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Sepsis-induced acute kidney injury  [cached]
Majumdar Arghya
Indian Journal of Critical Care Medicine , 2010,
Abstract: Acute kidney injury (AKI) is a common sequel of sepsis in the intensive care unit. It is being suggested that sepsis-induced AKI may have a distinct pathophysiology and identity. Availability of biomarkers now enable us to detect AKI as early as four hours after it′s inception and may even help us to delineate sepsis-induced AKI. Protective strategies such as preferential use of vasopressin or prevention of intra-abdominal hypertension may help, in addition to the other global management strategies of sepsis. Pharmacologic interventions have had limited success, may be due to their delayed usage. Newer developments in extracorporeal blood purification techniques may proffer effects beyond simple replacement of renal function, such as metabolic functions of the kidney or modulation of the sepsis cascade.
Management of Sepsis-Induced Acute Kidney Injury  [cached]
Senaka Rajapakse,Chaturaka Rodrigo,Eranga S. Wijewickrema
Sri Lanka Journal of Critical Care , 2009,
Abstract: Acute kidney injury (AKI) occurs in a significant proportion of patients with severe sepsis, and is an important cause of mortality in such patients. Current concepts of pathogenesis of AKI are shifting from vasoconstriction-ischaemia induced injury to toxic and immune mediated injury and hyperaemic injury resulting in apoptosis of renal cells. Renal replacement therapy is the mainstay of management of AKI. Adequacy of dialysis is likely to be linked to better outcome, but there is still no clear consensus on the timing, modality, intensity or frequency of dialysis. Haemodynamically unstable patients usually require modes of continuous renal replacement therapy. Biocompatible dialyser membranes are likely to be safer than older cellulose membranes. Bicarbonate is preferred to acetate and lactate as dialysate buffer. Anticoagulation has to be undertaken with care to prevent excessive haemorrhage in the setting of already deranged haemostasis. Adequate volume resuscitation and maintenance of renal perfusion by the use of vasopressors is beneficial; norepinephrine is the vasopressor of choice. There is no place for the use of low- or renal-dose dopamine, mannitol or frusemide in the setting of sepsis-induced AKI, and in fact they may be detrimental. Prevention of kidney damage by nephrotoxic drugs and radio-contrast media is of vital importance. Careful dose management of nephrotoxic drugs will prevent renal injury. Hydration prior to administration of contrast media prevents nephrotoxicity, but the benefit of N-Acetylcysteine is unclear. Tight glycaemic control may have renoprotective effects, though its place in the management of severe sepsis is now controversial. No clear evidence of benefit is seen with other newer therapies.
Acute Lung Injury and Acute Kidney Injury Are Established by Four Hours in Experimental Sepsis and Are Improved with Pre, but Not Post, Sepsis Administration of TNF-α Antibodies  [PDF]
Rhea Bhargava, Christopher J. Altmann, Ana Andres-Hernando, Ryan G. Webb, Kayo Okamura, Yimu Yang, Sandor Falk, Eric P. Schmidt, Sarah Faubel
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0079037
Abstract: Introduction Acute kidney injury (AKI) and acute lung injury (ALI) are serious complications of sepsis. AKI is often viewed as a late complication of sepsis. Notably, the onset of AKI relative to ALI is unclear as routine measures of kidney function (BUN and creatinine) are insensitive and increase late. In this study, we hypothesized that AKI and ALI would occur simultaneously due to a shared pathophysiology (i.e., TNF-α mediated systemic inflammatory response syndrome [SIRS]), but that sensitive markers of kidney function would be required to identify AKI. Methods Sepsis was induced in adult male C57B/6 mice with 5 different one time doses of intraperitoneal (IP) endotoxin (LPS) (0.00001, 0.0001, 0.001, 0.01, or 0.25 mg) or cecal ligation and puncture (CLP). SIRS was assessed by serum proinflammatory cytokines (TNF-α, IL-1β, CXCL1, IL-6), ALI was assessed by lung inflammation (lung myeloperoxidase [MPO] activity), and AKI was assessed by serum creatinine, BUN, and glomerular filtration rate (GFR) (by FITC-labeled inulin clearance) at 4 hours. 20 μgs of TNF-α antibody (Ab) or vehicle were injected IP 2 hours before or 2 hours after IP LPS. Results Serum cytokines increased with all 5 doses of LPS; AKI and ALI were detected within 4 hours of IP LPS or CLP, using sensitive markers of GFR and lung inflammation, respectively. Notably, creatinine did not increase with any dose; BUN increased with 0.01 and 0.25 mg. Remarkably, GFR was reduced 50% in the 0.001 mg LPS dose, demonstrating that dramatic loss of kidney function can occur in sepsis without a change in BUN or creatinine. Prophylactic TNF-α Ab reduced serum cytokines, lung MPO activity, and BUN; however, post-sepsis administration had no effect. Conclusions ALI and AKI occur together early in the course of sepsis and TNF-α plays a role in the early pathogenesis of both.
