Abstract Acute Kidney Injury Research Articles

ACUTE KIDNEY INJURY AND PREGNANCY

Acute kidney injury (AKI) in obstetrics is a serious complication of pregnancy, delivery and the postpartum period, which can have a negative impact on the outcome of pregnancy for both the mother and the fetus. Currently, in developing countries the incidence of AKI during pregnancy and in the postpartum period is 4-26% of all pregnancies, and in the economically developed regions of the world – not more than 2.8%. The frequency of obstetric AKI requiring dialysis is 1:10,000 pregnancies. The causes of kidney injury in pregnant women can be hypertensive disorders, various types of thrombotic microangiopathy (HELLP syndrome, atypical hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, catastrophic antiphospholipid syndrome), acute fatty liver of pregnancy, obstetric hemorrhages, sepsis and septic shock. The article discusses the diagnostic criteria, biomarkers and timing of development of AKI in pregnancy, the principles of treatment and prevention of this complication in obstetrics.

Renal Replacement Therapy in Acute Kidney Injury - Indication and Implementation

Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with a worse short- and long-term outcome. The KDIGO (Kidney Disease: Improving Global Outcomes) guidelines suggest to implement preventive strategies in high-risk patients. Definition and classification of acute kidney injury according to the KDIGO criteria are based on an increase in serum creatinine and/or a decrease in urinary output. Renal replacement therapy (RRT) is the only supportive measure in patients with severe AKI. The KDIGO guidelines recommend to initiate RRT immediately if an absolute indication exists. However, in the absence of absolute indication, there are no recommendations when to start RRT in AKI patients with a progressive decline of renal function. Continuous or intermittent techniques of renal replacement therapy may be used equally for treatment of acute kidney injury. In hemodynamically instable patients and patients with increased intracranial pressures continuous renal replacement therapy is recommended. Although weak evidence exists, regional citrate anticoagulation is suggested for patients receiving continuous renal replacement therapy and systemic heparin anticoagulation is suggested for patients receiving intermittent renal replacement therapy. The KDIGO guidelines recommend to deliver an effluent volume of 20 - 25 ml/kg/h for CRRT in AKI.

Conservative Management of Acute Kidney Injury

Acute kidney injury (AKI) is one of the most common complications occurring among intensive care unit (ICU) patients and is independently associated with a higher risk of mortality. In critically ill patients, AKI presentation is heterogeneous, varying from asymptomatic elevations in serum creatinine to the need for dialysis in the context of multiorgan failure. Within this range of clinical presentation, the kidney is often overlooked because improving and maintaining cardiac performance are the focus. In addition, aggressive fluid resuscitation may impose significant demands on the kidney wherein the normal excretory capacity may be overwhelmed. ICU patients often have underlying comorbidities, including chronic kidney disease and heart failure, which further limit the range of renal capacity. Drug and nutritional administration contribute to the demand for fluid removal to maintain fluid balance. The dissimilarities of the critical care environment and the extra demand kidney capacity highlight the need for different strategies for management and treatment of AKI in the critically ill patients. We focus this review on the general and nondialytic therapy of AKI. This reference contains 5 figures, 3 tables and 90 references Key words: Acute kidney injury, fluid resuscitation, loop diuretics, vasoactive agents, fluid overload, hiperkalemia, and metabolic acidosis.

Epidemiology of acute kidney injury in critically ill children living in the Kingdom of Saudi Arabia

Acute kidney injury (AKI) is very common in children admitted to pediatric intensive care and affected children are at increased risk of morbidity and mortality. The epidemiologic characteristics of children with AKI have not been well described in children living in the Kingdom of Saudi Arabia (KSA). This review of the epidemiology of AKI in critically ill children in KSA shows that AKI is common in this population and is chiefly attributed to sepsis, other infections and postcardiac surgery. The occurrence of AKI is linked to increased mortality and length of hospital stay. The severity of AKI correlates with increased inhospital mortality as well as risk of mortality after discharge. A considerable proportion of survivors develop evidence of chronic kidney disease. Cystatin C and urinary neutrophil gelatinase-associated lipocalin are useful in enabling early diagnosis of AKI in critically ill children.

