Septic AKI Research Articles

Two subphenotypes of septic acute kidney injury are associated with different 90-day mortality and renal recovery

BackgroundThe pathophysiology of septic acute kidney injury is inadequately understood. Recently, subphenotypes for sepsis and AKI have been derived. The objective of this study was to assess whether a combination of comorbidities, baseline clinical data, and biomarkers could classify meaningful subphenotypes in septic AKI with different outcomes.MethodsWe performed a post hoc analysis of the prospective Finnish Acute Kidney Injury (FINNAKI) study cohort. We included patients admitted with sepsis and acute kidney injury during the first 48 h from admission to intensive care (according to Kidney Disease Improving Global Outcome criteria). Primary outcomes were 90-day mortality and renal recovery on day 5. We performed latent class analysis using 30 variables obtained on admission to classify subphenotypes. Second, we used logistic regression to assess the association of derived subphenotypes with 90-day mortality and renal recovery on day 5.ResultsIn total, 301 patients with septic acute kidney injury were included. Based on the latent class analysis, a two-class model was chosen. Subphenotype 1 was assigned to 133 patients (44%) and subphenotype 2 to 168 patients (56%). Increased levels of inflammatory and endothelial injury markers characterized subphenotype 2. At 90 days, 29% of patients in subphenotype 1 and 41% of patients in subphenotype 2 had died. Subphenotype 2 was associated with a lower probability of short-term renal recovery and increased 90-day mortality.ConclusionsIn this post hoc analysis, we identified two subphenotypes of septic acute kidney injury with different clinical outcomes. Future studies are warranted to validate the suggested subphenotypes of septic acute kidney injury.

Pre-dilution continuous hemofiltration in septic AKI

Pre-dilution continuous hemofiltration in septic AKI

Lactate up-regulates the expression of PD-L1 in kidney and causes immunosuppression in septic Acute Renal Injury

This study aims to explore the mechanism of immunosuppression in septic Acute Renal Injury (AKI) and the role of programmed death-1 (PD-1/PD-L1) pathway in septic AKI. This study established a septic AKI model by Cecal ligation and puncture (CLP) in C57/B6 mice, ELISA was used to test the level of lactate and creatinine in serum, blood was collected for flow cytometry and kidney samples for Western blot analyses. This study further analyzed the expression of PD-L1 in kidney and the expression of PD-1 in CD4+, CD8+ T cell, and the number of CD3+ T cells to identify apoptosis in T cells in the blood. The CLP sepsis model induced AKI in C57/B6 mice; The expression of PD-1 and PD-L1 were increased in septic AKI mice; PD-1/PD-L1 induced apoptosis in T cells: the number of lymphocytes decreased by 64%, while the number of CD3+ T cells decreased by 27% compared with the sham group; Results also indicated that lactate up-regulates expression of PD-L1 in the kidney. Lactate activated PD-1/PD-L1 pathway can induce immunosuppression by inducing apoptosis in lymphocytes in septic AKI. Moreover, blocking the receptor of lactate or PD-1/PD-L1 might be a new therapy for septic AKI.

Association between intravenous contrast media exposure and non-recovery from dialysis-requiring septic acute kidney injury: a nationwide observational study.

This study aimed to examine the association between the use of intravenous contrast and non-recovery from dialysis-requiring acute kidney injury (AKI-D) and in-hospital mortality among patients with sepsis. This was a retrospective observational study using the Japanese Diagnosis Procedure Combination inpatient database between January 2011 and December 2016. We identified patients with septic AKI who began continuous renal replacement therapy (RRT) within 2-days of admission and underwent computed tomography. We compared patients with AKI-D with and without the use of intravenous contrast for computed tomography and performed propensity score matching to adjust for confounders for the association between exposure to intravenous contrast and outcomes, including a composite outcome of in-hospital mortality and RRT dependence at discharge and RRT duration. From 3782 and 6619 patients with septic AKI-D with and without intravenous contrast exposure, respectively, 3485 propensity score-matched pairs were generated. No significant differences were found in the outcomes between the propensity score-matched groups: a composite outcome of in-hospital mortality and RRT dependence, 49.6% vs. 50.2% (odds ratio (OR) 0.98; 95% CI (confidence interval) 0.88, 1.07); in-hospital mortality, 45.3% vs. 46.1% (OR 0.97; 95% CI 0.87, 1.06); RRT dependence, 4.4% vs 4.1% (OR 1.08; 95% CI 0.85, 1.31); and median (interquartile range) of RRT duration, 4 [2-11]days vs. 4 [2-11]days (P = 0.58). This large observational study did not support an association between intravenous contrast media and adverse in-hospital outcomes in patients with septic AKI-D. Further studies are warranted to assess the generalizability.

