Cytokine elevation and transaminitis after laparoscopic donor nephrectomy

2012 ◽  
Vol 302 (9) ◽  
pp. F1104-F1111 ◽  
Author(s):  
Steven Yap ◽  
Sang Won Park ◽  
Brian Egan ◽  
H. Thomas Lee
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Systemic Inflammation ◽  
Kidney Injury ◽  
Donor Nephrectomy ◽  
Enzyme Linked Immunosorbent Assay ◽  
Urinary Ngal ◽  
Laparoscopic Donor Nephrectomy ◽  
Potential Marker ◽  
Tnf Α

Acute kidney injury frequently occurs in the critically ill and often progresses into multiorgan dysfunction syndrome, resulting in high mortality. We previously showed that nephrectomized mice had increased interleukin (IL)-6 and tumor necrosis factor (TNF)-α that directly contributed to systemic inflammation and hepatic injury. In this study, we examined whether patients undergoing laparoscopic donor nephrectomy have increased postoperative cytokine levels with injury to the liver and whether the remaining kidney sustains injury. Serial serum and urine samples were collected from 32 patients undergoing laparoscopic donor nephrectomy and 17 patients undergoing nonrenal laparoscopic surgery. Serum IL-6, IL-18, TNF-α and monocyte chemotactic protein-1 (MCP-1) (markers of systemic inflammation) and urinary neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), MCP-1, and IL-18 (markers of acute kidney injury) were quantified by enzyme-linked immunosorbent assay. We also analyzed serum creatinine, aspartate transaminase (AST), and alanine transaminase to assess liver injury. Patients who underwent donor nephrectomy not only demonstrated increased serum creatinine but also had significant increases in serum IL-6, MCP-1, and AST. Serum TNF-α also trended upward in donor nephrectomy patients. Finally, the donor nephrectomy group showed increased urinary NGAL but not KIM-1 at 24 h. Taken together, our findings of increased serum IL-6, MCP-1, and AST after donor nephrectomy suggest that an acute reduction of kidney function induces systemic inflammation and may have distant effects on the liver. Further studies are needed to correlate increased urinary NGAL after donor nephrectomy both as a potential marker for renal tubular stress and/or hypertrophy in the contralateral kidney.

TAK-242 Attenuates Crush Injury Induced Acute Kidney Injury through Inhibiting TLR4/NF-κB Signaling Pathways in Rats

2020 ◽  
Vol 35 (6) ◽  
pp. 619-628
Author(s):  
Jinxiang Wang ◽  
Zhiguo Chen ◽  
Shike Hou ◽  
Ziquan Liu ◽  
Qi Lv
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Signaling Pathways ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Crush Injury ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Tnf Α ◽  
Blood Potassium

AbstractBackground:To investigate if toll-like receptor (TLR) 4/nuclear factor-kappa B (NF-κB) signaling pathways mediated crush injury induced acute kidney injury (AKI) in rats, and if TAK-242 (a specific inhibitor of TLR4) attenuates the injury through inhibiting the signaling pathways.Methods:This study was divided into two parts: (1) Establish the crush injury model: 50 rats were randomly divided into control group and four crush injury groups (n = 10/group). Crush injury groups were given 3kg pressure for eight hours and were sacrificed at the time points of 0h, 6h, 12h, and 24h after relieving pressure. And (2) Select the most obvious injury group (12h group) for drug intervention group. Thirty rats were randomly divided into control group, 12h group, and 12h+TAK-242 group (n = 10/group). Two parts detection were as follows: pathological changes of kidney tissues were observed in Haematoxylin and Eosin (HE) staining. Serum creatinine, blood urea nitrogen (BUN), myoglobin (Mb), and blood potassium were examined by automatic biochemical analysis instrument. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay (ELISA). The TLR4 messenger ribonucleic acid (mRNA), TLR4, and P65 were detected by real-time polymerase chain reaction (PCR), western blot, immunohistochemistry staining.Results:Compared with the control group, kidney tissues were damaged in crush injury groups, and most obvious in the 12h group. The level of serum creatinine, BUN, Mb, blood potassium, IL-6, TNF-α, and TLR4mRNA were increased in the crush injury groups and significantly increased in the 12h group (P <.05). The TLR4 and P65 were significantly increased in the 12h group (P <.05). Compared with the 12h group, kidney tissue damage was significantly reduced in the TAK-242 group (P <.05). The level of serum creatinine, BUN, Mb, blood potassium, IL-6, TNF-α, TLR4mRNA, TLR4, and P65 in the TAK-242 group were significantly reduced (P <.05).Conclusion:The present findings conclude that TLR4/NF-κB signaling pathways mediated crush injury induced AKI in rats, and TAK-242 attenuates the injury through inhibiting the signaling pathways.

