Browsing by Subject "ACUTE-RENAL-FAILURE"

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  • Palviainen, Mari J.; Junnikkala, Sami; Raekallio, Marja; Meri, Seppo; Vainio, Outi (2015)
  • Petaja, Liisa; Vaara, Suvi; Liuhanen, Sasu; Suojaranta-Ylinen, Raili; Mildh, Leena; Nisula, Sara; Korhonen, Anna-Maija; Kaukonen, Kirsi-Maija; Salmenpera, Markku; Pettila, Ville (2017)
    Objectives: Acute kidney injury (AKI) occurs frequently after cardiac surgery and is associated with increased mortality. The Kidney Disease: Improving Global Outcomes (KDIGO) criteria for diagnosing AKI include creatinine and urine output values. However, the value of the latter is debated. The authors aimed to evaluate the incidence of AKI after cardiac surgery and the independent association of KDIGO criteria, especially the urine output criterion, and 2.5-year mortality. Design: Prospective, observational, cohort study. Setting: Single-center study in a university hospital. Participants: The study comprised 638 cardiac surgical patients from September 1, 2011, to June 20, 2012. Interventions: None. Measurements and Main Results: Hourly urine output, daily plasma creatinine, risk factors for AKI, and variables for EuroSCORE II were recorded. AKI occurred in 183 (28.7%) patients. Patients with AKI diagnosed using only urine output had higher 2.5-year mortality than did patients without AKI (9/53 [17.0%] v 23/455 [5.1%], p = 0.001). AKI was associated with mortality (hazard ratios [95% confidence intervals]: 3.3 [1.8-6.1] for KDIGO I; 5.8 [2.7-12.1] for KDIGO 2; and 7.9 [3.5-17.6]) for KDIGO 3. KDIGO stages and AKI diagnosed using urine output were associated with mortality even after adjusting for mortality risk assessed using EuroSCORE II and risk factors for AKI. Conclusions: AKI diagnosed using only the urine output criterion without fulfilling the creatinine criterion and all stages of AKI were associated with long-term mortality. Preoperatively assessed mortality risk using EuroSCORE II did not predict this AKI-associated mortality. (C) 2017 Elsevier Inc. All rights reserved.
  • Bellomo, Rinaldo; Kellum, John A.; Ronco, Claudio; Wald, Ron; Martensson, Johan; Maiden, Matthew; Bagshaw, Sean M.; Glassford, Neil J.; Lankadeva, Yugeesh; Vaara, Suvi; Schneider, Antoine (2017)
    Acute kidney injury (AKI) and sepsis carry consensus definitions. The simultaneous presence of both identifies septic AKI. Septic AKI is the most common AKI syndrome in ICU and accounts for approximately half of all such AKI. Its pathophysiology remains poorly understood, but animal models and lack of histological changes suggest that, at least initially, septic AKI may be a functional phenomenon with combined microvascular shunting and tubular cell stress. The diagnosis remains based on clinical assessment and measurement of urinary output and serum creatinine. However, multiple biomarkers and especially cell cycle arrest biomarkers are gaining acceptance. Prevention of septic AKI remains based on the treatment of sepsis and on early resuscitation. Such resuscitation relies on the judicious use of both fluids and vasoactive drugs. In particular, there is strong evidence that starch-containing fluids are nephrotoxic and decrease renal function and suggestive evidence that chloride-rich fluid may also adversely affect renal function. Vasoactive drugs have variable effects on renal function in septic AKI. At this time, norepinephrine is the dominant agent, but vasopressin may also have a role. Despite supportive therapies, renal function may be temporarily or completely lost. In such patients, renal replacement therapy (RRT) becomes necessary. The optimal intensity of this therapy has been established, while the timing of when to commence RRT is now a focus of investigation. If sepsis resolves, the majority of patients recover renal function. Yet, even a single episode of septic AKI is associated with increased subsequent risk of chronic kidney disease.
