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Antihypertensive therapy is pivotal for reducing cardiovascular events. The 2019 Guidelines for the Management of Hypertension set a target blood pressure (BP) of

Background: Risk factors of mortality in chronic hemodialysis patients have not yet been sufficiently evaluated. In particular, chronological transits and interactions of the impact of risk factors have rarely been described. Methods: This study is a post hoc analysis of the participants in the Olme­sartan Clinical Trial in Okinawan Patients under OKIDS (OCTOPUS) study conducted between June 2006 and June 2011. We additionally followed up on the prognosis of the participants until July 31, 2018. Standardized univariable and multivariable Cox regression analyses were used to evaluate the influences of the participants’ baseline characteristics on all-cause mortality. We also evaluated chronological changes in the impacts of risk factors, interactions among predictors, and the influence of missing values using sensitivity analyses. Results: Of the 469 original trial participants, 461 participants were evaluated. The median time of follow-up was 10.2 years. A total of 211 (45.8%) participants were deceased. The leading causes of death were infection (n = 72, 34.1%) and cardiovascular disease (n = 66, 31.3%). Univariate and multivariate Cox regression analyses revealed that the impact of diabetes mellitus, history of coronary intervention, and hypoalbuminemia were significant risk factors for mortality during the whole follow-up period. During the early follow-up period (≤3 years), standardized univariate Cox regression analyses revealed that history of amputation (hazard ratio [HR] = 4.61, p < 0.001), lower dry weight, higher cardiothoracic ratio, and lower potassium levels were statistically significant risks. In those who survived for longer than 3 years, a history of stroke (HR = 1.73, p = 0.006), higher systolic blood pressure, lower serum sodium levels, and higher levels of hemoglobin, and serum phosphate were significant risks. We also observed a stable interaction between the impacts of serum phosphate and albumin on all-cause mortality. Conclusion: In chronic hemodialysis patients, targets to improve the short-term prognosis and long-term prognosis are not equivalent. Hyperphosphatemia was a significant risk factor for the all-cause mortality among patients with normal serum albumin levels but not among patients with compromised albumin levels.

Both frailty and chronic kidney disease (CKD) increase with age and share many similarities. Many studies have demonstrated an association between frailty and chronic kidney disease (CKD), but an association with dipstick proteinuria is limited. This is the cross-sectional analysis of the Nambu Cohort Study at the beginning of observation. Frailty was diagnosed using Kihon Checklist. Logistic analysis was used to evaluate the association between frailty and CKD or dipstick proteinuria. Among a total of 630 outpatients [age, 78 (70–84) years, men, 50%], the prevalence of patients with pre-frailty and frailty was 32% and 40%, respectively. The proportion of patients with pre-frailty and frailty increased with decreasing estimated glomerular filtration rate (eGFR) and increasing dipstick proteinuria levels. The odds ratios (95% confidence intervals) for CKD stage of 60

Background and Aims Serial decrease in body weight can be a prognostic marker reflecting Protein Energy Wasting (PEW) condition in haemodialysis patients. However, the impact of longitudinal body weight changes on mortality have rarely been evaluated. Therefore, we applied landmark analysis and time-scale mixed regression analyses to clarify the impact of long-term changes in body weight on all-cause mortality. Method This study is a post-hoc analysis of the participants in the Olmesartan Clinical Trial in Okinawan Patients Under OKIDS (OCTOPUS) conducted between June 2006 and June 2011. We additionally followed up with the participants until 31 July, 2018. During the OCTOPUS trial, the body weight of surviving participants was repeatedly measured every 6 months. The primary aim of the study was to clarify the association of serial change in body weights and all-cause mortality. The participants were categorized into 4 groups based on weight change slope during the first 2 years (bottom to highest group correspond with the first quartile to the fourth quartile group). We conducted a landmark analysis to evaluate the influence of weight change slope on the subsequent survival with Cox-proportional hazard regression. We also conducted time-scale multilevel regression analyses to draw marginal plots of body weight with a backward time scale to describe the difference in trajectories of body weight between deceased and surviving patients. Results Out of 461 patients in the cohort, 404 participants were analysed in the landmark analysis. Of the participants, 168 (41.6%) were deceased, and 236 participants (58.4%) survived. Although baseline body weights and indices about body components such as a creatinine index were similar among the 4 groups, multivariate Cox-proportional hazard regression showed that the higher rate of body weight loss was associated with higher mortality. Hazard ratios were 2.02 (1.28–3.20), 1.77 (1.10–2.85), 1.00 (Reference), and 1.11 (0.67–1.83) for first quartile, second quartile, third quartile (Reference), and fourth quartile group, respectively (P for trend was Conclusion In chronic haemodialysis patients, the higher rate of body weight loss, such as a decrease in body weight by 1 kg (1.7%) per 6 months, was significantly associated with higher mortality. Persistent loss of body weight is a significant predictor of death among chronic dialysis patients.

