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      Clinical Characteristics and Outcomes of Community- and Hospital-Acquired Acute Kidney Injury with COVID-19 in a US Inner City Hospital System

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          Emerging data have described poor clinical outcomes from infection with the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV 2) among African American patients and those from underserved socioeconomic groups. We sought to describe the clinical characteristics and outcomes of acute kidney injury (AKI) in this special population.


          This is a retrospective study conducted in an underserved area with a predominance of African American patients with coronavirus disease 2019 (COVID-19). Descriptive statistics were used to characterize the sample population. The onset of AKI and relation to clinical outcomes were determined. Multivariate logistic regression was used to determine factors associated with AKI.


          Nearly half (49.3%) of the patients with COVID-19 had AKI. Patients with AKI had a significantly lower baseline estimated glomerular filtration rate (eGFR) and higher FiO<sub>2</sub> requirement and D-dimer levels on admission. More subnephrotic proteinuria and microhematuria was seen in these patients, and the majority had a pre-renal urine electrolyte profile. Patients with hospital-acquired AKI (HA-AKI) as opposed to those with community-acquired AKI (CA-AKI) had higher rates of in-hospital death (52 vs. 23%, p = 0.005), need for vasopressors (42 vs. 25%, p = 0.024), and need for intubation (55 vs. 25%, p = 0.006). A history of heart failure was significantly associated with AKI after adjusting for baseline eGFR (OR 3.382, 95% CI 1.121–13.231, p = 0.032).


          We report a high burden of AKI among underserved COVID-19 patients with multiple comorbidities. Those who had HA-AKI had worse clinical outcomes compared to those who with CA-AKI. A history of heart failure is an independent predictor of AKI in patients with COVID-19.

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          Most cited references 18

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          The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988-1994.

          The metabolic syndrome is an important cluster of coronary heart disease risk factors with common insulin resistance. The extent to which the metabolic syndrome is associated with demographic and potentially modifiable lifestyle factors in the US population is unknown. Metabolic syndrome-associated factors and prevalence, as defined by Adult Treatment Panel III criteria, were evaluated in a representative US sample of 3305 black, 3477 Mexican American, and 5581 white men and nonpregnant or lactating women aged 20 years and older who participated in the cross-sectional Third National Health and Nutrition Examination Survey. The metabolic syndrome was present in 22.8% and 22.6% of US men and women, respectively (P =.86). The age-specific prevalence was highest in Mexican Americans and lowest in blacks of both sexes. Ethnic differences persisted even after adjusting for age, body mass index, and socioeconomic status. The metabolic syndrome was present in 4.6%, 22.4%, and 59.6% of normal-weight, overweight, and obese men, respectively, and a similar distribution was observed in women. Older age, postmenopausal status, Mexican American ethnicity, higher body mass index, current smoking, low household income, high carbohydrate intake, no alcohol consumption, and physical inactivity were associated with increased odds of the metabolic syndrome. The metabolic syndrome is present in more than 20% of the US adult population; varies substantially by ethnicity even after adjusting for body mass index, age, socioeconomic status, and other predictor variables; and is associated with several potentially modifiable lifestyle factors. Identification and clinical management of this high-risk group is an important aspect of coronary heart disease prevention.
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            Plasma cytokine levels predict mortality in patients with acute renal failure.