Transitional care program to facilitate recovery following severe acute kidney injury.

Patients with acute kidney injury needing prolonged renal replacement therapy (AKI-RRT) may benefit from a structured care process in form of an AKI transitional care program (ATCP), to facilitate RRT weaning and recovery. We examined outcomes following ATCP implementation in adults with AKI-RRT from a tertiary institution (versus pre-ATCP controls), including mortality, cumulative hospital days, and renal function over one year; RRT and haemodialysis catheter days in initial 90days. We studied 89 patients with age 62 ( ± 15) years. 47% had septic AKI, 20% cardiorenal syndrome, and 29% had baseline eGFR < 30mL/min/1.73 m2. Comparing 45 ATCP patients with 44 controls: 64% and 45% received continuous RRT (CRRT) (p = 0.07), with comparable rates of heart failure (24% versus 25%), ICU care (67% versus 70%), RRT successfully weaned (71% versus 75%), respectively; corresponding mortality rates were 24% and 32% (p = 0.44), hospital days of 205 (197-213) and 223 (215-232) per 1000 patient-days alive over one year (p = 0.002); with comparable RRT and catheter days. Serial serum creatinine in months following RRT cessation were comparable between either survivor-group. On multivariate analysis, heart failure or having received CRRT independently predicted mortality and longer hospital days (p < 0.05); ATCP was independently associated with reduced hospital days (p < 0.001). 17 ATCP patients and 14 controls required outpatient RRT weaning, with catheter days of 607 (568-648) and 683 (638-731) per 1000 patient-days in initial 90days, respectively (p = 0.01). Implementing a structured care pathway in patients with AKI-RRT may help reduce hospitalization, and reduce haemodialysis catheter days in the subgroup for outpatient RRT weaning.

CXCL8(3\u201372) K11R/G31P protects against sepsis-induced acute kidney injury via NF-\u03baB and JAK2/STAT3 pathway

BackgroundAcute kidney injury (AKI), which is mainly caused by sepsis, has high morbidity and mortality rates. CXCL8(3–72) K11R/G31P (G31P) can exert therapeutic effect on inflammatory diseases and malignancies. We aimed to investigate the effect and mechanism of G31P on septic AKI.MethodsAn AKI mouse model was established, and kidney injury was assessed by histological analysis. The contents of serum creatinine (SCr) and blood urea nitrogen (BUN) were measured by commercial kits, whereas neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were detected by enzyme-linked immunosorbent assay (ELISA) kits. The expressions of CXCL8 in serum and kidney tissues were determined using ELISA and immunohistochemical analysis, respectively. Apoptosis rate of renal tissue was detected by terminal deoxynucleotidyl transfer-mediated dUTP nick end labeling (TUNEL) analysis. The expressions of inflammatory cytokines were measured by quantitative real-time PCR and Western blot, respectively. The apoptosis-related proteins, JAK2, STAT3, NF-κB and IκB were determined by Western blot.ResultsG31P could reduce the levels of SCr, BUN, HGAL and KIM-1 and inhibit the renal tissue injury in AKI mice. G31P was also found to suppress the serum and nephric CXCL8 expressions and attenuated the apoptosis rate. The levels of inflammatory cytokines, pro-apoptotic proteins were decreased, while the anti-apoptotic proteins were increased by G31P in AKI mice. G31P also inhibited the activation of JAK2, STAT3 and NF-κB in AKI mice.ConclusionThese results suggest that G31P could protect renal function and attenuate the septic AKI. Our findings provide a potential target for the treatment of AKI.

Sepsis-induced acute kidney injury: A disease of the microcirculation.

AKI is a common complication of sepsis and is significantly associated with mortality. Sepsis accounts for more than 50% of the cases of AKI, with a mortality rate of up to 40%. The pathogenesis of septic AKI is complex, but there is emerging evidence that, at least in the first 48hours, the defects may be functional rather than structural in nature. For example, septic AKI is associated with an absence of histopathological changes, but with microvascular abnormalities and tubular stress. In this context, renal medullary hypoxia due to redistribution of intra-renal perfusion is emerging as a critical mediator of septic AKI. Clinically, vasopressor drugs remain the cornerstone of therapy for maintenance of blood pressure and organ perfusion. However, in septic AKI, there is insensitivity to vasopressors such as norepinephrine, leading to persistent hypotension and organ failure. Vasopressin, angiotensin II, and, paradoxically, α2 -adrenergic receptor agonists (clonidine and dexmedetomidine) may be feasible adjunct therapies for catecholamine-resistant vasodilatory shock. In this review, we outline the recent progress made in understanding how these drugs may influence the renal microcirculation, which represents a crucial step toward developing better approaches for the circulatory management of patients with septic AKI.