  • Perner, Anders; Haase, Nicolai; Wetterslev, Jorn; Aneman, Anders; Tenhunen, Jyrki; Guttormsen, Anne Berit; Klemenzson, Gudmundur; Pott, Frank; Bodker, Karen Doris; Badstolokken, Per Martin; Bendtsen, Asger; Soe-Jensen, Peter; Tousi, Hamid; Bestle, Morten; Pawlowicz, Malgorzata; Winding, Robert; Bulow, Hans-Henrik; Kancir, Claude; Steensen, Morten; Nielsen, Jonas; Fogh, Bjarne; Madsen, Kristian R.; Larsen, Nils H.; Carlsson, Marcela; Wiis, Jorgen; Petersen, John Asger; Iversen, Susanne; Schoidt, Ole; Leivdal, Siv; Berezowicz, Pawel; Pettilä, Ville; Ruokonen, Esko; Klepstad, Pal; Karlsson, Sari; Kaukonen, Maija; Rutanen, Juha; Karason, Sigurbergur; Kjaelgaard, Anne Lene; Holst, Lars Brokso; Wernerman, Jan; Scandinavian Critical Care Trials (2011)
  • Steegmann, J. L.; Baccarani, M.; Breccia, M.; Casado, L. F.; Garcia-Gutierrez, V.; Hochhaus, A.; Kim, D-W; Kim, T. D.; Khoury, H. J.; Le Coutre, P.; Mayer, J.; Milojkovic, D.; Porkka, Kimmo; Rea, D.; Rosti, G.; Saussele, S.; Hehlmann, R.; Clark, R. E. (2016)
    Most reports on chronic myeloid leukaemia (CML) treatment with tyrosine kinase inhibitors (TKIs) focus on efficacy, particularly on molecular response and outcome. In contrast, adverse events (AEs) are often reported as infrequent, minor, tolerable and manageable, but they are increasingly important as therapy is potentially lifelong and multiple TKIs are available. For this reason, the European LeukemiaNet panel for CML management recommendations presents an exhaustive and critical summary of AEs emerging during CML treatment, to assist their understanding, management and prevention. There are five major conclusions. First, the main purpose of CML treatment is the antileukemic effect. Suboptimal management of AEs must not compromise this first objective. Second, most patients will have AEs, usually early, mostly mild to moderate, and which will resolve spontaneously or are easily controlled by simple means. Third, reduction or interruption of treatment must only be done if optimal management of the AE cannot be accomplished in other ways, and frequent monitoring is needed to detect resolution of the AE as early as possible. Fourth, attention must be given to comorbidities and drug interactions, and to new events unrelated to TKIs that are inevitable during such a prolonged treatment. Fifth, some TKI-related AEs have emerged which were not predicted or detected in earlier studies, maybe because of suboptimal attention to or absence from the preclinical data. Overall, imatinib has demonstrated a good long-term safety profile, though recent findings suggest underestimation of symptom severity by physicians. Second and third generation TKIs have shown higher response rates, but have been associated with unexpected problems, some of which could be irreversible. We hope these recommendations will help to minimise adverse events, and we believe that an optimal management of them will be rewarded by better TKI compliance and thus better CML outcomes, together with better quality of life.
  • Rakkolainen, I.; Lindbohm, J. V.; Vuola, J. (2018)
    BackgroundAcute kidney injury (AKI) is a common complication in severe burns and can lead to significantly poorer outcomes. Although the prognosis has improved in recent decades, the mortality of AKI remains considerable. We investigated the factors that increase the risk of AKI and death after severe burn injury.MethodsIntensive care patients with 20% burned total body surface area (TBSA%) between January 2006 and December 2015 treated in Helsinki Burn Centre were enrolled retrospectively. Patients who arrived >36h after burn injury or died 80. Multivariate logistic regression model detected age, TBSA%, sepsis, and rhabdomyolysis as independent risk factors for AKI. Age (per 10yrs. OR 1.99), TBSA% (per 10% OR 1.64), and AKI predicted mortality during hospital stay; AKI had an odds ratio of (OR) of 5.97 (95% confidence interval [CI] 2.2-16.2).ConclusionsAge, TBSA%, and AKI were the strongest independent factors in predicting outcome in severe burns. Even a major burn (>50% TBSA) has a relatively good prognosis without simultaneous AKI. Prognosis is poorer even in minor burns for patients with AKI.
  • Vilander, Laura M.; Kaunisto, Mari A.; Pettila, Ville (2015)
    Background: The risk of an individual to develop an acute kidney injury (AKI), or its severity, cannot be reliably predicted by common clinical risk factors. Whether genetic risk factors have an explanatory role poses an interesting question, however. Thus, we conducted a systematic literature review regarding genetic predisposition to AKI or outcome of AKI patients. Methods: We searched Ovid SP (MEDLINE) and EMBASE databases and found 4027 references to AKI. Based on titles and abstracts, we approved 37 articles for further analysis. Nine were published only as abstracts, leaving 28 original articles in the final analysis. We extracted the first author, year of publication, study design, clinical setting, number of studied patients, patients with AKI, ethnicity of patients, studied polymorphisms, endpoints, AKI definition, phenotype, significant findings, and data for quality scoring from each article. We summarized the findings and scored the quality of articles. Results: The articles were quite heterogeneous and of moderate quality (mean 6.4 of 10). Conclusions: Despite different gene polymorphisms with suggested associations with development or severity or outcome of AKI, definitive conclusions would require replication of associations in independent cohort studies and, preferably a hypothesis-free study design.
