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2008, Clinical Journal of the American Society of Nephrology
The evaluation and initial management of patients with acute kidney injury (AKI) should include: (1) an assessment of the contributing causes of the kidney injury, (2) an assessment of the clinical course including comorbidities, (3) a careful assessment of volume status, and (4) the institution of appropriate therapeutic measures designed to reverse or prevent worsening of functional or structural kidney abnormalities. The initial assessment of patients with AKI classically includes the differentiation between prerenal, renal, and postrenal causes. The differentiation between so-called "prerenal" and "renal" causes is more difficult, especially because renal hypoperfusion may coexist with any stage of AKI. Using a modified Delphi approach, the multidisciplinary international working group, generated a set of testable research questions. Key questions included the following: Is there a difference in prognosis between volume-responsive and volume-unresponsive AKI? Are there biomarkers whose patterns (dynamic changes) predict the severity and recovery of AKI (maximal stage of AKI, need for RRT, renal recovery, mortality) and guide therapy? What is the best biomarker to assess prospectively whether AKI is volume responsive? What is the best biomarker to assess the optimal volume status in AKI patients? In evaluating the current literature and ongoing studies, it was thought that the answers to the questions posed herein would improve the understanding of AKI, and ultimately patient outcomes.
Anaesthesia Critical Care & Pain Medicine, 2016
Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years. The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen and serum creatinine, have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. However, using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, also called "functional renal insufficiency" or "pre-renal insufficiency". This situation is characterized by an oliguria and an increase in creatininemia as a consequence of a reduction in renal blood flow related to systemic haemodynamic abnormalities. In this situation, "renal insufficiency" seems rather inappropriate as kidney function is not impaired. On the contrary, the kidney delivers an appropriate response aiming to recover optimal systemic physiological haemodynamic conditions. Considering the kidney as insufficient is erroneous because this suggests that it does not work correctly, whereas the opposite is occurring, because the kidney is healthy even in a threatening situation. With current definitions of AKI, normalization of volaemia is needed before defining AKI in order to avoid this pitfall.
Acute kidney injury (AKI) is the most common cause of organ dysfunction in critically ill adults, with a single episode of AKI, regardless of stage, carrying a significant morbidity and mortality risk. Since the consensus on AKI nomenclature has been reached, data reflecting outcomes have become more apparent allowing investigation of both short-and long-term outcomes. Classically the short-term effects of AKI can be thought of as those reflecting an acute deterioration in renal function per se. However, the effects of AKI, especially with regard to distant organ function ("organ cross-talk"), are being elucidated as is the increased susceptibility to other conditions. With regards to the long-term effects, the consideration that outcome is a simple binary endpoint of dialysis or not, or survival or not, is overly simplistic, with the reality being much more complex. Also discussed are currently available treatment strategies to mitigate these adverse effects, as they have the potential to improve patient outcome and provide considerable economic health savings. Moving forward, an agreement for defining renal recovery is warranted if we are to assess and extrapolate the efficacy of novel therapies. Future research should focus on targeted therapies assessed by measure of long-term outcomes.
Nephron, 2019
Acute kidney injury (AKI) is a frequent event in hospitalized patients, with an incidence that continues to rise, reaching as high as 70–80% in intensive care settings. The need for dialysis and progression to end-stage kidney disease (ESKD) after an episode of AKI is relatively low, from 5 to 20%. However, it is now recognized that patients with AKI may have very different kidney outcomes, varying from complete recovery, incipient chronic kidney disease (CKD), to progression to ESKD. Recent studies have shown that even mild AKI episodes can be associated with a 90% increased risk of developing CKD during long-term follow-up. There is a significant need to focus our efforts on factors that could mitigate the progression of kidney dysfunction and ultimately improve outcomes from AKI. The first step toward this goal encompasses a better understanding of tubular and glomerular alterations during and following an AKI episode. Our current approach, based solely on glomerular filtration r...