CEST MRI of sepsis-induced acute kidney injury.

Sepsis-induced acute kidney injury (SAKI) is a major complication of kidney disease associated with increased mortality and faster progression. Therefore, the development of imaging biomarkers to detect septic AKI is of great clinical interest. In this study, we aimed to characterize the endogenous chemical exchange saturation transfer (CEST) MRI contrast in the lipopolysaccharide (LPS)-induced SAKI mouse model and to investigate the use of CEST MRI for detecting such injury. We used a SAKI mouse model that was generated by i.p. injection of 10mg/kg LPS. The resulting kidney injury was confirmed by the elevation of serum creatinine and histology. MRI assessments were performed 24h after LPS injection, including CEST MRI at different B1 strengths (1, 1.8 and 3 μT), T1 mapping, T2 mapping and conventional magnetization transfer contrast (MTC) MRI. The CEST MRI results were analyzed using Z-spectra, in which the normalized water signal saturation (Ssat /S0 ) is measured as a function of saturation frequency. Substantial decreases in CEST contrast were observed at both 3.5 and-3.5ppm frequency offset from water at all B1 powers, with the most significant difference obtained at a B1 of 1.8 μT. The average Ssat /S0 differences between injured and normal kidneys were 0.07 (0.55±0.04 versus 0.62±0.04, P=0.0028) and 0.07 (0.50±0.04 versus 0.57±0.03, P=0.0008) for 3.5 and-3.5ppm, respectively. In contrast, the T1 and T2 relaxation times and MTC contrast in the injured kidneys did not show a significant change compared with the normal control. Our results showed that CEST MRI is more sensitive to the pathological changes in injured kidneys than the changes in T1 , T2 and MTC effect, indicating its potential clinical utility for molecular imaging of renal diseases.

Septic acute kidney injury patients in emergency department: The risk factors and its correlation to serum lactate

BackgroundAcute kidney injury (AKI) is a common complication in septic patients, imposing a heavy burden of illness in terms of morbidity and mortality. Serum lactate is a widely used marker predicting the severity of sepsis. A paucity of research has investigated septic AKI in emergency departments (EDs) and its correlation with initial serum lactate level. This study aimed at identifying risk factors for septic AKI and clarifying the link between initial serum lactate level and septic AKI in ED patients. MethodsA retrospective cohort study was conducted at a single tertiary referral medical center. The medical records of all adult ED patients with measurement of serum lactate and creatinine between January 2012 and December 2016 were reviewed. A total of 696 septic patients were stratified into AKI and non-AKI groups according to Acute Kidney Injury Network (AKIN) criteria for further statistical analysis. ResultsNinety-nine septic patients (14.2%) had AKI, with AKIN-I, AKIN-II, and AKIN-III in 71.7%, 11.1%, and 17.2% of patients, respectively. Compared with the non-AKI group, the AKI group had a significantly higher mortality rate (71.7% vs. 21.3%, p < 0.001). Independent risk factors for septic AKI included liver disease (adjusted odds ratio [AOR] = 2.02, 95% confidence interval [CI] = 1.16–3.52), diabetes mellitus (AOR = 1.73, 95% CI = 1.11–2.69), chronic kidney disease (AOR = 1.68, 95% CI = 1.06–2.66), and initial serum lactate (AOR = 1.08, 95% CI = 1.02–1.14). ConclusionsPatients with septic AKI had an overwhelmingly higher mortality rate. The comorbidities of liver disease, diabetes mellitus, and chronic kidney disease were correlated with septic AKI and in combination with an elevated initial serum lactate level had predictive regarding AKI and further mortality in ED septic patients.

Genetic or pharmacologic inhibition of EGFR ameliorates sepsis-induced AKI.