            Critically ill patients with acute renal failure (ARF) experience a high mortality rate. Animal and human studies suggest that proinflammatory cytokines lead to the development of a systemic inflammatory response syndrome (SIRS), which is temporally followed by a counter anti-inflammatory response syndrome (CARS). This process has not been specifically described in critically ill patients with ARF. The Program to Improve Care in Acute Renal Disease (PICARD) is a prospective, multicenter cohort study designed to examine the natural history, practice patterns, and outcomes of treatment in critically ill patients with ARF. In a subset of 98 patients with ARF, we measured plasma proinflammatory cytokines [interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha)], the acute-phase reactant C-reactive protein (CRP), and the anti-inflammatory cytokine IL-10 at study enrollment and over the course of illness. When compared with healthy subjects and end-stage renal disease patients on maintenance hemodialysis, patients with ARF had significantly higher plasma levels of all measured cytokines. Additionally, the proinflammatory cytokines IL-6 and IL-8 were significantly higher in nonsurvivors versus survivors [median 234.7 (interdecile range 64.8 to 1775.9) pg/mL vs. 113.5 (46.1 to 419.3) pg/mL, P= 0.02 for IL-6; 35.5 (14.1 to 237.9) pg/mL vs. 21.2 (8.5 to 87.1) pg/mL, P= 0.03 for IL-8]. The anti-inflammatory cytokine IL-10 was also significantly higher in nonsurvivors [3.1 (0.5 to 41.9) pg/mL vs. 2.4 (0.5 to 16.9) pg/mL, P= 0.04]. For each natural log unit increase in the levels of IL-6, IL-8, and IL-10, the odds of death increased by 65%, 54%, and 34%, respectively, corresponding to increases in relative risk of approximately 30%, 25%, and 15%. The presence or absence of SIRS or sepsis was not a major determinant of plasma cytokine concentration in this group of patients. There is evidence of ongoing SIRS with concomitant CARS in critically ill patients with ARF, with higher levels of plasma IL-6, IL-8, and IL-10 in patients with ARF who die during hospitalization. Strategies to modulate inflammation must take into account the complex cytokine biology in patients with established ARF.
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              Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure.

              Fractional excretion of sodium (FENa) has been used in the diagnosis of acute renal failure (ARF) to distinguish between the two main causes of ARF, prerenal state and acute tubular necrosis (ATN). However, many patients with prerenal disorders receive diuretics, which decrease sodium reabsorption and thus increase FENa. In contrast, the fractional excretion of urea nitrogen (FEUN) is primarily dependent on passive forces and is therefore less influenced by diuretic therapy. To test the hypothesis that FEUN might be more useful in evaluating ARF, we prospectively compared FEUN with FENa during 102 episodes of ARF due to either prerenal azotemia or ATN. Patients were divided into three groups: those with prerenal azotemia (N = 50), those with prerenal azotemia treated with diuretics (N = 27), and those with ATN (N = 25). FENa was low only in the patients with untreated plain prerenal azotemia while it was high in both the prerenal with diuretics and the ATN groups. FEUN was essentially identical in the two pre-renal groups (27.9 +/- 2.4% vs. 24.5 +/- 2.3%), and very different from the FEUN found in ATN (58.6 +/- 3.6%, P < 0.0001). While 92% of the patients with prerenal azotemia had a FENa <1%, only 48% of those patients with prerenal and diuretic therapy had such a low FENa. By contrast 89% of this latter group had a FEUN <35%. Low FEUN (

                Author and article information

                Cardiorenal Med
                Cardiorenal Med
                Cardiorenal Medicine
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, )
                18 June 2020
                : 10
                : 4
                : 223-231
                aDepartment of Medicine, Einstein Medical Center Philadelphia, Philadelphia, Pennsylvania, USA
                bDepartment of Medicine, The Brooklyn Hospital Center, Brooklyn, New York, USA
                cDivision of Pulmonary and Critical Care and Sleep Medicine, Einstein Medical Center Philadelphia, Philadelphia, Pennsylvania, USA
                dSidney Kimmel College of Thomas Jefferson University, Philadelphia, Pennsylvania, USA
                Author notes
                *Jerald Pelayo, Internal Medicine, Einstein Medical Center, 5501 Old York Road, Philadelphia, PA 19141 (USA), pelayoje@
                Copyright © 2020 by S. Karger AG, Basel

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

                Page count
                Figures: 3, Tables: 2, References: 27, Pages: 9
                Research Article


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