Acute Kidney Injury and Information Technology.

Acute kidney injury (AKI) is a common complication that occurs in critically ill patients and it is associated with a worse outcome. Since therapy options are limited, prevention and early detection are the essential cornerstones to improve patient outcomes. Therefore, using health information technology (HIT) to detect AKI early might be useful for clinicians. Patient data can be extracted real-time from electronic health records. Programmed electronic alert systems (e-alerts) can increase clinicians' awareness for AKI. Integrated into clinical decision support systems, implementation of HIT might improve clinical processes and patient outcomes. Several studies show the application of e-alerts in AKI detection and the implementation in processes of care. Monitoring nephrotoxic medication is one successful approach of implementing e-alerts in prevention of AKI. Information technology in AKI is in an early phase of development and further multicenter prospective studies are required to draw optimally on the maximum potential of this concept.

Risk factors for acute kidney injury after orthotopic liver transplantation: A single-center data analysis.

Acute kidney injury (AKI) is a common complication following orthotopic liver transplantation (OLT) and is associated with increased morbidity and mortality. The aim of the current study was to determine the risk factors for AKI in patients undergoing OLT. A total of 103 patients who received OLT between January 2015 and May 2016 in Tongji Hospital, China, were retrospectively analyzed. Their demographic characteristics and perioperative parameters were collected, and AKI was diagnosed using 2012 Kidney Disease: Improving Global Outcomes (KDIGO) staging criteria. It was found that the incidence of AKI was 40.8% in this cohort and AKI was significantly associated with body mass index, urine volume, operation duration (especially > 480 min), and the postoperative use of vasopressors. It was concluded that relative low urine output, long operation duration, and the postoperative use of vasopressors are risk factors for AKI following OLT.

Reducing Inflammatory Cytokine Production from Renal Collecting Duct Cells by Inhibiting GATA2 Ameliorates Acute Kidney Injury.

Acute kidney injury (AKI) is a leading cause of chronic kidney disease. Proximal tubules are considered to be the primary origin of pathogenic inflammatory cytokines in AKI. However, it remains unclear whether other cell types, including collecting duct (CD) cells, participate in inflammatory processes. The transcription factor GATA2 is specifically expressed in CD cells and maintains their cellular identity. To explore the pathophysiological function of GATA2 in AKI, we generated renal tubular cell-specific Gata2 deletion (G2CKO) mice and examined their susceptibility to ischemia reperfusion injury (IRI). Notably, G2CKO mice exhibited less severe kidney damage, with reduced granulomacrophagic infiltration upon IRI. Transcriptome analysis revealed that a series of inflammatory cytokine genes were downregulated in GATA2-deficient CD cells, suggesting that GATA2 induces inflammatory cytokine expression in diseased kidney CD cells. Through high-throughput chemical library screening, we identified a potent GATA inhibitor. The chemical reduces cytokine production in CD cells and protects the mouse kidney from IRI. These results revealed a novel pathological mechanism of renal IRI, namely, that CD cells produce inflammatory cytokines and promote IRI progression. In injured kidney CD cells, GATA2 exerts a proinflammatory function by upregulating inflammatory cytokine gene expression. GATA2 can therefore be considered a therapeutic target for AKI.

Pharmacokinetic/Toxicodynamic Analysis of Colistin-Associated Acute Kidney Injury in Critically Ill Patients.

Acute kidney injury (AKI) occurs in a substantial proportion of critically ill patients receiving intravenous colistin. In the pharmacokinetic/toxicodynamic analysis reported here, the relationship of the occurrence of AKI to exposure to colistin and a number of potential patient factors was explored in 153 critically ill patients, none of whom were receiving renal replacement therapy. Tree-based modeling revealed that the rates of AKI were substantially higher when the average steady-state plasma colistin concentration was greater than ∼2 mg/liter.

