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      Indoxyl sulfate is associated with mortality after AKI – more evidence needed!

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          Abstract

          Patients who develop acute kidney injury (AKI) have significantly higher short-term outcomes including in-hospital mortality. The development of AKI has been associated with long-term consequences including progression to chronic kidney disease (CKD) and higher rates of cardiovascular disease (CVD) and mortality. In recent years there has been a growing push for the discovery of novel methods to diagnose AKI at earlier stages, and for an improvement in risk stratification and prognosis following AKI.

          Wang and colleagues assessed the association of total serum indoxyl sulfate (IS) levels, a protein bound uremic toxin, with 90-day mortality after hospital-acquired AKI (HA-AKI). These authors found that serum IS levels were significantly elevated in patients with HA-AKI (2.74 ± 0.75 μg/mL) compared to healthy subjects (1.73 ± 0.11 μg/ml, P < 0.001) and critically ill patients (2.46 ± 0.35 μg/ml, P = 0.016).

          The mechanisms of this relationship remain unclear, with a limited understanding of cause-specific mortality associated with either the high or low-IS group. One limitation of this current study is an understanding of the acceptable or expected higher level in IS during episodes of AKI. IS levels remained persistently elevated at day 7 compared to β2-microglobulin and serum creatinine which were both lower at 7 days. It is unclear, however, if levels of β2-microglobulin and serum creatinine were lower for other reasons, such as if any patients with AKI required dialysis.

          This work provides an important addition to the field of AKI research, specifically in the evaluation of readily measurable biomarkers and outcomes after AKI. Moving forward, further validation in studies of acute kidney injury are needed to develop a better understanding of IS levels at the time of AKI diagnosis and trends during the course of AKI.

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          Most cited references 23

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          Acute kidney injury, mortality, length of stay, and costs in hospitalized patients.

          The marginal effects of acute kidney injury on in-hospital mortality, length of stay (LOS), and costs have not been well described. A consecutive sample of 19,982 adults who were admitted to an urban academic medical center, including 9210 who had two or more serum creatinine (SCr) determinations, was evaluated. The presence and degree of acute kidney injury were assessed using absolute and relative increases from baseline to peak SCr concentration during hospitalization. Large increases in SCr concentration were relatively rare (e.g., >or=2.0 mg/dl in 105 [1%] patients), whereas more modest increases in SCr were common (e.g., >or=0.5 mg/dl in 1237 [13%] patients). Modest changes in SCr were significantly associated with mortality, LOS, and costs, even after adjustment for age, gender, admission International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis, severity of illness (diagnosis-related group weight), and chronic kidney disease. For example, an increase in SCr >or=0.5 mg/dl was associated with a 6.5-fold (95% confidence interval 5.0 to 8.5) increase in the odds of death, a 3.5-d increase in LOS, and nearly 7500 dollars in excess hospital costs. Acute kidney injury is associated with significantly increased mortality, LOS, and costs across a broad spectrum of conditions. Moreover, outcomes are related directly to the severity of acute kidney injury, whether characterized by nominal or percentage changes in serum creatinine.
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            The effect of acute renal failure on mortality. A cohort analysis.

            To determine if the high mortality in acute renal failure is explained by underlying illnesses (comorbidity). Cohort analytic study. An 826-bed general hospital providing primary, secondary, and tertiary care. From 16,248 inpatients undergoing radiocontrast procedures between 1987 and 1989, we identified 183 index subjects who developed contrast media-associated renal failure (defined as an increase in serum creatinine level of at least 25%, to at least 177 micromol/L [2 mg/dL], within 2 days of receiving contrast material) and 174 paired subjects, matched for age and baseline serum creatinine level, who underwent similar contrast procedures without developing renal failure. Death during hospitalization. The mortality rate in subjects without renal failure was 7%, compared with 34% in the corresponding index subjects with renal failure (odds ratio, 6.5; P<.001). After adjusting for differences in comorbidity, renal failure was associated with an odds ratio of dying of 5.5. Subjects who died after developing renal failure had complicated clinical courses characterized by sepsis, bleeding, delirium, and respiratory failure; most of these complications developed after the onset of renal failure. Deaths from renal causes were rare. The high mortality rate in acute renal failure is not explained by the underlying conditions alone. Renal failure appears to increase the risk of developing severe nonrenal complications that lead to death and should not be regarded as a treatable complication of serious illness.
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              AKI in the ICU: definition, epidemiology, risk stratification, and outcomes.

              Acute kidney injury (AKI) has emerged as a major public health problem that affects millions of patients worldwide and leads to decreased survival and increased progression of underlying chronic kidney disease (CKD). Recent consensus criteria for definition and classification of AKI have provided more consistent estimates of AKI epidemiology. Patients, in particular those in the ICU, are dying of AKI and not just simply with AKI. Even small changes in serum creatinine concentrations are associated with a substantial increase in the risk of death. AKI is not a single disease but rather a syndrome comprising multiple clinical conditions. Outcomes from AKI depend on the underlying disease, the severity and duration of renal impairment, and the patient's renal baseline condition. The development of AKI is the consequence of complex interactions between the actual insult and subsequent activation of inflammation and coagulation. Contrary to the conventional view, recent experimental and clinical data argue against renal ischemia-reperfusion as a sine qua non condition for the development of AKI. Loss of renal function can occur without histological signs of tubular damage or even necrosis. The detrimental effects of AKI are not limited to classical well-known symptoms such as fluid overload and electrolyte abnormalities. AKI can also lead to problems that are not readily appreciated at the bedside and can extend well beyond the ICU stay, including progression of CKD and impaired innate immunity. Experimental and small observational studies provide evidence that AKI impairs (innate) immunity and is associated with higher infection rates.
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                Author and article information

                Contributors
                bjaar@jhmi.edu
                Journal
                BMC Nephrol
                BMC Nephrol
                BMC Nephrology
                BioMed Central (London )
                1471-2369
                26 July 2019
                26 July 2019
                2019
                : 20
                Affiliations
                [1 ]ISNI 0000 0001 2171 9311, GRID grid.21107.35, Division of Nephrology, Department of Medicine, , Johns Hopkins University School of Medicine, ; 1830 E. Monument Street, Suite 416, Baltimore, MD 21287 USA
                [2 ]ISNI 0000 0001 2171 9311, GRID grid.21107.35, Department of Epidemiology, , Johns Hopkins Bloomberg School of Public Health, ; 615 N. Wolfe Street, Baltimore, MD 21205 USA
                [3 ]ISNI 0000 0001 2171 9311, GRID grid.21107.35, Welch Center for Prevention, Epidemiology and Clinical Research, , Johns Hopkins University, ; 2024 E. Monument Street, Baltimore, MD 21205 USA
                [4 ]Nephrology Center of Maryland, 5601 Loch Raven Boulevard, Suite 3 North, Baltimore, MD 21239 USA
                [5 ]ISNI 0000 0004 1937 0407, GRID grid.410721.1, Division of Nephrology, Department of Medicine, , University of Mississippi Medical Center, ; Jackson, MS USA
                Article
                1465
                10.1186/s12882-019-1465-0
                6659241
                31345164
                © The Author(s). 2019

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: 5T32HL007024
                Award Recipient :
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                © The Author(s) 2019

                Nephrology

                indoxyl sulfate, risk factors, mortality, aki

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