Despite recent studies have demonstrated that the EGF receptor (EGFR) activation provided a renoprotective role during ischemic and folic acid-induced AKI, the role and regulation mechanism of EGFR in septic AKI remains unclear. Here, gefitinib, a highly selective EGFR inhibitor, abrogated LPS-induced phosphorylation of EGFR, ERK1/2, and STAT3 as well as expression of COX, eNOS, and proinflammatory cytokines in HK-2 cells. In addition, c-Src is an upstream of EGFR signaling pathway and mediates LPS-induced EGFR transactivation. In vivo, either gefitinib or genetic approaches (Wave-2 mutant mice, which have reduced EGFR tyrosine kinase activity) protected against LPS or cecal ligation and puncture (CLP) induced AKI respectively. Interestingly, the beneficial effects of gefitinib or genetic approaches were accompanied by the dephosphorylation of EGFR, ERK1/2, and STAT3, the down regulation of expression of COX, eNOS, macrophage infiltration, proinflammatory cytokines production and the renal cell apoptosis. Furthermore, mRNA array results indicated that gene families involved in cell death, inflammation, proliferation and signal transduction were down regulated in Wave-2 (Wa-2) mice. Take together, these data suggest that EGFR may mediate renal injury by promoting production of inflammatory factors and cell apoptosis. Inhibition of EGFR may have therapeutic potential for AKI during endotoxemia.

Cardiac surgery-associated acute kidney injury: risk factors, pathophysiology and treatment.

Cardiac surgery-associated acute kidney injury (CSA-AKI) is the most common clinically important complication in adult patients undergoing open heart surgery, and is associated with increased mortality and morbidity. In patients in intensive care units, CSA-AKI is the second most common type of AKI after septic AKI. In this Review, we explore the definition of CSA-AKI, discuss its epidemiology and identify its risk factors. We discuss current theories of the pathophysiology of CSA-AKI and describe its clinical course. Furthermore, we introduce diagnostic tools with particular reference to novel biomarkers of AKI and their potential utility; we analyse currently applied interventions aimed at attenuating AKI in patients undergoing cardiac surgery; and describe evidence from randomized controlled trials aimed at preventing or treating CSA-AKI. Finally, we explore issues in the use of renal replacement therapy, its timing, its intensity and its preferred modalities in patients with CSA-AKI, and we discuss the prognosis of CSA-AKI in terms of patient survival and kidney recovery.

062 PREVALENCE OF ACUTE KIDNEY INJURY AND SEPSIS IN A MALAYSIAN INTENSIVE CARE SETTING

Introduction Acute Kidney Injury (AKI) is common in patients admitted to the intensive care unit, occurring in 30 to 60% of patients. The high incidence of AKI in our population may be attributed to sepsis. Sepsis is the leading cause of ICU admission. The Malaysian Registry of Intensive Care (MRIC), an annual ICU audit performed in all Malaysian ICUs. This registry serves as an excellent avenue to explore the incidence of septic AKI in our local ICU. Methods This retrospective cohort study extracted de-identified data from the Malaysian Registry of Intensive Care (MRIC) for patients admitted to Hospital Tengku Ampuan Afzan between January and December 2014. The study was registered under the NMRR (NMRR-14-1938-23183) and approved by the ethics committee. AKI was defined as doubling of serum creatinine from baseline value. Results A total of 1059 ICU admissions were analysed. Of these 230 (21.7%) had AKI and 253 (23.9%) had sepsis within 24 hours of admission. Patients with AKI were older and had higher severity of illness compared to those without AKI (p<0.0001). Diabetes mellitus, chronic renal failure and hypertension were more common in patients with AKI. Twenty percent of patients received dialysis, and 23% died. Of those who survived, AKI patients had longer duration of mechanical ventilation, length of ICU and hospital stay (p<0.0001). Seventy-three percent (n=168) of patients with sepsis had AKI (p<0.0001). Conclusions AKI is common in our ICU, with higher morbidity and mortality. Risk factors of AKI includes age, severity of illness, the presence of sepsis and pre-existing diabetes mellitus, chronic renal failure, and hypertension. Future analysis will explore a larger cohort of data involving four tertiary hospitals over a five-year duration.