Background and Aims Increase in resting heart rate might influence mortalities of dialysis patients, and the use of β-blocker might improve their survival probability. However, the influence of heart rate and benefits of β-blocker on their survival are difficult to quantify because of following obstacles: prone to measurement errors; inherent association of heart rate with blood pressures, comorbidities, and medication use; and a necessity of repeated measurements of vital signs and medication use. Therefore, at the design process of our previous randomized control trial on the Olmesartan Clinical Trial in Okinawan patients under OKIDS (OCTOPUS), we included the repeated measures design to quantify the influence of vital sign values on the survival retrospectively. We combined the repeated measurement data and additional the long-term prognosis information of the participants obtained after the OCTOPUS with aim of investigating the influence of time varying covariates: heart rates, blood pressures, and β-blocker use, on the long-term survival of hemodialysis patients. Method We investigated 461 adult OCTOPUS participants who received chronic hemodialysis and antihypertensive medications in Okinawa. The OCTOPUS trial, which was conducted between June 2006 and June 2011, did not detect the survival benefit of angiotensin receptor blocker (ARB)NDT 2013, but the study and the additional follow-up of participants’ prognosis provided us with information to investigate influence of predictors on long-term survival in the population. Throughout the OCTOPUS trial, study participants were measured pre-dialysis blood pressures, pre-dialysis resting heart rates, and their medication use for one week at their dialysis centers every six months after their participations. Following the trial, we collected the prognosis information of all participants until July 31st, 2018. Finally, we merged the multiple-measured data during the OCTOPUS with the prognosis data. Mean values of three measurements of blood pressures and heart rates and β-blocker use were introduced to the Cox-regression model as time-varying covariates with essential non-time varying covariates, which include age, gender, and diabetes. Results In this retrospective cohort study, 221 (47.9%) out of 461 participants deceased, and the median follow-up length was 10.21 years. Initial mean resting heart rate and pre-dialysis mean blood pressure were 78(±10) per minute and 159.5(±14) mmHg, respectively. 10% of participants were prescribed β-blocker initially. The resting heart rate of all participants significantly decreased by 1.75 and 2.45 per minutes after two and four years respectively. β-blocker could significantly decrease the mean heart rate by 3.54 and 2.90 per minutes after two and four years. With our Cox-regression with the time varying covariates, increase of heart rate was significantly associated with higher mortality (P=0.002), but the use of β-blocker was not associated with the mortality. (P=0.691) Additionally, we could not detect the interaction of heart rate and β-blocker use on the mortality. (P= 0.796) Although lower blood pressure was significantly associated with higher mortality in our initial Cox-regression analysis, an introduction of interaction term of heart rate and blood pressure remove the significance of influence of blood pressure on the survival. Conclusion In hypertensive chronic hemodialysis patients, higher heart rate is associated with higher mortality. However, use of beta-blocker was not associated with improvement of their mortality.

The association between nutritional status and mortality in critically ill patients is unclear based on the current literature. To clarify this relation, we analyzed the association between nutrition and mortality in a large population of critically ill patients and hypothesized that mortality would be impacted by nutritional status.Retrospective observational study.Single academic medical center.Six thousand five hundred eighteen adults treated in medical and surgical ICUs between 2004 and 2011.None.All cohort patients received a formal, in-person, standardized evaluation by a registered dietitian. The exposure of interest, malnutrition, was categorized as nonspecific malnutrition, protein-energy malnutrition, or well nourished and determined by data related to anthropometric measurements, biochemical indicators, clinical signs of malnutrition, malnutrition risk factors, and metabolic stress. The primary outcome was all-cause 30-day mortality determined by the Social Security Death Master File. Associations between nutrition groups and mortality were estimated by bivariable and multivariable logistic regression models. Adjusted odds ratios were estimated with inclusion of covariate terms thought to plausibly interact with both nutrition status and mortality. We used propensity score matching on baseline characteristics to reduce residual confounding of the nutrition status category assignment. In the cohort, nonspecific malnutrition was present in 56%, protein-energy malnutrition was present in 12%, and 32% were well nourished. The 30-day and 90-day mortality rates for the cohort were 19.1% and 26.6%, respectively. Nutritional status is a significant predictor of 30-day mortality following adjustment for age, gender, race, medical versus surgical patient type, Deyo-Charlson index, acute organ failure, vasopressor use, and sepsis: nonspecific malnutrition 30-day mortality odds ratio, 1.17 (95% CI, 1.01-1.37); protein-energy malnutrition 30-day mortality odds ratio, 2.10 (95% CI, 1.70-2.59), all relative to patients without malnutrition. In the matched cohort, the adjusted odds of 30-day mortality in the group of propensity score-matched patients with protein-energy malnutrition was two-fold greater than that of patients without malnutrition.In a large population of critically ill adults, an association exists between nutrition status and mortality.