2018
Acute Kidney Injury (AKI) occurs frequently in the critically ill and has an extremely high shortterm mortality. The long-term risks of death, Chronic Kidney Disease (CKD) and End Stage Renal Disease (ESRD) have not been fully established and have never been investigated in the Swedish intensive care (ICU) population. Nephrological surveillance and intervention could improve outcome for AKI survivors at particular risk of persistent renal dysfunction; these patients need to be identified and their renal function, reflected in the glomerular filtration rate (GFR) ought to be followed. However, the performance of endogenous biomarkers in estimating GFR in the recovery period has not been evaluated. Sarcopenia during ICU stay confounds creatinine ́s use during admission and this effect could persist beyond ICU discharge. All studies were cohort in design. In studies I and II, we used the Swedish intensive care registry (2005-2011) comprising 130,134 adult patients and applied epidemiol...
Plos One, 2013
Current consensus definitions of Acute Kidney Injury (AKI) utilise thresholds of change in serum or plasma creatinine and urine output. Biomarkers of renal injury have been validated against these definitions. These biomarkers have also been shown to be independently associated with mortality and need for dialysis. For AKI definitions to include these structural biomarkers, there is a need for an independent outcome against which to judge both markers of functional change and structural markers of injury. We illustrate how sensitivity to need for dialysis and death can be used to link functional and structural (biomarker) based definitions of AKI. We demonstrated the methodology in a representative cohort of critically ill patients, in which an increase of plasma creatinine of .26.4 mmol/L in 48 hours or .50% in 7 days (Functional-AKI) had a sensitivity of 62% for death or dialysis within 30 days. In a development sub-cohort the urinary neutrophil-gelatinaseassociated-lipocalin threshold with a 62% sensitivity for death or dialysis was 140 ng/ml (Structural-AKI). Using these thresholds in a validation sub-cohort, the risk of death or dialysis relative to those with no AKI by either definition was, for combined Structural-AKI and Functional-AKI 3.11 (95% Confidence interval: 2.53 to 3.55), for those with Structural-AKI but not Functional-AKI 1.51 (1.26 to 1.62), and for those with Functional-AKI but not Structural-AKI 1.34 (1.16 to 1.42). Linking functional and structural biomarkers via sensitivity for death and dialysis is a viable method by which to define thresholds for novel biomarkers of AKI.
Canadian Journal of Anesthesia/Journal canadien d'anesthésie, 2012
The Clinical biochemist. Reviews / Australian Association of Clinical Biochemists
Acute kidney injury (AKI) is an independent risk factor for morbidity and mortality. This review provides essential information for the diagnosis and management of AKI. Blood urea nitrogen and serum creatinine are used for the diagnosis of AKI. The review also focuses on recent studies on the diagnosis of AKI using the RIFLE (R-renal risk, I-injury, F-failure, L-loss of kidney function, E-end stage kidney disease) and Acute Kidney Injury Network criteria, and serum and urine AKI biomarkers. Dialysis is the only Food and Drug Administration-approved therapy for AKI. Recent studies on the dose of dialysis in AKI are reviewed.
Advances in Chronic Kidney Disease, 2008
Acute kidney injury (AKI) is a common condition with a high risk of death. The standard metrics used to define and monitor the progression of AKI, such as serum creatinine and blood urea nitrogen levels, are insensitive, nonspecific, and change significantly only after significant kidney injury and then with a substantial time delay. This delay in diagnosis not only prevents timely patient management decisions, including administration of putative therapeutic agents, but also significantly affects the preclinical evaluation of toxicity thereby allowing potentially nephrotoxic drug candidates to pass the preclinical safety criteria only to be found to be clinically nephrotoxic with great human costs. Studies to establish effective therapies for AKI will be greatly facilitated by two factors: (a) development of sensitive, specific, and reliable biomarkers for early diagnosis/prognosis of AKI in preclinical and clinical studies, and (b) development and validation of high-throughput innovative technologies that allow rapid multiplexed detection of multiple markers at the bedside. Keywords acute renal failure; clusterin; cystatin-C; cysteine-rich protein-61 (CYR-61); ELISA; Interleukin-18 (IL-18); kidney injury molecule-1 (Kim-1); microfluidics; nanotechnology; neutrophil gelatinaseassociated lipocalin (NGAL) ACUTE KIDNEY INJURY Definition and Prevalence Acute kidney injury (AKI) is currently recognized as the preferred nomenclature for the clinical disorder formally called acute renal failure (ARF). This transition in terminology served to emphasize that the spectrum of disease is much broader than that subset of patients who experience failure requiring dialysis support (1). This new nomenclature underscores the fact that kidney injury exists along a continuum: The more severe the injury, the more likely the overall outcome will be unfavorable. The Acute Kidney Injury Network (AKIN), which was formed recently in an effort to facilitate improved care of patients who are at risk for AKI, described AKI as "functional or structural abnormalities or markers of kidney damage
Advances in Chronic Kidney Disease, 2008
Changes in terminology and new consensus definitions of acute kidney injury (AKI) and stages of severity have simplified some of the problems in the clinical approach to this complex syndrome. Nevertheless, new proactive approaches to the diagnosis of kidney injury instead of kidney failure are required to allow clinical translation of successful therapies developed for experimental AKI. The recent development of novel urinary and plasma biomarkers, which predict kidney failure, has allowed the development of new paradigms for detection, prevention, and stage-specific treatment.