Acute Kidney Injury in the Cancer Patient

Acute kidney injury (AKI) is a problem frequently encountered in patients with cancer that significantly impacts their well-being and outcomes. In addition to the usual prerenal, intrarenal, and postrenal etiologies of AKI, patients with cancer experience unique causes of AKI. Nephrologists caring for this population must be able to identify and manage these conditions, which often require distinguishing between causes resulting from the cancer itself and those related to chemotherapeutic or other concurrent treatment, to institute appropriate preventive or therapeutic strategies. In this review, we present a suggested systematic approach to the diagnosis of AKI in patients with cancer and discuss common clinical scenarios specific to this patient population, with a special emphasis on tumor infiltration of the kidney parenchyma, myeloma-related AKI, tumor lysis syndrome, thrombotic microangiopathy, AKI in the patient with hematopoietic stem cell transplantation, and renal disease in patients with renal cell carcinoma. We cover the latest evidence-based strategies for management of these disorders in this evolving field. In addition, we provide an updated table of potentially nephrotoxic chemotherapeutic agents with their associated mechanisms of kidney injury as a reference for clinicians to build on as they encounter the ever-expanding list of oncologic agents in practice. As the subspecialty of onconephrology continues to evolve, it will be increasingly important for clinicians to have the skills to effectively diagnose and treat AKI in cancer patients to minimize morbidity and mortality, decrease the incidence of subsequent chronic kidney disease, and maintain chemotherapeutic options for these patients. This review contains 5 figures, 5 tables, and 61 references. Key words: acute kidney injury, cancer, chemotherapy, onconephrology, renal failure

Assessing renal changes after remote ischemic preconditioning (RIPC) of the upper extremity using BOLD imaging at 3T.

Acute kidney injury (AKI) is an important risk factor for a number of adverse outcomes including end-stage renal disease and cardiovascular morbidity and mortality. Whilst many clinical situations that can induce AKI are known-e.g. drug toxicity, contrast agent exposure or ischemia during surgery-targeted preventive or therapeutic measures are still lacking. As to renoprotective strategies, remote ischemic preconditioning (RIPC) is one of the most promising novel approaches and has been examined by a number of clinical trials. The aim of this study was to use blood oxygenation level-dependent (BOLD) MRI as a surrogate parameter to assess the effect of RIPC in healthy volunteers. In this IRB-approved, prospective study, 40 healthy volunteers were stratified with 20 undergoing an RIPC procedure (i.e. RIPC group) with a transient ischemia of the right arm, and 20 undergoing a sham procedure. Before and after the procedure, both kidneys of all participants were scanned using a 12-echo mGRE sequence for functional BOLD imaging at 3T. For each volunteer, 180 ROIs were placed in the cortex and the medulla of the kidneys. Ultimately, R2* values, which have an inverse correlation with the oxygenation level of tissue, were averaged for the RIPC and control groups. Following intervention, mean R2* values significantly decreased in the RIPC group in both the cortex (18.6±2.3 vs. 17.5±1.7Hz; p=0.0047) and medulla (34±5.2 vs. 32.2±4.2Hz; p=0.0001). However, no significant differences were observed in the control group. RIPC can be non-invasively assessed in healthy volunteers using BOLDMRI at 3T, demonstrating a higher oxygen content in kidney tissue. This study presents a first-in-man trial establishing a quantifiable readout of RIPC and its effects on kidney physiology. BOLD measurements may advance clinical trials in further evaluating RIPC for future clinical care.

Diagnostic prediction of urinary [TIMP-2] x [IGFBP7] for acute kidney injury: A meta-analysis exploring detection time and cutoff levels.

Acute kidney injury (AKI) most commonly occurs in critically ill and postoperative patients. Tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) are two newly-identified urinary biomarkers that can help to detect early AKI, yet their predictive accuracies range widely. Here, we conduct a systematic meta-analysis to evaluate the diagnostic values of [TIMP-2] x [IGFBP7] for AKI at different detection times and cutoff levels. Ten studies were meta-analyzed on 1606 patients. Overall, urinary [TIMP-2] x [IGFBP7] had a pooled sensitivity of 58% and specificity of 79%. Subgroup analysis showed that the sensitivity and specificity were 0.72 and 0.58 with a cutoff value of 0.3 (ng/mL)2/1000, and 0.38 and 0.94 with a cutoff value of 2.0 (ng/mL)2/1000, respectively. Moreover, when 0.3 was chosen as the cutoff value, restricting analysis to patients who were tested within 4 hours showed a sensitivity of 0.71 and specificity of 0.73, with the AUROC of 0.75. When 2.0 was chosen as the cutoff value, the sensitivity and specificity were 0.43 and 0.93, respectively in patients who were tested within 24 hours, with the AUROC of 0.70. In summary, urinary [TIMP-2] x [IGFBP7] can predict the occurrence of AKI with moderate diagnostic accuracy. In the earlier administrative periods (less than 4 hours), 0.3 (ng/mL)2/1000 is recommended to be used; whereas for patients who were administrated more than 24 hours, 2.0 (ng/mL)2/1000 is more appropriate.