Objective In animal models of renal, intestinal, liver, cardiac, and cerebral ischemia, alcohol exposure is shown to reduce ischemia-reperfusion injury. Inpatient mortality of trauma patients is shown to be decreased in a dose-dependent fashion relative to blood alcohol concentration (BAC) at hospital admission. In this study, we examined the association between BAC at hospital admission and risk of 30-day mortality in critically ill patients. Design We performed a 2-center observational study of patients treated in medical and surgical intensive care units in Boston, Massachusetts. Setting Medical and surgical intensive care units in 2 teaching hospitals in Boston, Massachusetts. Patients We studied 11 850 patients, 18 years or older, who received critical care between 1997 and 2007. The exposure of interest was the BAC determined in the first 24 hours of hospital admission and categorized a priori as BAC less than 10 mg/dL (below level of detection), 10 to 80 mg/dL, 80 to 160 mg/dL, and greater than 160 mg/dL. The primary outcome was all-cause mortality in the 30 days after critical care initiation. Secondary outcomes included 90- and 365-day mortality after critical care initiation. Mortality was determined using the US Social Security Administration Death Master File, and 365-day follow-up was present in all cohort patients. Adjusted odds ratios (ORs) were estimated by multivariable logistic regression models with inclusion of covariate terms thought to plausibly interact with both BAC and mortality. Adjustment included age, sex, race (white or nonwhite), type (surgical vs medical), Deyo-Charlson index, sepsis, acute organ failure, trauma, and chronic liver disease. Results Thirty-day mortality of the cohort was 13.7%. Compared to patients with BAC levels less than 10 mg/dL, patients with levels greater than or equal to 10 mg/dL had lower odds of 30-day mortality; for BAC levels 10 to 79.9 mg/dL, the OR was 0.53 (95% confidence interval [CI], 0.40-0.70); for BAC levels 80 to 159.9 mg/dL, it was 0.36 (95% CI, 0.26-0.49); and for BAC levels greater than or equal to 160 mg/dL, it was 0.35 (95% CI, 0.27-0.44). After multivariable adjustment, the OR of 30-day mortality was 0.97 (0.72-1.31), 0.79 (0.57-1.10), and 0.69 (0.54-0.90), respectively. When the cohort was analyzed with sepsis as the outcome of interest, the multivariable adjusted odds of sepsis in patients with BAC 80 to 160 mg/dL or greater than 160 mg/dL were 0.72 (0.50-1.04) or 0.68 (0.51-0.90), respectively, compared to those with BAC less than 10 mg/dL. In a subset of patients with blood cultures drawn (n = 4065), the multivariable adjusted odds of bloodstream infection in patients with BAC 80 to 160 mg/dL or greater than 160 mg/dL were 0.53 (0.27-1.01) or 0.49 (0.29-0.83), respectively, compared to those with BAC less than 10 mg/dL. Conclusions Analysis of 11 850 adult patients showed that having a detectable BAC at hospitalization was associated with significantly decreased odds of 30-day mortality after critical care. Furthermore, BAC greater than 160 mg/dL is associated with significantly decreased odds of developing sepsis and bloodstream infection.