European Journal of Internal Medicine, 2017
Acute kidney injury (AKI) is common in critically ill patients and is associated with high morbidity and mortality. The availability of several biomarkers of kidney injury offers new tools for its early recognition and management. The early identification of high-risk patients provides an opportunity to develop strategies for the prevention, early diagnosis and treatment of AKI. Despite progress in critical care medicine over the past decade, the treatment strategies for AKI in critically ill patients, such as when to start renal replacement therapy, remain controversial. A recently proposed risk prediction score for AKI, based on routinely available clinical variables, presents a new means of identifying patients at high risk of AKI.
BMC nephrology, 2010
The incidence of acute kidney injury (AKI) has been increasing over time and is associated with a high risk of short-term death. Previous studies on hospital-acquired AKI have important methodological limitations, especially their retrospective study designs and limited ability to control for potential confounding factors.
The incidence of acute kidney injury (AKI) is increasing and is associated with increased morbidity and mortality. AKI is now recognized as a risk factor for progressive chronic kidney disease (CKD). Additionally, patients with CKD are at increased risk for development of AKI due to structural and functional abnormalities, comorbidities, need for invasive procedures and multiple medications. Patients with rapid progression to end-stage renal disease (ESRD) often have courses marked by decline in kidney function due to one or more episodes of AKI. It is important to identify and counsel patients at risk for AKI and to employ risk reduction measures prior to the development of AKI. A rapid assessment for reversible cause of AKI should occur, especially in patients with CKD and treatment aimed at timely optimization of volume and hemodynamic status should be pursued. Early consultation with a nephrologist is indicated if the cause is not immediately clear, evidence of progressive AKI or the complications emerge, or if a tissue diagnosis is required. Finally, patients who experience AKI should be followed for the resolution of AKI and evaluated for development or progression of complications. The key elements in any AKI prevention and management strategy, whenever feasible, are optimization of hemodynamics, correction of fluid and electrolyte imbalances, discontinuation of nephrotoxic drugs, dose adjustment of administered medications and avoidance of contrast media.
Nephrology, 2018
There is an imminent need to increase awareness among general physicians about the long term risk of an episode of AKI and the improved outcomes with early referral and follow up by a nephrologist. This review highlights the importance of recognising the renal and non-renal consequences following an episode of AKI, and the available biomarkers for this condition. LONG-TERM SYSTEMIC CONSEQUENCES OF AKI Patients surviving an episode of AKI are at an increased risk of death. This was observed in the extended follow-up
Journal of Critical …, 2010
This research aims to apply the definition proposed by the Acute Kidney Injury Network (AKIN) research group to assess the incidence, risk factors, and outcomes in acute kidney injury (AKI) patients admitted at the intensive care unit (ICU). Design: This is a retrospective cohort study. Patients who were admitted to the ICU from January 1, 2003 to December 31, 2004 were studied. Interventions: Medical records of all patients were reviewed. Demographic information, diagnoses, risk factors for AKI, laboratory data, urinary output, frequency and days of exposure to mechanical ventilation, ICU and hospital stay, and outcomes were recorded. Measurements and Main Results: A total of 794 patients were studied. There were 39.8% of patients who presented AKI (stage 1: 13.9%, stage 2: 12%, stage 3: 13.9%). The variables that were associated with the presence of AKI in the multivariable analysis were as follows: sepsis (odds ratio [OR], 5.29; 95% confidence interval [CI], 3.36-8.33), heart failure (OR, 3.01; 95% CI, 1.59-5.67), vasopressor use (OR, 1.89; 95% CI, 1.26-2.83), and age (β = 1.02; 95% CI, 1.01-1.03). The mean hospital stay increased with renal commitment: patients without AKI, 10.9 days; AKIN stage 1, 17.8; AKIN stage 2, 21.1; and AKIN stage 3, 22.1 days (P b .0001). Mortality rate increased as more advanced the AKI stage was (no AKI,
Journal of renal injury prevention, 2014
The first consensus definition of Acute Kidney Injury (AKI) was published a decade ago. In this mini narrative review we look at the history of the changes in the definition of AKI and consider how it may change again in the near future. The epidemiology of small changes in creatinine and the difficulties with determining baseline creatinine have driven the changes. Recent evidence on urinary output and the application of structural injury biomarkers are likely to change the definition once more.