Injuria renal aguda en la sepsis grave Acute kidney injury in severe sepsis
Hernán Trimarchi,Christian Nozieres,Vicente Cámpolo Girard,Fernando Lombi
Medicina (Buenos Aires) , 2009,
Abstract: La sepsis afecta al 40% de los pacientes críticos, siendo su mortalidad de aproximadamente un 30% en el caso de la sepsis grave, y de 75% con injuria renal aguda, la cual sucede en el 20-51% de los casos. Se realizó un estudio prospectivo, observacional, longitudinal, en 80 pacientes sépticos graves en el lapso de 1 a o para determinar el desarrollo de injuria renal aguda y su relación con la mortalidad; correlacionar antecedentes clínicos y variaciones del laboratorio con la mortalidad; determinar la tasa de mortalidad de la sepsis grave; relacionar óbito y foco séptico primario; evaluar la predictibilidad de mortalidad según niveles de creatinina de ingreso y sus variaciones finales. Se definieron dos grupos: Obito (n = 25) y No-óbito (n = 55). Analizados según la creatinina de ingreso, 39 tenían valores normales de creatinina (10 óbitos) y 41 la presentaban elevada (15 óbitos); según la creatinina de egreso, 48 presentaron creatinina normal y fallecieron 7, mientras que 32 tenían da o renal agudo, de los cuales 18 fallecieron. De los 25 pacientes fallecidos, el 72% presentaron da o renal. De éstos, 7 pacientes vivos y 2 fallecidos requirieron hemodiálisis. El foco primario más frecuente fue el respiratorio (26.4%). El desarrollo de da o renal es un alto predictor de mortalidad en la sepsis, independientemente de los valores iniciales de creatinina. Edad más avanzada, hipertensión arterial, score APACHE más elevado, anemia más grave, hipoalbuminemia, hiperfosfatemia e hiperkalemia se asociaron a mayor mortalidad. La mortalidad global fue 31.3%. La imposibilidad de identificar el foco séptico primario se asoció a mayor mortalidad. El foco respiratorio se relacionó a mayor riesgo de requerir hemodiálisis. Sepsis affects 40% of critically ill patients, with a reported mortality of approximately 30% in severe sepsis, raising to 75% when acute kidney injury ensues, which occurs in about 20-51% of cases. The present study consists on a one-year prospective, observational, longitudinal trial undergone in 80 severe septic patients to determine the risk of development of acute kidney injury and its relationship with mortality; the association of the clinical course and blood parameter variations with mortality; the severe sepsis mortality rate; an eventual correlation between death and septic focus, and to assess mortality predictibility based on initial creatinine levels and final variations. Two groups were defined: Dead (n=25) and Not-dead (n=55). According to creatinine on admission, 39 subjects presented with normal creatinine levels (10 deaths) and 41 pr
Early acute kidney injury and sepsis: a multicentre evaluation
Sean M Bagshaw, Carol George, Rinaldo Bellomo, the ANZICS Database Management Committee
Critical Care , 2008, DOI: 10.1186/cc6863
Abstract: The study was a retrospective interrogation of prospectively collected data from the Australian New Zealand Intensive Care Society Adult Patient Database. Data were collected from 57 intensive care units (ICUs) across Australia. In total, 120,123 patients admitted to ICU for more than 24 hours from 1 January 2000 to 31 December 2005 were included in the analysis. The main outcome measures were clinical and laboratory data and outcomes.Of 120,123 patients admitted, 33,375 had a sepsis-related diagnosis (27.8%). Among septic patients, 14,039 (42.1%) had concomitant AKI (septic AKI). Sepsis accounted for 32.4% of all patients with AKI. For septic AKI stratified by RIFLE (risk of renal failure, injury to the kidney, failure of kidney function, loss of kidney function and end-stage kidney disease) category, 38.5% of patients belonged to the risk category, 38.8% to the injury category and 22.7% to the failure category. Septic AKI patients had greater acuity of illness (P < 0.0001), lower blood pressure (P < 0.0001), higher heart rates (P < 0.0001), worse pulmonary function measures by arterial oxygen tension/fraction of inspired