Objectives:Prediction models for ICU mortality rely heavily on physiologic variables that may not be available in large retrospective studies. An alternative approach when physiologic variables are absent stratifies mortality risk by acute organ failure classification.Design:Retrospective cohort stu

Community-acquired bloodstream infections have not been studied related to diabetes mellitus in the critically ill.We hypothesized that the diagnosis of diabetes mellitus and poor chronic glycemic control would increase the risk of community-acquired bloodstream infections (CA-BSIs) in the critically ill.We performed an observational cohort study between 1998 and 2007 in 2 teaching hospitals in Boston, Massachusetts. We studied 2551 patients 18 years or older, who received critical care within 48 hours of admission and had blood cultures obtained within 48 hours of admission. The exposure of interest was diabetes mellitus defined by International Classification of Diseases, Ninth Revision, Clinical Modification, code 250.xx in outpatient or inpatient records. The primary end point was CA-BSI (48 hours of hospital admission). Patients with a single coagulase-negative Staphylococcus positive blood culture were not considered to have bloodstream infection. Associations between diabetes groups and bloodstream infection were estimated by bivariable and multivariable logistic regression models. Subanalyses included evaluation of the association between hemoglobin A1c (HbA1c) and bloodstream infection, diabetes and risk of sepsis, and the proportion of the association between diabetes and CA-BSI that was mediated by acute glycemic control.Diabetes is a predictor of CA-BSI. After adjustment for age, sex, race, patient type (medical vs surgical), and acute organ failure, the risk of bloodstream infection was significantly higher in patients with diabetes (odds ratio [OR], 1.42; 95% confidence interval [CI], 1.10-1.82; P = .006) relative to patients without diabetes. The adjusted risk of bloodstream infection was increased in patients with HbA1c of 6.5% or higher (OR, 1.31; 95% CI, 1.04-1.65; P = .02) relative to patients with HbA1c less than 6.5%. Furthermore, the adjusted risk of sepsis was significantly higher in patients with diabetes (OR, 1.26; 95% CI, 1.04-1.54; P = .02) relative to patients without diabetes. Maximum glucose did not significantly mediate the relationship between diabetes mellitus diagnosis and CA-BSI.A diagnosis of diabetes mellitus and HbA1c of 6.5% or higher is associated with the risk of CA-BSI in the critically ill.

The study objective was to investigate the association between primary language spoken and all-cause mortality in critically ill patients.We performed a cohort study on 48 581 patients 18 years or older who received critical care between 1997 and 2007 in 2 Boston hospitals. The exposure of interest was primary language spoken determined by the patient or family members who interacted with administrative staff during hospital registration. The primary outcome was 30-day mortality. Associations between language and mortality were estimated by bivariable and multivariable logistic regression models with inclusion of covariate terms thought to plausibly interact with both language and mortality. Adjustment included age, race, sex, Deyo-Charlson index, patient type (medical vs surgical), sepsis, creatinine, hematocrit, white blood count, and number of organs with acute failure.Validation showed that primary language spoken was highly accurate for a statement in the medical record noting the language spoken that matched the assigned language. Patients whose primary language spoken was not English had improved outcomes (odds ratio 30-day mortality, 0.69 [95% confidence interval, 0.60-0.81; P.001), relative to patients with English as the primary language spoken, fully adjusted. Similar significant associations are seen with death by days 90 and 365 as well as in-hospital mortality. The improved survival in patients with a non-English primary language spoken is not confounded by indicators of severity of disease and is independent of the specific language spoken and neighborhood poverty rate, a proxy for socioeconomic status. There are significant limitations inherent to large database studies that we have acknowledged and addressed with controlling for measured confounding and evaluation of effect modification.In a regional cohort, not speaking English as a primary language is associated with improved outcomes after critical care. Our observations may have clinical relevance and illustrate the intersection of several factors in critical illness outcome including severity of illness, comorbidity, and social and economic factors.