PLoS ONE, 2014
Aims: Acute kidney injury is a classical complication of diabetic ketoacidosis. However, to the best of our knowledge, no study has reported the incidence and characteristics of acute kidney injury since the consensus definition was issued.
Comprehensive Physiology, 2011
The term "acute renal failure" (ARF) has traditionally been used to describe a syndrome with a rapid decline in glomerular filtration rate (GFR) occurring over a period of hours to weeks as the key feature. Recently, a consortium of nephrologists and intensivists, the Acute Kidney Injury Network (AKIN), representing many of the professional societies involved in the care of critically ill patients, recommended that the term "acute kidney injury" (AKI) replace ARF. This term includes the entire spectrum of ARF and recognizes that minor changes in kidney function (reflected by a change in serum creatinine [SCr] of 0.3 mg/dL) can portend worse patient outcome, 1 whereas the term "failure" is reserved for those patients whose renal functional impairment is so severe that replacement therapy is indicated, or at least considered. The previous issue of Nephrology Rounds reviewed the epidemiology, diagnosis, and treatment of AKI in various settings. This issue of Nephrology Rounds examines the pathophysiological underpinnings of AKI.
Seminars in Dialysis, 2011
Acute kidney injury (AKI) is now well recognized as an independent risk factor for increased morbidity and mortality particularly when dialysis is needed. Although renal replacement therapy (RRT) has been used in AKI for more than five decades, there is no standard methodology to predict which AKI patients will need dialysis and who will recover renal function without requiring dialysis. The lack of consensus on what parameters should guide the decision to start dialysis has led to a wide variation in dialysis utilization. A contributing factor is the lack of studies in the modern era
Seminars in dialysis
The decision to provide dialytic support and choosing the ideal moment to initiate therapy are common impasses for physicians treating patients with acute kidney injury (AKI). Although renal replacement therapy (RRT) has been extensively used in clinical practice for more than 30 years, there is a paucity of evidence to guide clinicians on the optimal utilization of RRT in AKI. In the absence of traditional or urgent indications, there is no consensus on whether dialysis should be offered and when it should be started. The lack of agreed-upon parameters to guide the decision, the fear of the risk of the procedure, and the possible contribution to worse prognosis with RRT have resulted in a considerable variation in practice among physicians and centers. In this review, we summarize the evidence evaluating time of initiation of RRT and discuss possible approaches for future trials in addressing this issue.
Critical Care, 2011
Introduction: Septic-shock-associated acute kidney injury (SSAKI) carries high morbidity in the pediatric population. Effective treatment strategies are lacking, in part due to poor detection and prediction. There is a need to identify novel candidate biomarkers of SSAKI. The objective of our study was to determine whether microarray data from children with septic shock could be used to derive a panel of candidate biomarkers for predicting SSAKI. Methods: A retrospective cohort study compared microarray data representing the first 24 hours of admission for 179 children with septic shock with those of 53 age-matched normal controls. SSAKI was defined as a >200% increase of baseline serum creatinine, persistent to 7 days after admission. Results: Patients with SSAKI (n = 31) and patients without SSAKI (n = 148) were clinically similar, but SSAKI carried a higher mortality (45% vs. 10%). Twenty-one unique gene probes were upregulated in SSAKI patients versus patients without SSAKI. Using leave-one-out cross-validation and class prediction modeling, these probes predicted SSAKI with a sensitivity of 98% (95% confidence interval (CI) = 81 to 100) and a specificity of 80% (95% CI = 72 to 86). Serum protein levels of two specific genes showed high sensitivity for predicting SSAKI: matrix metalloproteinase-8 (89%, 95% CI = 64 to 98) and elastase-2 (83%, 95% CI = 58 to 96). Both biomarkers carried a negative predictive value of 95%. When applied to a validation cohort, although both biomarkers carried low specificity (matrix metalloproteinase-8: 41%, 95% CI = 28 to 50; and elastase-2: 49%, 95% CI = 36 to 62), they carried high sensitivity (100%, 95% CI = 68 to 100 for both). Conclusions: Gene probes upregulated in critically ill pediatric patients with septic shock may allow for the identification of novel candidate serum biomarkers for SSAKI prediction.