Evaluation of urinary neutrophil gelatinase-associated lipocalin and urinary kidney injury molecule-1 as biomarkers of renal function in cancer patients treated with cisplatin

2020 ◽  
Vol 26 (7) ◽  
pp. 1643-1649
Author(s):  
Elliyeh Ghadrdan ◽  
Sholeh Ebrahimpour ◽  
Sanambar Sadighi ◽  
Samira Chaibakhsh ◽  
Zahra Jahangard-Rafsanjani
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Characteristic Curve ◽  
Kidney Injury ◽  
Acute Kidney Injury Network ◽  
The Novel ◽  
Urinary Ngal ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Kidney Injury Molecule 1 ◽  
Neutrophil Gelatinase

Introduction Cisplatin-associated acute kidney injury (AKI) is the major limitation to the use of cisplatin-based chemotherapy regimens. Serum creatinine as a traditional marker did not increase in a timely enough fashion in AKI patients. Therefore, recently, the novel markers such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were considered for early detection of AKI. The aim of this study was to compare the sensitivity and specificity of urinary NGAL and KIM-1 with serum creatinine in cisplatin related AKI. Methods Patients ≥18 years with solid tumors who received cisplatin-based chemotherapy were included. Urine samples were collected 0, 6 and 24 h after cisplatin infusion and the urinary NGAL, KIM-1, and creatinine concentrations were evaluated. NGAL and KIM-1 concentrations were adjusted based on urine creatinine to eliminate hydration effects. Serum creatinine levels were assessed at the base and 72 h after cisplatin administration. Results Seven out of the 35 recruited patients (20%) suffered from AKI defined by Acute Kidney Injury Network criteria. In AKI patients, the ratio of urinary KIM-1–creatinine at 24 h compared to baseline (24 h/baseline) and NGAL–creatinine 24 h/baseline were significantly higher than those of non-AKI group ( p = 0.037 and 0.047 respectively). The area under the receiver-operating characteristic curve for KIM-1–creatinine 24 h/baseline and NGAL–creatinine 24 h/baseline were 0.78 (0.59–0.96, p = 0.032) and 0.77 (0.57–0.97, p = 0.036) respectively. Conclusions Our findings showed that the changes in urinary NGAL–creatinine and KIM-1–creatinine ratios, 24 h after cisplatin administration can be utilized to predict AKI in cisplatin recipients.

scholarly journals P0521TICAGRELOR PROTECTS KIDNEY FROM SEPSIS INDUCED ACUTE KIDNEY INJURY THROUGH ADENOSINE DEPENDENT WAY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yuhan Cao ◽  
Qiancheng Xu ◽  
Yuwei Wang ◽  
Cong Fu
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Western Blot ◽  
Receptor Antagonist ◽  
Adenosine Receptor ◽  
Kidney Injury ◽  
Tunel Staining ◽  
Adenosine Receptor Antagonist ◽  
Tnf Α ◽  
Pas Staining