Outcomes of acute kidney injury in a nephrology ward.

Acute kidney injury (AKI) is a global problem which predicts immediate and long-term adverse outcomes. We evaluated the AKI progression to end-stage renal disease, as well as the mortality associated with AKI and the in-hospital readmission rate because of a cardiovascular event in AKI patients admitted in a nephrology ward. A 5-year retrospective study was set in a nephrology department, with a follow-up period of up to 8years. In a total of 191 patients, mean age was 73.83±12.49years, and 137 (71.7%) patients had history of chronic kidney disease. One hundred and twenty-four (65%) patients needed RRT and two (1%) needed surgery. Upon discharge, 107 (56%) patients had recovered the renal function, 41 (21.6%) patients had partial recovery, 25 (13%) patients were RRT dependent, 16 (8.4%) died, and two (1%) patients had outcomes unknown to us, because they were transferred to other hospitals. The median survival time free of RRT was 74months. The median survival time of the followed patients was 34months (95% CI 23.3-44.7). The mortality rate in the follow-up period in this sample was 18 deaths/100 patients-years, and the incidence of a composite cardiovascular endpoint of heart failure, acute coronary syndrome, and stroke was 6 events/100 patients-years. The mortality rate in the follow-up period was higher than usually described for patients outside intensive care unit, probably because our patients were old and had many comorbidities.

The Role of Natural Killer T Cells in Acute Kidney Injury: Angel or Evil?

Acute kidney injury (AKI) is manifested by inflammation, and an early feature in the pathogenesis is the accumulation of immune cells in the kidney. Natural killer T (NKT) cells, a peculiar T cells subtype, serve as a bridge between innate and adaptive immunity. Due to the difference between type I and type II subsets, NKT cells were supposed to play a dual role in IR-related tissue injury. Furthermore, membrane receptors and clinical immunosuppressive agents remain involved in the modulation of NKT cell function. Therefore, regulation of the amount and viability of NKT cells becomes a potential strategy in amelioration of AKI. This review will highlight the recent insights gained into the role and mechanisms of NKT cells in AKI.

TCT-676 Utility of Urinary Neutrophil Gelatinase Associated Lipocalin to predict Acute Kidney Injury after coronary intervention

Acute kidney injury (AKI) is a troublesome complication and is associated with an increased risk of mortality after coronary intervention. It usually takes over 48 hours to diagnose the development of AKI based on the elevation of serum creatinine. Recent developed the urinary neutrophil gelatinase

TCT-199 Acute Kidney Recovery in Patients Undergoing Transcatheter Aortic Valve Replacement

Acute Kidney Injury (AKI) after TAVR is associated with increased mortality. As significant hemodynamic improvement may occur with relief of aortic stenosis, we hypothesized that TAVR patients may demonstrate the opposite phenomena: Acute Kidney Recovery (AKR). We studied the incidence and

TCT-34 Prediction of acute kidney injury after TAVR by new biomarkers

Acute kidney injury (AKI) is a common complication after transcatheter aortic valve replacement (TAVR) and is associated with increased morbidity and mortality. Routinely used biomarkers such as creatinine show a diagnostic gap in the first hours after kidney injury. Thus, new biomarkers for earlier

Beyond hematopoietic property; administration of erythropoietin for nephroprotection