Nature Reviews Nephrology, 2011
| Acute kidney injury (AKI) as a consequence of ischemia is a common clinical event leading to unacceptably high morbidity and mortality, development of chronic kidney disease (CKD), and transition from pre-existing CKD to end-stage renal disease. Data indicate a close interaction between the many cell types involved in the pathophysiology of ischemic AKI, which has critical implications for the treatment of this condition. Inflammation seems to be the common factor that links the various cell types involved in this process. In this Review, we describe the interactions between these cells and their response to injury following ischemia. We relate these events to patients who are at high risk of AKI, and highlight the characteristics that might predispose these patients to injury. We also discuss how therapy targeting specific cell types can minimize the initial and subsequent injury following ischemia, thereby limiting the extent of acute changes and, hopefully, long-term structural and functional alterations to the kidney.
Acta physiologica (Oxford, England), 2017
Acute kidney injury (AKI) is a common complication following cardiac surgery performed on cardiopulmonary bypass (CPB) and has important implications for prognosis. The aetiology of cardiac surgery-associated AKI is complex, but renal hypoxia, particularly in the medulla, is thought to play at least some role. There is strong evidence from studies in experimental animals, clinical observations and computational models, that medullary ischaemia and hypoxia occurs during CPB. There are no validated methods to monitor or improve renal oxygenation during CPB, and thus possibly decrease the risk of AKI. Attempts to reduce the incidence of AKI by early transfusion to ameliorate intra-operative anaemia, refinement of protocols for cooling and rewarming on bypass, optimisation of pump flow and arterial pressure, or the use of pulsatile flow, have not been successful to date. This may in part reflect the complexity of renal oxygenation, which may limit the effectiveness of individual interve...
Aspects in Continuous Renal Replacement Therapy [Working Title]
Acute kidney injury (AKI), previously named acute renal failure, is characterized by abrupt deterioration in renal function. The incidence of AKI has increased lately, both in the hospital and community setting. It is estimated that more than 13 million people are affected by AKI annually worldwide. Despite all the advances in the field, AKI still carries a high mortality rate. In addition to mortality, AKI is an important risk factor for the development of chronic kidney disease. In this chapter, various aspects of AKI will be discussed including definition and staging, etiology, pathophysiology, clinical presentation, diagnosis, management, prognosis, and prevention.
Molecular and Cellular Biochemistry, 2011
The pathogenesis of acute kidney injury (AKI) occurring due to sepsis is incompletely understood. Endothelial activation, defined as up-regulation of adhesion molecules by proinflammatory cytokines, may be central to the development of sepsis-induced AKI. Our aim was to determine levels of circulating adhesion molecules endothelial (E)-selectin, intercellular adhesion molecule (ICAM), and vascular cell adhesion molecule (VCAM), inflammatory mediators; tumor necrosis factor-a (TNF-a) and transforming growth factor-b (TGF-b), vasoactive mediators; endothelin-1 (ET-1) and nitric oxide (NO), soluble receptor for advanced glycated end products (sRAGE) and serum fetuin-A in septic AKI patients before and after antibiotic therapy. Nineteen AKI patients with sepsis and fifteen healthy controls were enrolled in this prospective study. Results revealed that 12 weeks of therapy caused amelioration of endothelial and inflammatory injuries as well as renal function markers. Moreover, the positive correlations between levels of RAGE and E-selectin (r = 0.88), ET-1 (r = 0.90), and TNF-a (r = 0.94) and negative with NO (r =-0.75-0.95) suggest that possible interaction of RAGE and inflammation may contribute to endothelial dysfunction in septic AKI patients.