Abstract Background and Aims Sepsis induced acute kidney injury (AKI) is common in intensive care unit in multiple organ failure patients. Ticagrelor is an anti-platelet drug that widely applied in coronary artery disease. In addition, ticagrelor can increase the level of adenosine. Recent study had indicated that ticagrelor can protect renal function in sepsis induced AKI. However, the detailed mechanism was still unknown. Accordingly, we designed this trial to investigate if the ticagrelor alleviated sepsis induced AKI and demonstrated the potential mechanism that how ticagrelor works. Method C57BL6J mouse received oral ticagrelor (20mg/kg and 50mg/kg) for 7 days and caecum ligation and puncture (CLP) were performed. Adenosine-receptor antagonist was administered (10mg/kg, intraperitoneal injection) to block the adenosine pathway 2h before CLP. After 24h, serum creatinine was measured. PAS staining was used and TUNEL staining was applied to determine the pathological changes and cell apoptosis. Plasma concentrations of TNF-α and IL-1β were detected. Kidney tissue level of TNF-α and IL-1β were determined via qRT-PCR. Western blot was used to determine the expression of signal molecular in kidney. Results In ticagrelor group, PAS staining (fig. 1) showed that less swelling of renal tubules and TUNEL staining (fig. 2) showed the less cell apoptosis compared to CLP. Serum creatinine was significantly lower in ticagrelor group. Plasma TNF-α and IL-1β and kidney expression of TNF-α and IL-1β were significantly lower in ticagrelor group. Adenosine-receptor antagonist significantly blocked the effect of ticagrelor (fig. 3 ang 4). Western blot showed that ticagrelor activate the phosphorylation of AKT and mTOR in kidney. Adenosine-receptor antagonist inhibited the activation of AKT and mTOR (fig. 5). Conclusion The protective effect of ticagrelor was dependent on adenosine-receptor activation with downstream upregulation of phosphorylation of AKT and mTOR in sepsis induced AKI.

scholarly journals Early Identification of Acute Kidney Injury after Bariatric Surgery: Role of NGAL and Cystatin C

2014 ◽  
Vol 6 (1) ◽  
pp. 50-59
Author(s):  
Sidoti Anna ◽  
Giacalone Marilu ◽  
Abramo Antonio ◽  
Anselmino Marco ◽  
Carlo Donadio ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Cystatin C ◽  
Kidney Injury ◽  
Urinary Ngal ◽  
Paired Data ◽  
Serum Cystatin C ◽  
Serum Cystatin ◽  
Significant Difference

Background: The aim of our study was to evaluate plasmatic and urinary NGAL and serum cystatin C as early diagnostic markers of acute kidney injury in obese patients undergoing bariatric surgery. Methods: For this this prospective observational study, we recruited 23 patients undergoing gastric by-pass or sleeve gastrectomy, and admitted to the Low Dependence Unit after the surgery. Plasma NGAL (pNGAL), urinary NGAL (uNGAL), serum cystatin C, serum creatinine, and serum urea were measured before surgery as well as 10 h and 24 h after surgery. Mean values of pNGAL, uNGAL, cystatin C, creatinine, and urea concentrations of pre- and post-surgery periods were compared using Student’s t test for paired data. We also evaluated the presence of correlation between modifications of NGAL and cystatin C after surgery and fluid balance, hydration (ml/kg) and diuresis using Pearson’s coefficient of correlation. Results: No patient developed AKI according to the AKIN criteria. pNGAL was significantly higher at T10h than T0 (p=0.004). There was no significant difference between uNGAL at T0 and T10h (p=0.53) and between uNGAL at T0 and T24h (p=0.31). uNGAL at T was significantly higher in comparison to T10h (p=0.024). uNGAL concentrations were normal in all patients at every time step. Cystatin C concentration did not increase after surgery. Serum creatinine level was significantly higher at T48h, despite being still within the normal range, when compared to T0 (p=0.038). Conclusion: Our study shows that pNGAL can reflect mild tubular damage as its levels increase within a few hours from surgery and return to normal limits afterwards. Concerning uNGAL, there is a minimal increase at T24h, when NGAL concentration in plasma has already decreased. Serum cystatin C does not show any relevant kidney changes, or at least, no more than those ones shown by pNGAL.

scholarly journals The role of hepatocellular death and systemic inflammation in the development of acute kidney injury in acute decompensation of alcoholic liver cirrhosis

2021 ◽  
pp. 66-71
Author(s):  
A. S. Rodina ◽  
M. E. Shubina ◽  
I. V. Kurbatova ◽  
L. V. Topchieva ◽  
O. P. Dudanova
Keyword(s):  
Acute Kidney Injury ◽  
Systemic Inflammation ◽  
Kidney Injury ◽  
Alcoholic Liver Cirrhosis ◽  
Group I ◽  
Tnf Α ◽  
Acute Decompensation ◽  
Group Ii ◽  
Hepatocellular Death