oxygen ratio (P < 0.0001), greater acidaemia (P < 0.0001) and higher white cell counts (P < 0.0001) compared with patients with nonseptic AKI. Septic AKI was also associated with greater severity of AKI (RIFLE category injury or failure) compared with nonseptic AKI. Septic AKI was associated with a significantly higher crude and co-variate adjusted mortality in the ICU (19.8% versus 13.4%; odds ratio 1.60, 95% confidence interval 1.5 to 1.7; P < 0.001) and in hospital (29.7% versus 21.6%; odds ratio 1.53, 95% confidence interval 1.46 to 1.60; P < 0.001) compared with nonseptic AKI. Septic AKI was associated with higher ICU and hospital mortality across all strata of RIFLE categories. Septic AKI patients had longer durations of stay in both ICU and hospital across all strata of RIFLE categories.Septic AKI is common during the first 24 hours after I
Long-term risk of mortality after acute kidney injury in patients with sepsis: a contemporary analysis
José António Lopes, Paulo Fernandes, Sofia Jorge, Cristina Resina, Carla Santos, álvaro Pereira, José Neves, Francisco Antunes, António Gomes da Costa
BMC Nephrology , 2010, DOI: 10.1186/1471-2369-11-9
Abstract: We retrospectively evaluated the impact of AKI, defined by the "Risk, Injury, Failure, Loss of kidney function, End-stage kidney disease" (RIFLE) classification based on creatinine criteria, on 2-year mortality in a cohort of 234 hospital surviving septic patients who had been hospitalized at the Infectious Disease Intensive Care Unit of our Hospital.Mean-follow-up was 21 ± 6.4 months. During this period, 32 patients (13.7%) died. At 6 months, 1 and 2 years of follow-up, the cumulative probability of death of patients with previous AKI was 8.3, 16.9 and 34.2%, respectively, as compared with 2.2, 6 and 8.9% in patients without previous AKI (log-rank, P < 0.0001). In the univariate analysis, age (hazard ratio 1.4, 95% CI 1.2-1.7, P < 0.0001), as well as pre-existing cardiovascular disease (hazard ratio 3.6, 95% CI 1.4-9.4, P = 0.009), illness severity as evaluated by nonrenal APACHE II (hazard ratio 1.3, 95% CI 1.1-1.6, P = 0.002), and previous AKI (hazard ratio 4.2, 95% CI 2.1-8.5, P < 0.0001) were associated with increased 2-year mortality, while gender, race, pre-existing hypertension, cirrhosis, HIV infection, neoplasm, and baseline glomerular filtration rate did not. In the multivariate analysis, however, only previous AKI (hazard ratio 3.2, 95% CI 1.6-6.5, P = 0.001) and age (hazard ratio 1.4, 95% CI 1.2-1.6, P < 0.0001) emerged as independent predictors of 2-year mortality.Acute kidney injury had a negative impact on long-term mortality of patients with sepsis.Acute kidney injury (AKI) is a common complication among hospitalized patients, particularly in the Intensive Care Unit (ICU) setting, and it portends an ominous outcome. In fact, the incidence of AKI in critically ill patients varies from 35 to 70%, and it is associated with increased in-hospital mortality (10 to 60%) [1-4].Although AKI is a common complication in the hospital and has an immediate impact on morbidity, mortality, and resource utilization, its detrimental effect appears to persist also aft
Effects of Continuous Erythropoietin Receptor Activator in Sepsis-Induced Acute Kidney Injury and Multi-Organ Dysfunction  [PDF]
Camila E. Rodrigues, Talita R. Sanches, Rildo A. Volpini, Maria H. M. Shimizu, Patrícia S. Kuriki, Niels O. S. Camara, Antonio C. Seguro, Lúcia Andrade
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0029893
Abstract: Background Despite advances in supportive care, sepsis-related mortality remains high, especially in patients with acute kidney injury (AKI). Erythropoietin can protect organs against ischemia and sepsis. This effect has been linked to activation of intracellular survival pathways, although the mechanism remains unclear. Continuous erythropoietin receptor activator (CERA) is an erythropoietin with a unique pharmacologic profile and long half-life. We hypothesized that pretreatment with CERA would be renoprotective in the cecal ligation and puncture (CLP) model of sepsis-induced AKI. Methods Rats were randomized