  • Törnblom, Sanna; Nisula, Sara; Vaara, Suvi T.; Poukkanen, Meri; Andersson, Sture; Pettilä, Ville; Pesonen, Eero (2019)
    Background Inflammation, reflected by high plasma interleukin-6 concentration, is associated with acute kidney injury (AKI) in septic patients. Neutrophil activation has pathophysiological significance in experimental septic AKI. We hypothesized that neutrophil activation is associated with AKI in critically ill sepsis patients. Methods We measured plasma (n = 182) and urine (n = 118) activin A (a rapidly released cytosolic neutrophil protein), interleukin-8 (a chemotactic factor for neutrophils), myeloperoxidase (a neutrophil biomarker released in tissues), and interleukin-6 on intensive care unit admission (plasma and urine) and 24 hours later (plasma) in sepsis patients manifesting their first organ dysfunction between 24 hours preceding admission and the second calendar day in intensive care unit. AKI was defined by the Kidney Disease: Improving Global Outcomes criteria. Results Plasma admission interleukin-8 (240 [60-971] vs 50 [19-164] pg/mL, P <.001) and activin A (845 [554-1895] vs 469 [285-862] pg/mL, P <.001) were but myeloperoxidase (169 [111-300] vs 144 [88-215] ng/mL, P = .059) was not higher among patients with AKI compared with those without. Urine admission interleukin-8 (50.4 [19.8-145.3] vs 9.5 [2.7-28.7] ng/mL, P <.001) and myeloperoxidase (7.7 [1.5-12.6] vs 1.9 [0.4-6.9] ng/mL, P <.001) were but activin A (9.7 [1.4-42.6] vs 4.0 [0.0-33.0] ng/mL, P = .064) was not higher in AKI than non-AKI patients. Urine myeloperoxidase correlated with urine interleukin-8 (R = .627, P <.001) but not with plasma myeloperoxidase (R = .131, P = .158). Conclusion Interleukin-8 in plasma and urine was associated with septic AKI. Elevated plasma activin A indicates intravascular neutrophil activation in septic AKI. Concomitant plasma and urine myeloperoxidase measurements suggest neutrophil accumulation into injured kidneys.
  • Vaara, Suvi T.; Lakkisto, Paivi; Immonen, Katariina; Tikkanen, Ilkka; Ala-Kokko, Tero; Pettila, Ville; FINNAKI Study Grp (2016)
    Background Apoptosis is a key mechanism involved in ischemic acute kidney injury (AKI), but its role in septic AKI is controversial. Biomarkers indicative of apoptosis could potentially detect developing AKI prior to its clinical diagnosis. Methods As a part of the multicenter, observational FINNAKI study, we performed a pilot study among critically ill patients who developed AKI (n = 30) matched to critically ill patients without AKI (n = 30). We explored the urine and plasma levels of cytokeratin-18 neoepitope M30 (CK-18 M30), cell-free DNA, and heat shock protein 70 (HSP70) at intensive care unit (ICU) admission and 24h thereafter, before the clinical diagnosis of AKI defined by the Kidney Disease: Improving Global Outcomes - creatinine and urine output criteria. Furthermore, we performed a validation study in 197 consecutive patients in the FINNAKI cohort and analyzed the urine sample at ICU admission for CK-18 M30 levels. Results In the pilot study, the urine or plasma levels of measured biomarkers at ICU admission, at 24h, or their maximum value did not differ significantly between AKI and non-AKI patients. Among 20 AKI patients without severe sepsis, the urine CK-18 M30 levels were significantly higher at 24h (median 116.0, IQR [32.3-233.0] U/L) than among those 20 patients who did not develop AKI (46.0 [0.0-54.0] U/L), P = 0.020. Neither urine cell-free DNA nor HSP70 levels significantly differed between AKI and non-AKI patients regardless of the presence of severe sepsis. In the validation study, urine CK-18 M30 level at ICU admission was not significantly higher among patients developing AKI compared to non-AKI patients regardless of the presence of severe sepsis or CKD. Conclusions Our findings do not support that apoptosis detected with CK-18 M30 level would be useful in assessing the development of AKI in the critically ill. Urine HSP or cell-free DNA levels did not differ between AKI and non-AKI patients.