Acute kidney injury (AKI) is defined as an abrupt or rapid decline in renal filtration function. Erythropoietin (EPO) as a hematopoietic and multifunctional hormone is produced primarily by kidney. Many investigations have shown that EPO as an antioxidant agent has shown several effects such as anti-apoptotic, antioxidant, and anti-inflammatory and also angiogenic activities. The biological activities of EPO are mediated by binding to its receptor (EPOR). The potential role of EPO in kidney is related to the presence of functional EPOR in renal mesangial cells, tubular epithelial cells and the glomerulus. Antioxidants and reactive oxygen species (ROS) scavengers such as EPO, can protect the kidneys against conditions that induce nephrotoxicity. Most studies in the field of renoprotective effects of EPO have focused on AKI models. In this paper we sought to review the ameliorative effects of EPO against various agents or conditions that induce nephrotoxicity including ischemia/reperfusion injury (IRI), cisplatin, gentamicin, rhabdomyolysis, amikacin and vancomycin.

Acute Kidney Injury in the Cancer Patient

Acute kidney injury (AKI) is a problem frequently encountered in patients with cancer that significantly impacts their well-being and outcomes. In addition to the usual prerenal, intrarenal, and postrenal etiologies of AKI, patients with cancer experience unique causes of AKI. Nephrologists caring for this population must be able to identify and manage these conditions, which often require distinguishing between causes resulting from the cancer itself and those related to chemotherapeutic or other concurrent treatment, to institute appropriate preventive or therapeutic strategies. In this review, we present a suggested systematic approach to the diagnosis of AKI in patients with cancer and discuss common clinical scenarios specific to this patient population, with a special emphasis on tumor infiltration of the kidney parenchyma, myeloma-related AKI, tumor lysis syndrome, thrombotic microangiopathy, AKI in the patient with hematopoietic stem cell transplantation, and renal disease in patients with renal cell carcinoma. We cover the latest evidence-based strategies for management of these disorders in this evolving field. In addition, we provide an updated table of potentially nephrotoxic chemotherapeutic agents with their associated mechanisms of kidney injury as a reference for clinicians to build on as they encounter the ever-expanding list of oncologic agents in practice. As the subspecialty of onconephrology continues to evolve, it will be increasingly important for clinicians to have the skills to effectively diagnose and treat AKI in cancer patients to minimize morbidity and mortality, decrease the incidence of subsequent chronic kidney disease, and maintain chemotherapeutic options for these patients. This review contains 5 figures, 5 tables, and 61 references. Key words: acute kidney injury, cancer, chemotherapy, onconephrology, renal failure

Essential Elements as Biomarkers of Acute Kidney Injury and Spontaneous Reversion.

Acute kidney injury (AKI) is an important health problem and can be caused by number of factors. The use of aminoglycosides, such as gentamicin, is one of these factors. Recently, an effort has been made to find biomarkers to guide treatment protocols. Inductively coupled plasma optical emission spectroscopy (ICP-OES) was used to estimate the contents of Ca, Cu, Fe, K, Mg, Mn, Na, P, and Zn in serum and urine of the healthy, AKI, and spontaneous recovery (SR) groups of animals. The animal model of AKI and SR was validated by measuring serum and urinary urea and creatinine. The quantitative determination of the elements showed a decrease in serum levels of Ca, and Fe in the AKI group (P<0.01 vs. healthy), with a return to normal levels in the SR group, without a significant difference between the healthy and SR groups. In the urine samples, there was a decrease in P and Na levels in the AKI group (P<0.001 and P<0.01 vs. healthy), but Ca levels were increased in this group compared with the healthy and SR groups (P<0.01). These findings indicate that mineral elements might be useful as biomarkers for AKI.

Acute kidney injury in critically ill

Acute kidney injury (AKI) is frequent in hospitalised critically ill patients with a high incidence in ICU patients. It is associated with increased mortality, greater cost, prolonged intensive care and hospital stay and progress to development of chronic kidney disease. AKI is an independent risk factor for increased mortality and severe morbidity. Sepsis is a leading cause of AKI in critically ill patients. The management is still supportive and early recognition, haemodynamic optimisation, avoidance of nephrotoxic medications, treatment of the underlying cause and renal replacement therapy are important. AKI is a preventable and outcome can be improved by early diagnosis and effective management. The aim of this review is to provide a comprehensive update on recent evidence in the field of AKI in critically ill patients, including risk factors, causes, pathophysiology, diagnosis/classification, prevention and management.