Background: Alterations in immune function can predispose patients to nosocomial infections. Few studies have explored potentially modifiable host factors that may improve immune function and decrease risk of hospital-acquired bloodstream infection (HABSI). Vitamin D is a key regulator of innate and adaptive immune systems that may influence host susceptibility to infections. Objective: We investigated the association between prehospital serum 25-hydroxyvitamin D [25(OH)D] concentrations and risk of HABSI. Design: We performed a retrospective cohort study of 2135 adult patients from 2 Boston teaching hospitals. All patients had 25(OH)D concentrations measured before hospitalization between 1993 and 2010. The main outcome measure was HABSI, which was defined as positive blood cultures from samples drawn 48 h after hospital admission. Coagulase-negative Staphylococcus isolates were not considered to be bloodstream infections. Associations between 25(OH)D groups and HABSI were estimated by using bivariable and multivariable logistic regression models. Adjusted ORs were estimated with the inclusion of covariate terms thought to plausibly interact with both 25(OH)D concentration and HABSI. Results: Compared with patients with 25(OH)D concentrations $30 ng/mL, patients with concentrations ,30 ng/mL had higher odds of HABSI. For 25(OH)D concentrations ,10 ng/mL, the OR was 2.33 (95% CI: 1.45, 3.74); for 25(OH)D concentrations from 10 to 19.9 ng/mL, the OR was 1.60 (95% CI: 1.04, 2.46); and for 25(OH)D concentrations from 20 to 29.9 ng/mL, the OR was 1.13 (95% CI: 0.69, 1.84). After adjustment for age, sex, race (nonwhite compared with white), patient type (medical compared with surgical), and DeyoCharlson index, the ORs of HABSI were 1.95 (95% CI: 1.22, 3.12), 1.36 (95% CI: 0.89, 2.07), and 0.98 (95% CI: 0.60, 1.62), respectively. Conclusions: The analysis of 2135 adult patients showed that 25 (OH)D concentrations ,10 ng/mL before hospitalization were associated with significantly increased odds of developing HABSI. These data support the initiation of randomized trials to test the role of vitamin D supplementation in HABSI prevention. Am J Clin Nutr doi: 10.3945/ajcn.113.058909.

Background Little is known about risk factors associated with out-of-hospital outcomes in survivors of critical illness. We hypothesized that the presence of nucleated red blood cells in patients who survived critical care would be associated with adverse outcomes following hospital discharge. Methods We performed a two-center observational cohort study of patients treated in medical and surgical intensive care units in Boston, Massachusetts. All data were obtained from the Research Patient Data Registry at Partners HealthCare. We studied 2878 patients, age ≥ 18 years, who received critical care between 2011 and 2015 and survived hospitalization. The exposure of interest was nucleated red blood cells occurring from 2 days prior to 7 days after critical care initiation. The primary outcome was mortality in the 90 days following hospital discharge. Secondary outcome was unplanned 30-day hospital readmission. Adjusted odds ratios were estimated by multivariable logistic regression models with inclusion of covariate terms thought to plausibly interact with both nucleated red blood cells and outcome. Adjustment included age, race (white versus nonwhite), gender, Deyo–Charlson Index, patient type (medical versus surgical), sepsis and acute organ failure. Results In patients who received critical care and survived hospitalization, the absolute risk of 90-day postdischarge mortality was 5.9%, 11.7%, 15.8% and 21.9% in patients with 0/μl, 1–100/μl, 101–200/μl and more than 200/μl nucleated red blood cells respectively. Nucleated red blood cells were a robust predictor of postdischarge mortality and remained so following multivariable adjustment. The fully adjusted odds of 90-day postdischarge mortality in patients with 1–100/μl, 101–200/μl and more than 200/μl nucleated red blood cells were 1.77 (95% CI, 1.23–2.54), 2.51 (95% CI, 1.36–4.62) and 3.72 (95% CI, 2.16–6.39) respectively, relative to patients without nucleated red blood cells. Further, the presence of nucleated red blood cells is a significant predictor of the odds of unplanned 30-day hospital readmission. Conclusion In critically ill patients who survive hospitalization, the presence of nucleated red blood cells is a robust predictor of postdischarge mortality and unplanned hospital readmission. Electronic supplementary material The online version of this article (doi:10.1186/s13054-017-1724-z) contains supplementary material, which is available to authorized users.

Objective: Early diagnosis of pyogenic vertebral osteomyelitis (PVO) is frequently difficult. There are, however, few studies that have investigated the diagnostic performance of PVO in Japan. Our aim was to analyze the diagnostic performance and identify clinical factors associated with the diagnostic delay of PVO. Materials and Methods: We performed hospital-based retrospective case analysis. All patients with PVO were identified from the computerized medical database at Okinawa Chubu Hospital in Okinawa, Japan, from January 1985 to December 2004. We collected the following data; baseline information; laboratory tests; clinical and microbiologic outcomes; and diagnostic process. We used multivariable-adjusted linear regression to identify significant factors associated with patient and hospital delay to the diagnosis of PVO. Results: We reviewed total of 209,428 patients hospitalized during the 20-year study period. Of those, we identified 51 patients with PVO. Eighty percent of these patients were misdiagnosed at their initial clinical encounters. Median duration from the symptom onset to the diagnosis was 19 days. Median durations of patient factor and hospital factor that contributed to the total delay were 1 and 8 days, respectively. Significant patient factor that contributed to delay was cognitive dysfunction. Conclusions: Cognitive dysfunction is a risk factor for patient delay for visiting physicians in patients with PVO. Diagnosis of PVO is difficult at the initial clinical encounter. High index of suspicion is needed for more rapid diagnosis of PVO.

