Dataset Information

Relationship of body mass index, serum creatine kinase, and acute kidney injury after severe trauma.

ABSTRACT:

Objectives

Body mass index (BMI) is associated with acute kidney injury (AKI) after trauma, but underlying mechanisms are unclear. Body mass index correlates with both excess adiposity and increased muscle mass. Since the latter could predispose to severe rhabdomyolysis after trauma, we hypothesized that the BMI-AKI association may be partially explained by a direct relationship of BMI with serum creatine kinase (CK).

Methods

Prospective cohort study of 463 critically ill patients admitted to a level I trauma center from 2005 to 2015 with Injury Severity Score of >15 and serum CK measured in the first 7 days. We defined AKI by AKI Network creatinine criteria. We used simple linear regression to determine the association of BMI with peak CK and multivariable logistic regression to adjust the BMI-AKI association for peak CK and confounders.

Results

Median age was 43 years, 350 (76%) were male, 366 (79%) had blunt mechanism, and median Injury Severity Score was 24. Body mass index was associated with peak CK (R = 0.05, p < 0.001). Acute kidney injury developed in 148 patients (32%), and median time to peak CK was 29 hours (interquartile range, 15-56 hours) after presentation. Body mass index was significantly associated with AKI in multivariable models adjusted for age, race, sex, diabetes, injury mechanism and severity, and red blood cell transfusions (odds ratio [OR], 1.31 per 5 kg/m; 95% confidence interval [CI], 1.09-1.58; p = 0.004). Adding peak CK to the model partially attenuated the association of BMI with AKI (OR, 1.26 per 5 kg/m; 95% CI, 1.04-1.52; p = 0.018), and peak CK was also associated with AKI (OR, 1.19 per natural log; 95% CI, 1.00-1.41; p = 0.049). Peak CK remained associated with AKI when restricted to patients with values of <5,000 U/L (OR, 1.31 per natural log; 95% CI, 1.01-1.69; p = 0.043).

Conclusion

Serum CK correlated with BMI and partially attenuated the association of BMI with AKI after major trauma, suggesting that excess muscle injury may contribute to the BMI-AKI association.

Level of evidence

Epidemiologic study, level III.

SUBMITTER: Vasquez CR

PROVIDER: S-EPMC7830741 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:ImportanceAlthough high body mass index (BMI) is associated with adverse birth outcomes, the association with severe maternal morbidity is unclear.ObjectiveTo examine the association between prepregnancy BMI and severe maternal morbidity.Design, setting, and participantsRetrospective population-based cohort study including all singleton hospital births in Washington State, 2004-2013. Demographic data and morbidity diagnoses were obtained from linked birth certificates and hospitalization files.ExposuresPrepregnancy BMI (weight in kilograms divided by height in meters squared) categories included underweight (<18.5), normal BMI (18.5-24.9), overweight (25.0-29.9), obesity class 1 (30.0-34.9), obesity class 2 (35.0-39.9), and obesity class 3 (≥40).Main outcomes and measuresComposite severe maternal morbidity or mortality included life-threatening conditions and conditions leading to serious sequelae (eg, amniotic fluid embolism, hysterectomy), complications requiring intensive care unit admission, and maternal death. Logistic regression was used to obtain adjusted odds ratios (ORs) and adjusted rate differences with 95% confidence intervals, adjusted for confounders (eg, maternal age and parity).ResultsOverall, 743 630 women were included in the study (mean age, 28.1 [SD, 6.0] years; 41.4% nulliparous). Prepregnancy BMI was distributed as follows: underweight, 3.2%; normal weight, 47.5%; overweight, 25.8%; obesity class 1, 13.1%; obesity class 2, 6.2%; and obesity class 3, 4.2%. Rates of severe maternal morbidity or mortality were 171.5, 143.2, 160.4, 167.9, 178.3 and 202.9 per 10 000 women, respectively. Adjusted ORs were 1.2 (95% CI, 1.0-1.3) for underweight women; 1.1 (95% CI, 1.1-1.2) for overweight women; 1.1 (95% CI, 1.1-1.2) for women with class 1 obesity; 1.2 (95% CI, 1.1-1.3) for women with class 2 obesity; and 1.4 (95% CI, 1.3-1.5) for women with class 3 obesity compared with women with normal BMI. Absolute risk increases (adjusted rate differences per 10 000 women, compared with women with normal BMI) were 28.8 (95% CI, 12.2-47.2) for underweight women, 17.6 (95% CI, 10.5-25.1) for overweight women, 24.9 (95% CI, 15.7-34.6) for women with class 1 obesity, 35.8 (95% CI, 23.1-49.5) for women with class 2 obesity, and 61.1 (95% CI, 44.8-78.9) for women with class 3 obesity.Conclusions and relevanceAmong pregnant women in Washington State, low and high prepregnancy BMI, compared with normal BMI, were associated with a statistically significant but small absolute increase in severe maternal morbidity or mortality.

