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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.
Update on the diagnosis and management of acute kidney injury  [cached]
Ali Akcay,Kultigin Turkmen,DongWon Lee,et al
International Journal of Nephrology and Renovascular Disease , 2010,
Abstract: Ali Akcay, Kultigin Turkmen, DongWon Lee, Charles L EdelsteinDivision of Renal Diseases and Hypertension, University of Colorado and the Health Sciences Center, Aurora, Colorado, USAAbstract: 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.Keywords: acute kidney injury, biomarkers, interleukin-18
Volume Management in the Critically Ill Patient with Acute Kidney Injury  [PDF]
Mary Labib,Raeesa Khalid,Akram Khan,Supriya Khan
Critical Care Research and Practice , 2013, DOI: 10.1155/2013/792830
Abstract: Acute kidney injury (AKI) frequently occurs in the setting of critical illness and its management poses a challenge for the intensivist. Optimal management of volume status is critical in the setting of AKI in the ICU patient. The use of urine sodium, the fractional excretion of sodium (FeNa), and the fractional excretion of urea (FeUrea) are common clinical tools used to help guide fluid management especially further volume expansion but should be used in the context of the patient’s overall clinical scenario as they are not completely sensitive or specific for the finding of volume depletion and can be misleading. In the case of oliguric or anuric AKI, diuretics are often utilized to increase the urine output although current evidence suggests that they are best reserved for the treatment of volume overload and hyperkalemia in patients who are likely to respond to them. Management of volume overload in ICU patients with AKI is especially important as volume overload has several negative effects on organ function and overall morbidity and mortality. 1. Introduction Acute kidney injury (AKI) is a frequent complication in critically ill patients in the intensive care unit (ICU) with an incidence ranging from 17.5% to 78% [1–5]. Management of volume status in critically ill patients with AKI is difficult as it is often accompanied by oliguria or anuria as well as total body fluid overload and tissue edema. AKI increases the risk of mortality and often occurs in the setting of sepsis or other forms of shock [6]. While the early goal-directed therapy study showed the benefit of adequate volume repletion in critically ill patients with septic shock [7], there are detrimental effects associated with salt and water overload which can result from resuscitation with crystalloids or colloids. These include worsening of lung function and difficulty of wound healing [8, 9]. In this paper we will focus on the role of intravenous fluids (IVFs) and diuretics for the management of volume status in critically ill patients with AKI. We will also discuss the differences between oliguric and nonoliguric renal failure and the effects on outcomes of “converting” patients from oliguric to nonoliguric renal failure. 2. Epidemiology and Mortality of AKI in the ICU The Acute Dialysis Quality Initiative (ADQI) published the Risk, Injury, Failure, Loss, End-Stage Kidney Disease (RIFLE) definitions for AKI in 2004 [10], developing a consensus definition of AKI that could be used in studies rather than the 30 plus definitions that had been used in previous studies. This was revised
Update on the diagnosis and management of acute kidney injury
Ali Akcay, Kultigin Turkmen, DongWon Lee, et al
International Journal of Nephrology and Renovascular Disease , 2010, DOI: http://dx.doi.org/10.2147/IJNRD.S8641
Abstract: ate on the diagnosis and management of acute kidney injury Review (7713) Total Article Views Authors: Ali Akcay, Kultigin Turkmen, DongWon Lee, et al Published Date September 2010 Volume 2010:3 Pages 129 - 140 DOI: http://dx.doi.org/10.2147/IJNRD.S8641 Ali Akcay, Kultigin Turkmen, DongWon Lee, Charles L Edelstein Division of Renal Diseases and Hypertension, University of Colorado and the Health Sciences Center, Aurora, Colorado, USA Abstract: 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.
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.
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,
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
Bath Salts: A Newly Recognized Cause of Acute Kidney Injury
Jonathan McNeely,Samir Parikh,Christopher Valentine,Nabil Haddad,Ganesh Shidham,Brad Rovin,Lee Hebert,Anil Agarwal
Case Reports in Nephrology , 2012, DOI: 10.1155/2012/560854
Abstract: Bath salts are substance of abuse that are becoming more common and are difficult to recognize due to negative toxicology screening. Acute kidney injury due to bath salt use has not previously been described. We present the case of a previously healthy male who developed acute kidney injury and dialysis dependence after bath salt ingestion and insufflation. This was self-reported with negative toxicology screening. Clinical course was marked by severe hyperthermia, hyperkalemia, rhabdomyolysis, disseminated intravascular coagulation, oliguria, and sepsis. We discuss signs and symptoms, differential diagnoses, potential mechanisms of injury, management, and review of the literature related to bath salt toxicity.
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
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