BMC Nephrology
Background Electronic alerts (e-alerts) for Acute Kidney Injury (AKI) have been implemented into a variety of different Electronic Health Records (EHR) systems worldwide in order to improve recognition and encourage early appropriate management of AKI. We were interested in the impact on patient safety, specialist referral and clinical management. Methods All patients admitted to our institution with AKI were included in the study. We studied AKI progression, dialysis dependency, length of hospital stay, emergency readmission, ICU readmission, and death, before and after the introduction of electronic alerts. The impact on prescription of high risk drugs, fluid administration, and referral to renal services was also analysed. Results After the introduction of the e-alert, progression to higher AKI stage, emergency readmission to hospital and death during admission were significantly reduced. More prescriptions were stopped for drugs that adversely affect renal function in AKI and th...
Journal of community hospital internal medicine perspectives, 2017
Early stage acute kidney injury (AKI) is an independent risk factor for an increase in mortality. Accurate assessment of volume status is a major challenge during the early stages of acute renal injury. Determining volume status based on the history and physical exam lacks accuracy. Urine sodium and free excretion of sodium (FENa) provide objective evidence of intravascular volume status when interpreted carefully and is helpful to delineate prerenal from intrinsic renal failure. In recent years point of care ultrasound has been used to assess volume status. Our team conducted a retrospective chart review to assess the association of inferior vena cava collapsibility by point of care ultrasound (POCUS) and urine electrolytes (urine sodium, fractional excretion of sodium) during early stage AKI (Stage 1-2 of KDIGO guidelines). We reviewed 150 cases based on the provisional diagnosis. 36 patients met the criteria for further review. Using bivariate analysis, we found a strong associat...
Journal of Clinical Medicine, 2023
This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY
Frontiers in Physiology, 2023
Hydrodynamic fluid delivery has shown promise in influencing renal function in disease models. This technique provided pre-conditioned protection in acute injury models by upregulating the mitochondrial adaptation, while hydrodynamic injections of saline alone have improved microvascular perfusion. Accordingly, hydrodynamic mitochondrial gene delivery was applied to investigate the ability to halt progressive or persistent renal function impairment following episodes of ischemia-reperfusion injuries known to induce acute kidney injury (AKI). The rate of transgene expression was approximately 33% and 30% in rats with prerenal AKI that received treatments 1 (T 1hr) and 24 (T 24hr) hours after the injury was established, respectively. The resulting mitochondrial adaptation via exogenous IDH2 (isocitrate dehydrogenase 2 (NADP+) and mitochondrial) significantly blunted the effects of injury within 24 h of administration: decreased serum creatinine (≈60%, p < 0.05 at T 1hr ; ≈50%, p < 0.05 at T 24hr) and blood urea nitrogen (≈50%, p < 0.05 at T 1hr ; ≈35%, p < 0.05 at T 24hr) levels, and increased urine output (≈40%, p < 0.05 at T 1hr ; ≈26%, p < 0.05 at T 24hr) and mitochondrial membrane potential, Δψ m , (≈ by a factor of 13, p < 0.001 at T 1hr ; ≈ by a factor of 11, p < 0.001 at T 24hr), despite elevated histology injury score (26%, p < 0.05 at T1 hr ; 47%, p < 0.05 at T 24hr). Therefore, this study identifies an approach that can boost recovery and halt the progression of AKI at its inception.
Journal of Medicine and Life
Ischemic reperfusion injury (IRI) of the kidneys is a direct sequela of surgical procedures associated with the interruption of blood supply. The pathophysiology of IRI is complicated, and several inflammatories, apoptosis, and oxidative stress pathways are implicated. Among the major receptors directly involved in renal IRI are the toll-like receptors (TLRs), specifically TLR2 and TLR4. In this study, we investigated the effects of Lipopolysaccharide from Rhodobacter Sphaeroides (TLR2 and TLR4 antagonist, LPS-RS) and the ultrapure form (pure TLR4 antagonist, ULPS-RS) on the histopathological changes and TLRs expression in an animal model of bilateral renal IRI. Forty-eight adult male rats were allocated into six groups (N=8) as follows: sham group (negative control without IRI), control group (rats underwent bilateral renal ischemia for 30 minutes and 2 hours of reperfusion), vehicle group (IRI+ vehicle), LPS-RS group (IRI+ 0.5 mg/kg of LPS-RS), ULPS-RS group (IRI+ 0.1 mg/kg of ULP...
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