The aim of the study was to assess the role of hepatocellular death and systemic inflammation in the development of acute kidney injury (AKI) in acute decompensation of alcoholic liver cirrhosis (AD ALC).Materials and methods. 125 patients with ALC were examined: 20 (16.0%) (group I) with signs of hepatorenal syndromeacute kidney injury (HRS-AKI) at the age of 57.13 ± 9,08 years, 13 men (65.0%) and 105 (84.0%) patients (group II) without such a syndrome at the age of 56.30 ± 9.6 years., 62 men (59.0%). Along with liver tests, a markers of hepatocyte apoptosis and cytokines were determined by ELISA: fragments of cytokeratin-18 (FCK-18) ("Biotech" Sweden), cytokines — TNF-α, IL-1β, IL-4, IL-6, IL-8 (“Vector-Best”, Russia). Grade and index of acute on chronic liver failure (ACLF) were determined using an on-line calculator (www.efclif.com/scientific-activity/score-calculators/clif-c-aclf).Results. The hepatocellular death indicators were significantly higher in patients of group I with HRS-AKI compared with patients of group II without HRS-AKI: FCK-18-1609.44 ± 542.79 U / l versus 975.77±607.59 U / l, bilirubin — 242.64 ± 98.14 pmol/l versus 145.09 ± 79.35 pmol/l, inflammation indicators — TNF-α — 9.28 ± 3,11 pg/ml versus 6.59 ± 2.21 pg/ml, IL-6-54.79 ± 17.7 pg/ml versus 36.71 ± 18.05 pg/ml, CRP — 49.68 ± 23.23 mg/l versus 22.07 ± 20.40 mg/l, leukocytes — 12.23 ± 3.28x109/l versus 8,66 ± 2,31x109/l (everywhere p <0.05). ACLF developed in all (100.0%) patients of group I, its grade was 2.73±0.76 and score — 56.33 ± 4.01; ACLF developed only in 37 (35,2%) patients of group II, its grade was1.05±0.24 (p<0,05) and score was 47.45 ± 4,80 (p <0.05).Conclusion. The development of HRS-AKI in patients with acute decompensation of ALC was associated with significantly higher rates of hepatocytic apoptosis, hyperbilirubinemia, systemic inflammation, frequency and severity of ACLF.

PO-0634 Factors Limiting Usefulness Of Serum And Urinary Ngal As A Marker Of Acute Kidney Injury In Preterm Newborns

2014 ◽  
Vol 99 (Suppl 2) ◽  
pp. A461.2-A461
Author(s):  
A Suchojad ◽  
M Smertka ◽  
A Tarko ◽  
M Majcherczyk ◽  
A Brzozowska ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Urinary Ngal ◽  
Preterm Newborns

scholarly journals Perioperative use of serum creatinine and postoperative acute kidney injury: a single-centre, observational retrospective study to explore physicians’ perception and practice

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Gianluca Villa ◽  
Silvia De Rosa ◽  
Caterina Scirè Calabrisotto ◽  
Alessandro Nerini ◽  
Thomas Saitta ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Retrospective Study ◽  
High Risk ◽  
Abdominal Surgery ◽  
Serum Creatinine ◽  
Malignant Disease ◽  
Kidney Injury ◽  
Major Surgery ◽  
Single Centre

Abstract Background Postoperative acute kidney injury (PO-AKI) is a leading cause of short- and long-term morbidity and mortality, as well as progression to chronic kidney disease (CKD). The aim of this study was to explore the physicians’ attitude toward the use of perioperative serum creatinine (sCr) for the identification of patients at risk for PO-AKI and long-term CKD. We also evaluated the incidence and risk factors associated with PO-AKI and renal function deterioration in patients undergoing major surgery for malignant disease. Methods Adult oncological patients who underwent major abdominal surgery from November 2016 to February 2017 were considered for this single-centre, observational retrospective study. Routinely available sCr values were used to define AKI in the first three postoperative days. Long-term kidney dysfunction (LT-KDys) was defined as a reduction in the estimated glomerular filtration rate by more than 10 ml/min/m2 at 12 months postoperatively. A questionnaire was administered to 125 physicians caring for the enrolled patients to collect information on local attitudes regarding the use of sCr perioperatively and its relationship with PO-AKI. Results A total of 423 patients were observed. sCr was not available in 59 patients (13.9%); the remaining 364 (86.1%) had at least one sCr value measured to allow for detection of postoperative kidney impairment. Among these, PO-AKI was diagnosed in 8.2% of cases. Of the 334 patients who had a sCr result available at 12-month follow-up, 56 (16.8%) developed LT-KDys. Data on long-term kidney function were not available for 21% of patients. Interestingly, 33 of 423 patients (7.8%) did not have a sCr result available in the immediate postoperative period or long term. All the physicians who participated in the survey (83 out of 125) recognised that postoperative assessment of sCr is required after major oncological abdominal surgery, particularly in those patients at high risk for PO-AKI and LT-KDys. Conclusion PO-AKI after major surgery for malignant disease is common, but clinical practice of measuring sCr is variable. As a result, the exact incidence of PO-AKI and long-term renal prognosis are unclear, including in high-risk patients. Trial registration ClinicalTrials.gov, NCT04341974.