Cytoprotective Effect of Heat Shock Protein 27 Against Lipopolysaccharide-Induced Apoptosis of Renal Epithelial HK-2 Cells

Background: In response to various stimuli, heat shock protein 27 (Hsp27) functions as an anti-apoptotic or/and anti-inflammatory factor which confers a survival advantage to cells. This study was aimed to explore whether Hsp27 also has a cytoprotective role in human renal tubular epithelial cells, and to evaluate its potential in treating septic acute kidney injury (septic AKI). Methods: HK-2 cells were subjected to different concentrations (0-10 µg/mL) of lipopolysaccharide (LPS) for various times (0-24 h) to establish a septic AKI model in vitro. Before LPS administration, HK-2 cells were transfected either with vectors or siRNA against Hsp27, and the changes in cell viability and apoptotic cells rate were assessed using CCK-8 and flow cytometry. The expression changes in apoptosis-related proteins, proinflammatory cytokines and chemokine, as well as main factors in NF-κB and JNK pathways were mainly determined by Western blotting. Besides, the relationship between Hsp27 and Bcl-2 was detected by co-immunoprecipitation. Results: LPS remarkably damaged HK-2 cells by reduction of cell viability, induction of apoptosis, and stimulation of proinflammatory cytokines and chemokine release. Hsp27 overexpression significantly impaired LPS-induced damage in HK-2 cells. Hsp27 overexpression couldn’t alter the mRNA level of Bcl-2, but could interact with Bcl-2 at an endogenous level. Both NF-κB and JNK pathways were activated by LPS, while were blocked in Hsp27-overexpressing cells. Conclusion: Hsp27 overexpression conferred a survival advantage to LPS-injured HK-2 cells by controlling cell viability, apoptosis and inflammation, possibly via interaction with Bcl-2 and modulation of NF-κB and JNK pathways.

Acute Kidney Injury in Pregnancy-specific Disorders.

The incidence of acute kidney injury in pregnancy (P-AKI) has declined significantly over the last three decades in developing countries. However, it is still associated with significant fetomaternal mortality and morbidity. The diagnosis of P-AKI is based on the serum creatinine increase. The usual formulas for estimating glomerular filtration rate (GFR) are not validated in this population. The incidence of P-AKI with respect to total AKI cases has decreased in the last three decades from 25% in 1980s to 9% in 2000s at our centre. During the first trimester of gestation, AKI develops most often due to septic abortion or hyperemesis gravidarum. Septic abortion related AKI with respect to total AKI decreased from 9% to 5% in our study. Prevention of unwanted pregnancy and avoidance of septic abortion are keys to eliminate abortion associated AKI in early pregnancy. However, we have not seen AKI on account of hyperemesis gravidarum over a period of 33 years at our center. In the third trimester, the differential diagnosis of AKI in association with pregnancy specific conditions namely preeclampsia/HELLP syndrome, acute fatty liver of pregnancy and thrombotic microangiopathies of pregnancy (P-TMA) is more challenging, because these 3 conditions share several clinical features of thrombotic microangiopathy which makes the diagnosis very difficult on clinical grounds. It is imperative to distinguish these conditions to make appropriate therapeutic decisions. Typically, AFLP and HELLP syndrome improve after delivery of the fetus, whereas plasma exchange is the first-line treatment for pregnancy associated thrombotic microangioathies (P-TMA). We observed that preclampsia/eclampsia is the most common cause of AKI in late third trimester and postpartum periods followed by puerperal sepsis and postpartum hemorrhage. Pregnancy-associated thrombotic microangiopathies (aHUS/TTP) and AFLP are rare causes of AKI during pregnancy in developing countries.

Septic acute kidney injury in critically ill patients – a single-center study on its incidence, clinical characteristics, and outcome predictors

Purpose The objective of this study is to examine the incidence, clinical characteristics, and outcome (90-day mortality) of critically ill Chinese patients with septic AKI. Methods Patients admitted to the ICU of a regional hospital from 1 January 2011 to 31 December 2013 were included, excluding those on chronic renal replacement therapy. AKI was defined using KDIGO criteria. Patients were followed till 90 days from ICU admission or death, whichever occurred earlier. Demographics, diagnosis, clinical characteristics, and outcome were analyzed. Results In total, 3687 patients were included and 54.7% patients developed AKI. Sepsis was the most common cause of AKI (49.2%). Compared to those without AKI, AKI patients had higher disease severity, more physiological and biochemical disturbance, and carried significant co-morbidities. Ninety-day mortality increased with severity of AKI (16.7, 27.5, and 48.3% for KDIGO stage 1, 2, and 3 AKI, p < 0.001). Full renal recovery was achieved in 71.6% of AKI patients. Compared with non-septic AKI, septic AKI was associated with higher disease severity and required more aggressive support. Non-recovery of renal function occurred in 2.5% of patients with septic AKI, compared with 6.4% in non-septic AKI (p < 0.001). Cox regression analysis showed that age, emergency ICU admission, post-operative cases, admission diagnosis, etiology of AKI, disease severity score, mechanical ventilation, vasopressor support, and blood parameters (like albumin, potassium and pH) independently predicted 90-day mortality. Conclusions AKI, especially septic AKI is common in critically ill Chinese patients and is associated with poor patient outcome. Etiology of AKI has a significant impact on 90-day mortality and may affect renal outcome.