We hypothesized that preexisting malnutrition in patients who survived critical care would be associated with adverse outcomes following hospital discharge.We performed an observational cohort study in 1 academic medical center in Boston. We studied 23,575 patients, aged ≥18 years, who received critical care between 2004 and 2011 and survived hospitalization.The exposure of interest was malnutrition determined at intensive care unit (ICU) admission by a registered dietitian using clinical judgment and on data related to unintentional weight loss, inadequate nutrient intake, and wasting of muscle mass and/or subcutaneous fat. The primary outcome was 90-day postdischarge mortality. Secondary outcome was unplanned 30-day hospital readmission. Adjusted odds ratios were estimated by logistic regression models adjusted for age, race, sex, Deyo-Charlson Index, surgical ICU, sepsis, and acute organ failure. In the cohort, the absolute risk of 90-day postdischarge mortality was 5.9%, 11.7%, 15.8%, and 21.9% in patients without malnutrition, those at risk of malnutrition, nonspecific malnutrition, and protein-energy malnutrition, respectively. The odds of 90-day postdischarge mortality in patients at risk of malnutrition, nonspecific malnutrition, and protein-energy malnutrition fully adjusted were 1.77 (95% confidence interval [CI], 1.23-2.54), 2.51 (95% CI, 1.36-4.62), and 3.72 (95% CI, 2.16-6.39), respectively, relative to patients without malnutrition. Furthermore, the presence of malnutrition is a significant predictor of the odds of unplanned 30-day hospital readmission.In patients treated with critical care who survive hospitalization, preexisting malnutrition is a robust predictor of subsequent mortality and unplanned hospital readmission.

Pre-hospital vitamin D status may be a modifiable risk factor for all-cause mortality among hospitalized patients.To examine the association between increases in serum 25-hydroxyvitamin D [25(OH)D] levels during the year before hospitalization and risk of 30-day all-cause mortality after hospital admission.Retrospective cohort study.Two Boston teaching hospitals.We studied 4344 adults hospitalized between 1993 and 2011 who had serum 25(OH)D concentrations measured at least twice within 7-365 days before the index hospitalization.None.The exposure of interest was change in pre-hospital serum 25(OH)D concentrations. The main outcome was 30-day all-cause mortality. We used mixed-effects logistic regression to describe how 30-day mortality differed with changes in pre-hospital 25(OH)D concentrations. Additionally, the odds of 30-day mortality in patients with pre-hospital 25(OH)D increases of ≥10 ng/mL was compared to that of patients with increases of10 ng/mL.In a mixed-effect logistic regression model adjusted for age, gender, race, type (medical/surgical), Deyo-Charlson Index, creatinine and hematocrit, 30-day all-cause mortality rate was 8% (95%CI: 1-15) lower for each 10 ng/mL increase in pre-hospital 25(OH)D (P = 0.025) compared with the 30-day all-cause mortality rate in the entire cohort. In an adjusted logistic regression model, absolute changes of ≥10 ng/mL in patients with initial 25(OH)D concentrations 20 ng/mL (n = 1944) decreased the odds of 30-day all-cause mortality by 48% (adjusted OR 0.52; 95%CI 0.30-0.93; P = 0.026) compared to patients with changes of10 ng/mL.In patients with initial 25(OH)D 20 ng/mL, subsequent improvements in vitamin D status before hospitalization are associated with decreased odds of 30-day all-cause mortality after hospital admission. A causal relation may not be inferred from this observational study.