into three groups: control; CLP; and CLP+CERA (5 μg/kg body weight, i.p. administered 24 h before CLP). At 24 hours after CLP, we measured creatinine clearance, biochemical variables, and hemodynamic parameters. In kidney tissue, we performed immunoblotting—to quantify expression of the Na-K-2Cl cotransporter (NKCC2), aquaporin 2 (AQP2), Toll-like receptor 4 (TLR4), erythropoietin receptor (EpoR), and nuclear factor kappa B (NF-κB)—and immunohistochemical staining for CD68 (macrophage infiltration). Plasma interleukin (IL)-2, IL-1β, IL-6, IL-10, interferon gamma, and tumor necrosis factor alpha were measured by multiplex detection. Results Pretreatment with CERA preserved creatinine clearance and tubular function, as well as the expression of NKCC2 and AQP2. In addition, CERA maintained plasma lactate at normal levels, as well as preserving plasma levels of transaminases and lactate dehydrogenase. Renal expression of TLR4 and NF-κB was lower in CLP+CERA rats than in CLP rats (p<0.05 and p<0.01, respectively), as were CD68-positive cell counts (p<0.01), whereas renal EpoR expression was higher (p<0.05). Plasma levels of all measured cytokines were lower in CLP+CERA rats than in CLP rats. Conclusion CERA protects against sepsis-induced AKI. This protective effect is, in part, attributable to suppression of the inflammatory response.
Sepsis as a major determinant of outcome in critically ill HIV/AIDS patients: don't forget acute kidney injury
José Lopes, Sofia Jorge
Critical Care , 2012, DOI: 10.1186/cc11870
Abstract: Rodrigo Teixeira Amancio, André Miguel Japiassú and Fernando Augusto BozzaAcute renal failure (ARF) is one of the major determinants of hospital outcome in the critically ill population, and severe sepsis is the main cause of ARF in this setting [5]. Patients with HIV/AIDS show a predisposition to renal dysfunction, as the HIV and antiretroviral drugs can lead to renal tubular dysfunction [6]. Lopes and colleagues [3,4] have reported that ARF is independently associated with hospital mortality of critically ill patients with HIV.We evaluated 88 HIV-positive critically ill patients, seeking the main risk factors for mortality [1]. Severe sepsis was the major factor associated with 28-day and 6-month mortality. CD4 cell count, viral load, and the use of antiretrovirals were not associated with survival. As suggested by Lopes and Jorge, we reanalyzed the data about organ dysfunctions in that cohort, targeting hospital outcome. Nonsurvivors presented higher rates of renal (63% versus 33%, P = 0.01) and hematological (42% versus 16%, P = 0.009) dysfunctions than survivors of HIV/AIDS. We included these organ dysfunctions in a new multivariate analysis; severe sepsis remained the main factor associated with hospital survival (odds ratio (OR) 4.2, 95% confidence interval (CI) 1.2 to 14.2, P = 0.02), and renal (OR 2.6, 95% CI 0.9 to 7.4, P = 0.06) and hematological (OR 2.7, 95% CI 0.9 to 8.5, P = 0.08) dysfunction had borderline results (Table 1). We also reevaluated our current cohort, reaching 139 patients with HIV, and the presence of renal failure was related to poorer prognosis but was not associated with hospital mortality in the multivariate analysis (OR 1.9, 95% CI 0.8 to 4.4, P = 0.15). We agree that renal dysfunction, especially when associated with severe sepsis, can reduce survival among critically ill patients with HIV/AIDS.AKI: acute kidney injury; ARF: acute renal failure; CI: confidence interval; OR: odds ratio.The authors declare that they have no competing
Doppler resistive index to reflect regulation of renal vascular tone during sepsis and acute kidney injury
Antoine Dewitte, Julien Coquin, Bertrand Meyssignac, Olivier Joannès-Boyau, Catherine Fleureau, Hadrien Roze, Jean Ripoche, Gérard Janvier, Christian Combe, Alexandre Ouattara
Critical Care , 2012, DOI: 10.1186/cc11517
