardiology. The massive use of contrast media exposes patients to a great risk of contrast-induced nephropathy and chronic kidney disease development, and increases morbidity and mortality rates. The serum creatinine concentration does not allow for a timely and accurate CI-AKI diagnosis; hence numerous other biomarkers of renal injury have been proposed. Renalase, a novel catecholamine-metabolizing amine oxidase, is synthesized mainly in proximal tubular cells and secreted into urine and blood. It is primarily engaged in the degradation of circulating catecholamines. Notwithstanding its key role in blood pressure regulation, renalase remains a potential CI-AKI biomarker, which was shown to be markedly downregulated in the aftermath of renal injury. In this sense, renalase appears to be the first CI-AKI marker revealing an actual loss of renal function and indicating disease severity. Summary: The purpose of this review is to summarize the contemporary knowledge about the application of novel biomarkers of CI-AKI and to highlight the potential role of renalase as a functional marker of contrast-induced renal injury. Key Messages: Renalase may constitute a missing biochemical link in the mutual interplay between kidney and cardiac pathology known as the cardiorenal syndrome.


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