The association between obesity and mortality in critically ill patients is unclear based on the current literature. To clarify this relationship, we analyzed the association between obesity and mortality in a large population of critically ill patients and hypothesized that mortality would be impacted by nutritional status.We performed a single-center observational study of 6,518 adult patients treated in medical and surgical ICUs between 2004 and 2011. All patients received a formal, in-person, and standardized evaluation by a registered dietitian. Body mass index was determined at the time of dietitian consultation from the estimated dry weight or hospital admission weight and categorized a priori as less than 18.5 kg/m (underweight), 18.5-24.9 kg/m (normal/referent), 25-29.9 kg/m (overweight), 30-39.9 kg/m (obesity class I and II), and more than or equal to 40.0 kg/m (obesity class III). Malnutrition diagnoses were categorized as nonspecific malnutrition, protein-energy malnutrition, or well nourished. The primary outcome was all-cause 30-day mortality determined by the Social Security Death Master File. Associations between body mass index groups and mortality were estimated by bivariable and multivariable logistic regression models. Adjusted odds ratios were estimated with inclusion of covariate terms thought to plausibly interact with both body mass index and mortality. We utilized propensity score matching on baseline characteristics and nutrition status to reduce residual confounding of the body mass index category assignment.In the cohort, 5% were underweight, 36% were normal weight, 31% were overweight, 23% had class I/II obesity, and 5% had class III obesity. Nonspecific malnutrition was present in 56%, protein-energy malnutrition was present in 12%, and 32% were well nourished. The 30-day and 90-day mortality rate for the cohort was 19.1 and 26.6%, respectively. Obesity is a significant predictor of improved 30-day mortality following adjustment for age, gender, race, medical versus surgical patient type, Deyo-Charlson index, acute organ failure, vasopressor use, and sepsis: underweight odds ratio 30-day mortality is 1.09 (95% CI, 0.80-1.48), overweight 30-day mortality odds ratio is 0.93 (95% CI, 0.80-1.09), class I/II obesity 30-day mortality odds ratio is 0.80 (95% CI, 0.67-0.96), and class III obesity 30-day mortality odds ratio is 0.69 (95% CI, 0.49-0.97), all relative to patients with body mass index 18.5-24.9 kg/m. Importantly, there is confounding of the obesity-mortality association on the basis of malnutrition. Adjustment for only nutrition status attenuates the obesity-30-day mortality association: underweight odds ratio is 0.74 (95% CI, 0.54-1.00), overweight odds ratio is 1.05 (95% CI, 0.90-1.23), class I/II obesity odds ratio is 0.96 (95% CI, 0.81-1.15), and class III obesity odds ratio is 0.81 (95% CI, 0.59-1.12), all relative to patients with body mass index 18.5-24.9 kg/m. In a subset of patients with body mass index more than or equal to 30.0 kg/m (n = 1,799), those with either nonspecific or protein-energy malnutrition have increased mortality relative to well-nourished patients with body mass index more than or equal to 30.0 kg/m: odds ratio of 90-day mortality is 1.67 (95% CI, 1.29-2.15; p0.0001), fully adjusted. In a cohort of propensity score matched patients (n = 3,554), the body mass index-mortality association was not statistically significant, likely from matching on nutrition status.In a large population of critically ill adults, the association between improved mortality and obesity is confounded by malnutrition status. Critically ill obese patients with malnutrition have worse outcomes than obese patients without malnutrition.

Objectives: Red cell distribution width is associated with mortality and bloodstream infection risk in the critically ill. In hospitalized patients with critical illness, it is not known if red cell distribution width can predict subsequent risk of all-cause mortality following hospital discharge. We hypothesized that an increase in red cell distribution width at hospital discharge in patients who survived to discharge following critical care would be associated with increased postdischarge mortality. Design: Two-center observational cohort study Setting: All medical and surgical ICUs at the Brigham and Women’s Hospital and Massachusetts General Hospital. Patients: We studied 43,212 patients, who were 18 years old or older and received critical care between 1997 and 2007 and survived hospitalization. Interventions: None. Measurements and Main Results: The exposure of interest was red cell distribution width within 24 hours of hospital discharge and categorized a priori in quintiles as less than or equal to 13.3%, 13.3–14.0%, 14.0–14.7%, 14.7–15.8%, and more than 15.8%. The primary outcome was all-cause mortality in the 30 days following hospital discharge. Secondary outcomes included 90-day and 365-day mortality following hospital discharge. Mortality was determined using the U.S. Social Security Administration Death Master File, and 365-day follow-up was present in all cohort patients. Adjusted odds ratios were estimated by multivariable logistic regression models with inclusion of covariate terms thought to plausibly interact with both red cell distribution width and mortality. Adjustment included age, race, gender, Deyo-Charlson Index, patient type (medical vs surgical), sepsis, and number of organs with acute failure. In patients who received critical care and survived hospitalization, the discharge red cell distribution width was a robust predictor of all-cause mortality and remained so following multivariable adjustment. Patients with a discharge red cell distribution width of 14.0–14.7%, 14.7–15.8%, and more than 15.8% have an odds ratio for mortality in the 30 days following hospital discharge of 2.86 (95% CI, 2.25–3.62), 4.57 (95% CI, 3.66–5.72), and 8.80 (95% CI, 7.15–10.83), respectively, all relative to patients with a discharge red cell distribution width less than or equal to 13.3%. Following multivariable adjustment, patients with a discharge red cell distribution width of 14.0–14.7%, 14.7–15.8%, and more than 15.8% have an odds ratio for mortality in the 30 days following hospital discharge of 1.63 (95% CI, 1.27–2.07), 2.36 (95% CI, 1.87–2.97), and 4.18 (95% CI, 3.36–5.20), respectively, all relative to patients with a discharge red cell distribution width less than or equal to 13.3%. Similar significant robust associations post multivariable adjustments are seen with death by days 90 and 365 postdischarge. Estimating the receiver-operating characteristic area under the curve shows that discharge red cell distribution width has moderate discriminative power for mortality 30 days following hospital discharge (area under the curve = 0.70; SE 0.006; 95% CI, 0.69–0.71; p Conclusion: In patients treated with critical care who survive hospitalization, an elevated red cell distribution width at the time of discharge is a robust predictor of subsequent all-cause patient mortality. Increased discharge red cell distribution width likely reflects the presence of proinflammatory state, oxidative stress, arterial underfilling, or a combination, thereof which may explain the observed impact on patient survival following discharge. Elevated red cell distribution width at hospital discharge may identify ICU survivors who are at risk for adverse outcomes following hospital discharge.