Project description:BACKGROUND:While restrictive and compensatory eating disorders (e.g. anorexia and bulimia) are associated with elevated risk of suicide, less is known about binge eating disorder (BED). There is suggestive evidence of a U-shaped relationship between body mass index (BMI) and completed suicide, but fewer studies on suicidal ideation or attempts. This study examined the association between BED, BMI, and suicidality, and assessed whether these relationships varied by gender. METHODS:Data come from the Collaborative Psychiatric Epidemiologic Surveys (N =?14,497). Binge episodes and BED were assessed using the Composite International Diagnostic Inventory (CIDI). BMI was calculated from self-reported height and weight. Suicidal ideation/attempts were assessed using the CIDI. Weighted logistic regression was used to assess the association between binging/BED, BMI and suicidality. Interaction terms were used to assess whether the relationship between BMI and suicidality was moderated by binging/BED, and whether the relationships between binging/BED and BMI differed by gender. RESULTS:One-third of adults with BED had a history of suicidality, compared to 19% of those without. Both binging (OR: 1.95, 95% CI: 1.50-2.53) and BED (OR: 2.01, 95% CI: 1.41-2.86) were associated with suicidality in fully-adjusted models. BMI was associated with suicidality in a curvilinear manner, and this relationship was exacerbated by binging/BED (ORBinge eating x BMI: 1.04, 95% CI: 1.01-1.09, p <?0.05). The relationship between BMI and suicidality did not differ by gender (ORgender x BMI: 1.00, p <?0.770). However, the relationship between binge eating and suicidality was stronger for women relative to men (ORgender X binge: 1.87, p <?0.012). CONCLUSIONS:Binge eating, even below the threshold for BED, is associated with suicidality. BMI is associated with suicidality in a curvilinear manner, and the BMI-suicidality relationship is potentiated by binge eating/BED. Findings support the thoughtful integration of psychiatric care into weight loss programs for adults with a history of binging behavior.

Project description:AimsThere are limited data examining whether body mass index (BMI) influences the association between cardiovascular biomarkers and incident heart failure (HF).Methods and resultsThirteen biomarkers representing key HF domains were measured: N-terminal pro-B-type natriuretic peptide (NT-proBNP), mid-regional pro-A-type natriuretic peptide (MR-proANP), cardiac troponin T (cTnT), C-reactive protein, procalcitonin, galectin-3, C-terminal pro-endothelin-1 (CT-proET-1), mid-regional pro-adrenomedullin, plasminogen activator inhibitor-1, copeptin, renin, aldosterone, and cystatin-C. Associations of biomarkers with BMI were examined using linear regression models, and with incident HF using Cox regression models. We selected biomarkers significantly associated with incident HF, and evaluated whether BMI modified these associations. Among 8202 individuals, 41% were overweight (BMI 25-30 kg/m2 ), and 16% were obese (BMI ≥30 kg/m2 ). Mean age of the cohort was 49 years (range 28-75), and 50% were women. All biomarkers except renin were associated with BMI: inverse associations were observed with NT-proBNP, MR-proANP, CT-proET-1 and aldosterone whereas positive associations were observed with the remaining biomarkers (all P ≤ 0.001). During 11.3 ± 3.1 years of follow-up, 357 HF events were recorded. Only NT-proBNP, MR-proANP and cTnT remained associated with incident HF (P < 0.001), and a significant biomarker*BMI interaction was not observed (interaction P > 0.1). Combined NT-proBNP and cTnT measurements modestly improved performance metrics of the clinical HF model in overweight (ΔC-statistic = 0.024; likelihood ratio χ2 = 38; P < 0.001) and obese (ΔC-statistic = 0.020; likelihood ratio χ2 = 32; P < 0.001) individuals.ConclusionsPlasma concentrations of several cardiovascular biomarkers are influenced by obesity. Only NT-proBNP, MR-proANP and cTnT were associated with incident HF, and BMI did not modify these associations. A combination of NT-proBNP and cTnT improves HF risk prediction in overweight and obese individuals.