Management of acute kidney injury in sepsis

Abstract Acute kidney injury and multiorgan dysfunction due to sepsis and septic shock increase the morbidity and mortality among critically ill patients. It remains an important challenge in critically ill patients. In this review, management of septic AKI in terms of prevention, medical therapies, and extracorporeal therapies is discussed. Stabilizing the hemodynamic parameters by fluid resuscitation and inotropic support are important strategies to prevent acute kidney injury in the initial stages. Controversies exist in the timing of initiating renal replacement therapy although some studies showed improved outcomes with early initiation. The recommended dose of renal replacement therapy (25 ml/kg/hr) had not shown to be associated with improved survival in randomized studies. The clinical benefit of other therapies, like hemoadsorption, and alkaline phosphatase use is still uncertain. Mesenchymal stem cell therapies are in phase I trials.

Reduction of Tubular Flow Rate as a Mechanism of Oliguria in the Early Phase of Endotoxemia Revealed by Intravital Imaging.

Urine output is widely used as a criterion for the diagnosis of AKI. Although several potential mechanisms of septic AKI have been identified, regulation of urine flow after glomerular filtration has not been evaluated. This study evaluated changes in urine flow in mice with septic AKI. The intratubular urine flow rate was monitored in real time by intravital imaging using two-photon laser microscopy. The tubular flow rate, as measured by freely filtered dye (FITC-inulin or Lucifer yellow), time-dependently declined after LPS injection. At 2 hours, the tubular flow rate was slower in mice injected with LPS than in mice injected with saline, whereas BP and GFR were similar in the two groups. Importantly, fluorophore-conjugated LPS selectively accumulated in the proximal tubules that showed reduced tubular flow at 2 hours and luminal obstruction with cell swelling at 24 hours. Delipidation of LPS or deletion of Toll-like receptor 4 in mice abolished these effects, whereas neutralization of TNF-α had little effect on LPS-induced tubular flow retention. Rapid intravenous fluid resuscitation within 6 hours improved the tubular flow rate only when accompanied by the dilation of obstructed proximal tubules with accumulated LPS. These findings suggest that LPS reduces the intratubular urine flow rate during early phases of endotoxemia through a Toll-like receptor 4-dependent mechanism, and that the efficacy of fluid resuscitation may depend on the response of tubules with LPS accumulation.

Risk factors for mortality in patients with septic acute kidney injury in intensive care units in Beijing, China: a multicenter prospective observational study.

Objective. To discover risk factors for mortality of patients with septic AKI in ICU via a multicenter study. Background. Septic AKI is a serious threat to patients in ICU, but there are a few clinical studies focusing on this. Methods. This was a prospective, observational, and multicenter study conducted in 30 ICUs of 28 major hospitals in Beijing. 3,107 patients were admitted consecutively, among which 361 patients were with septic AKI. Patient clinical data were recorded daily for 10 days after admission. Kidney Disease: Improving Global Outcomes (KDIGO) criteria were used to define and stage AKI. Of the involved patients, 201 survived and 160 died. Results. The rate of septic AKI was 11.6%. Twenty-one risk factors were found, and six independent risk factors were identified: age, APACHE II score, duration of mechanical ventilation, duration of MAP <65 mmHg, time until RRT started, and progressive KIDGO stage. Admission KDIGO stages were not associated with mortality, while worst KDIGO stages were. Only progressive KIDGO stage was an independent risk factor. Conclusions. Six independent risk factors for mortality for septic AKI were identified. Progressive KIDGO stage is better than admission or the worst KIDGO for prediction of mortality. This trial is registered with ChiCTR-ONC-11001875.

Dying Cells and Extracellular Histones in AKI

Dying Cells and Extracellular Histones in AKI

Significant microalbuminuria, on admission to the ICU, may indicate AKI in patients with sepsis

In sepsis, a generalised inflammatory onslaught causes systemic endothelial dysfunction; the glomerular manifestation of which is microalbuminuria. Recent histopathological evidence of extensive glomerular capillary infiltration by leucocytes in septic AKI suggests that endothelial dysfunction may play a particularly important role in this condition compared with patients with other causes of AKI. Markers of endothelial dysfunction such as microalbuminuria may therefore have a potential diagnostic role in septic AKI.