Objective: Given the importance of inflammation in acute kid ney injury and the relationship between vitamin D and inflamma tion, we sought to elucidate the effect of vitamin D on acute kidney injury. We hypothesized that deficiency in 25-hydroxyvitamin D prior to hospital admission would be associated with acute kidney injury in the critically ill. Design: Two-center observational study of patients treated in medical and surgical intensive care units. Setting: Two hundred nine medical and surgical intensive care beds in two teaching hospitals in Boston, Massachusetts. Patients: Two thousand seventy-five patients, aged ≥18 yrs, in whom serum 25-hydroxyvitamin D was measured prior to hospitalization between 1998 and 2009. Interventions: None. Measurements and Main Results: The exposure of interest was preadmission serum 25-hydroxyvitamin D and categorized a priori as deficiency (25-hydroxyvitamin D ≤15 ng/mL), insufficiency (25-hydroxyvitamin D 15–30 ng/mL), or sufficiency (25-hydroxyvi tamin D ≥30 ng/mL). The primary outcome was acute kidney injury defined as meeting Risk, Injury, Failure, Loss, and End-stage kidney disease (RIFLE) Injury or Failure criteria. Logistic regression examined the RIFLE criteria outcome. Adjusted odds ratios were estimated by multivariate logistic regression models. Preadmission 25-hydroxyvitamin D deficiency is predictive of acute kidney injury. Patients with 25-hydroxyvitamin D deficiency have an odds ratio for acute kidney injury of 1.73 (95% confidence interval 1.30–2.30; p < .0001) relative to patients with 25-hydroxyvitamin D sufficiency. 25-Hydroxyvitamin D deficiency remains a significant predictor of acute kidney injury following multivariable adjustment (adjusted odds ratio 1.50; 95% confidence interval 1.42–2.24; p < .0001). Patients with 25-hydroxyvitamin D insufficiency have an odds ratio for acute kidney injury of 1.49 (95% confidence interval 1.15–1.94; p = .003) and an adjusted odds ratio of 1.23 (95% confidence interval 1.12–1.72; p = .003) relative to patients with 25-hydroxyvitamin D sufficiency. In addition, preadmission 25-hydroxyvitamin D deficiency is predictive of mor tality. Patients with 25-hydroxyvitamin D insufficiency have an odds ratio for 30-day mortality of 1.60 (95% confidence interval 1.18–2.17; p = .003) and an adjusted odds ratio of 1.61 (95% confidence inter val 1.06–1.57; p = .004) relative to patients with 25-hydroxyvitamin D sufficiency. Conclusion: Deficiency of 25-hydroxyvitamin D prior to hos pital admission is a significant predictor of acute kidney injury and mortality in a critically ill patient population. (Crit Care Med 2012; 40:3170–3179)

Given the importance of inflammation in acute kidney injury and the relationship between vitamin D and inflammation, we sought to elucidate the effect of vitamin D status on acute kidney injury. We hypothesized that deficiency in 25-hydroxyvitamin D (25(OH)D) prior to hospital admission would be associated with acute kidney injury in the critically ill.