Abstract: This prospective observational study included 96 patients. AKI was defined according to RIFLE criteria and transient or persistent AKI according to renal recovery within 3 days.Median renal RIs were 0.72 (0.68-0.75) in patients without AKI and 0.76 (0.72-0.80) in patients with AKI (P=0.001). RIs were 0.75 (0.72-0.79) in transient AKI and 0.77 (0.70-0.80) in persistent AKI (P=0.84). RI did not differ in patients given norepinephrine infusion and was not correlated with norepinephrine dose. RI was correlated with MAP (ρ= -0.47; P=0.002), PaO2/FiO2 ratio (ρ= -0.33; P=0.04) and age (ρ=0.35; P=0.015) only in patients without AKI.A poor correlation between renal RI and MAP, age, or PaO2/FiO2 ratio was found in septic and critically ill patients without AKI compared to patients with AKI. These findings suggest that determinants of RI are multiple. Renal circulatory response to sepsis estimated by Doppler ultrasonography cannot reliably be predicted simply from changes in systemic hemodynamics. As many factors influence its value, the interest in a single RI measurement at ICU admission to determine optimal MAP remains uncertain.In critically ill patients, sepsis and acute kidney injury (AKI) are very common diseases and are associated with increased hospitalization and elevated in-hospital mortality rates [1,2]. AKI is a dynamic process that evolves from an early reversible condition to an established disease and leads to sustained renal impairment, cell death, and delayed renal recovery [3,4]. Consequently, prompt resuscitation of the circulation and optimal perfusion pressure are the primary therapies for critically ill patients with AKI. These methods are based principally on the appropriate management of intravenous fluid replacement and vasopressor administration under strict hemodynamic monitoring [5].To date, the pathogenesis of septic AKI is not completely known [6]. An increase in renal vascular resistance (RVR), associated with reduced renal blood flow (RBF) and,
A Multicentre Study of Acute Kidney Injury in Severe Sepsis and Septic Shock: Association with Inflammatory Phenotype and HLA Genotype  [PDF]
Didier Payen, Anne-Claire Lukaszewicz, Matthieu Legrand, Etienne Gayat, Valérie Faivre, Bruno Megarbane, Elie Azoulay, Fabienne Fieux, Dominique Charron, Pascale Loiseau, Marc Busson
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035838
Abstract: Background To investigate the association between severity of acute kidney injury (AKI) and outcome, systemic inflammatory phenotype and HLA genotype in severe sepsis. Methodology/Principal Findings Prospective multicenter observational study done in 4 intensive care units in two university hospitals. Severe sepsis and septic shock patients with at least 2 organ failures based on the SOFA score were classified: 1) "no AKI", 2) "mild AKI" (grouping stage 1 and 2 of AKIN score) and 3) "severe AKI" (stage 3 of AKIN score). Sequential measurements: The vasopressor dependency index (VDI; dose and types of drugs) to evaluate the association between hemodynamic status and the development of early AKI; plasma levels of IL-10, macrophage migration inhibitory factor (MIF), IL-6 and HLA-DR monocyte expression. Genotyping of the 13 HLA-DRB1 alleles with deduction of presence of HLA-DRB3, -DRB4 and -DRB5 genes. We used multivariate analysis with competitive risk model to study associations. Overall, 176 study patients (146 with septic shock) were classified from AKIN score as "no AKI" (n = 43), "mild AKI" (n = 74) or "severe AKI" (n = 59). The VDI did not differ between groups of AKI. After adjustment, "mild and severe AKI" were an independent risk factor for mortality (HR 2.42 95%CI[1.01-5.83], p = 0.048 and HR 1.99 95%CI[1.30-3.03], p = 0.001 respectively). "Severe AKI" had higher levels of plasma IL-10, MIF and IL-6 compared to “no AKI” and mild AKI (p<0.05 for each), with no difference in mHLA-DR at day 0. HLA-DRB genotyping showed a significantly lower proportion of 4 HLA-DRB alleles among patients requiring renal replacement therapy (RRT) (58%) than in patients with severe AKI who did not receive RRT (84%) (p = 0.004). Conclusions AKI severity is independently associated with mortality and plasma IL-10, MIF or IL-6 levels. Presence of 4 alleles of HLA-DRB in severe AKI patients seems associated with a lower need of RRT.
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