The Effect of a Short Course of Tocolytic Indomethacin on Urinary Biomarkers in Premature Infants

2021 ◽  
Author(s):  
Ahmad El Samra ◽  
Ayesa Mian ◽  
Marc Lande ◽  
Hongyue Wang ◽  
Ronnie Guillet
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Kidney Injury ◽  
Urinary Biomarkers ◽  
Bivariate Analysis ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Short Course ◽  
Medication Exposure ◽  
Epidermal Growth ◽  
Neutrophil Gelatinase

Objective The aim of this study was to determine the effects of a 2-day prenatal course of indomethacin on the premature kidney as reflected by serum creatinine and urinary biomarkers. Study Design Urine of infants ≤ 32 weeks was collected for the first 14 days and analyzed for cystatin C, neutrophil gelatinase-associated lipocalin, osteopontin, β2 microglobulin, epidermal growth factor, uromodulin, and microalbumin. Bivariate analysis compared serum creatinine and biomarkers of exposed (INDO) and unexposed (CONT) subjects. Results Fifty-seven infants (35 CONT and 22 INDO) were studied. The cohorts were similar in gestational age, birthweight, race, gender, nephrotoxic medication exposure, and Apgar scores. CONT had more dopamine exposure and included more pre-eclamptic mothers (p = 0.005). No difference in creatinine-based acute kidney injury or the log transformed mean, maximum, and minimum values of urinary biomarkers was detected. Conclusion Our findings suggest that a short course of tocolytic indomethacin does not result in neonatal acute kidney injury. Key Points

scholarly journals NEAT1 aggravates sepsis-induced acute kidney injury by sponging miR-22-3p

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 333-342
Author(s):  
Yawei Feng ◽  
Jun Liu ◽  
Ranliang Wu ◽  
Peng Yang ◽  
Zhiqiang Ye ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Noncoding Rna ◽  
Cell Injury ◽  
Kidney Injury ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Western Blot Assay

AbstractBackground and aimAcute kidney injury (AKI) is a common complication of sepsis. Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays a vital role in various diseases, including AKI. This study aimed to investigate the function and mechanism of NEAT1 in sepsis-induced AKI.Materials and methodsA septic AKI model was established by treating HK-2 cells with lipopolysaccharide (LPS). The levels of NEAT1 and miR-22-3p were measured by quantitative real-time PCR. Cell apoptosis was assessed by flow cytometry. The levels of apoptosis-related protein and autophagy-related factors were examined by the western blot assay. An enzyme-linked immunosorbent assay was used to calculate the contents of inflammatory factors. The interaction between NEAT1 and miR-22-3p was validated by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. The levels of nuclear factor (NF)-κB pathway-related proteins were evaluated by the western blot assay.ResultsNEAT1 was upregulated, while miR-22-3p was downregulated in patients with sepsis and in LPS-stimulated HK-2 cells. LPS treatment triggered cell apoptosis, autophagy, and inflammatory response in HK-2 cells. NEAT1 knockdown attenuated LPS-induced cell injury. NEAT1 modulated LPS-triggered cell injury by targeting miR-22-3p. Furthermore, NEAT1 regulated the NF-κB pathway by modulating miR-22-3p.ConclusionDepletion of NEAT1 alleviated sepsis-induced AKI via regulating the miR-22-3p/NF-κB pathway.

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