Objective: There is gap in knowledge about obesity prevalence in stroke patients from low-and middle-income countries. Therefore, we aimed to measure the prevalence of overweight and obesity status among patients with incident stroke in Brazil. Methods: In a crosssectional study, we measured the body mass index (BMI) of ischemic and hemorrhagic stroke patients. The sample was extracted in 2016, from the cities of Sobral (CE), Sertãozinho (SP), Campo Grande (MS), Joinville (SC) and Canoas (RS). Results: In 1,255 patients with first-ever strokes, 64% (95% CI, 62-67) were overweight and 26% (95%CI, 24-29) were obese. The obesity prevalence ranged from 15% (95%CI, 9-23) in Sobral to 31% (95%CI, 18-45) in Sertãozinho. Physical inactivity ranged from 53% (95%CI, 43-63) in Sobral to 80% (95%CI, 73-85) in Canoas. Conclusions: The number of overweight patients with incident stroke is higher than the number of patients with stroke and normal BMI. Although similar to other findings in high-income countries, we urgently need better policies for obesity prevention.Keywords: obesity; prevalence; stroke, epidemiology; cross-sectional studies RESUMO Objetivo: Há uma lacuna de conhecimento sobre a prevalência de obesidade em pacientes com AVC (acidente vascular cerebral) de países de baixa e média renda. Portanto, objetivamos medir a prevalência de sobrepeso e obesidade entre pacientes com AVC no Brasil. Métodos: Em um estudo transversal, medimos o índice de massa corporal (IMC) em pacientes com AVC isquêmico e hemorrágico. A amostra foi extraída em 2016, nas cidades de Sobral (CE), Sertãozinho (SP), Campo Grande (MS), Joinville (SC) e Canoas (RS). Resultados: Entre 1255 casos de AVC, 64% (95%CI, 62-67) apresentavam sobrepeso e 26% (95%CI, 24-29) obesidade. A prevalência de obesidade variou de 15% (95%CI, 9-23) em Sobral a 31% (95%CI, 18-45) em Sertãozinho. Conclusões: A quantidade de pacientes com AVC e IMC anormal é maior do que a de pacientes com AVC e IMC normal. Embora esta prevalência seja similar às de países de alta renda, precisamos urgentemente de melhores políticas de prevenção da obesidade. Atividade física deveria ser parte da prescrição médica.Palavras-chave: obesidade; prevalência; acidente vascular cerebral, epidemiologia; estudos transversais Obesity has reached epidemic proportions globally, with at least 2.8 million people dying each year as a result of being overweight or obese 1 . Once associated with high-income countries, obesity is now also prevalent in low-and middle-income countries 1 . In Brazil, a study by the Ministry of Health in 2011, showed that 48% of the population was either overweight (33%) or obese (15%) 2 . In 2006, these figures were 22.7% and 11.4% 2,3 . Because obesity is believed to cause a number of established risk factors for cardiovascular diseases such as hypertension, dyslipidemia and diabetes, the growing prevalence of obesity is assumed to increase the global cardiovascular disease burden 4 . For instance, in adults, the risk for ischemic stroke increases almost linear...

Introduction: Obesity is reported as an important contributor for vitamin D (VitD) deficiency. Nevertheless, most of the studies use body mass index (BMI) to evaluate this relationship and results are not clear. In CKD, obesity and VitD deficiency are common conditions, however the association of body adiposity and VitD in nondialyzed CKD patients is not known. Objective: Determine the association of VitD with total and central body adiposity in nondialyzed CKD patients. Methods: Cross-sectional study conducted in nondialyzed CKD outpatients under regular treatment. Inclusion criteria: clinically stable; age≥18 years; estimated glomerular filtration rate (CKD-EPI) (eGFR)≤ 60 ml/min. Body adiposity: BMI (classified by WHO criteria; 1998); waist circumference (WC); waist-to-height ratio (WheiR); waist-to-hip ratio (WHR); total body adiposity (TBA) by dual-energy X-ray absorptiometry (DXA) and by body adiposity index (BAI). VitD[25(OH)D] analysed by Passing-Bablok method and leptin, used as TBA marker, by radioimmunoassay. Participants were stratified as: VitD-deficient (<20 ng/ml; 23%/n=40; VitD=16±3 ng/ml) and VitD-no-deficient (≥20 ng/ml; 77%/n=135; VitD=31±8 ng/ml). Results: We studied 175 nondialyzed CKD (57.7% men/n=101), 66±13 years, eGFR=29±13ml/min., BMI=26±5 kg/m2, VitD=27±9.7 ng/ml. CKD stages (CKD-s) profile was (%/n): 3A-15%/26; 3B-32%/56; 4-39%/68; 5-14%/25. VitD-deficient patients compared with VitD-no-deficient showed higher TBA evaluated by DXA (38±7 vs. 33±9%,p=0.003), BAI (32±7 vs. 29±5%,p=0.009) and leptin (median; interquartil interval=6.2; 5-10 vs. 11; 10-19 ng/dl,p=0,01), but showed no differences (p≥0.05) for BMI and central adiposity parameters (WC;WheiR;WHR). Serum 25(OH)D values were negatively associated with TBA (DXA: r= -0.3; p=0.0008; BAI: r= -0.22; p=0.008), but was not associated with BMI and with WC, WheiR, WHR. In multiple regression analysis TBA (by DXA and by BAI), but not BMI, was independently associated with VitD (p=0.001) after adjusted by age, gender, eGFR. Conclusion: Total body adiposity, but not BMI or central adiposity, was independently associated with vitamin D levels in this population with CKD.

INTRODUCTION: Vitamin D deficiency is reported to be associated with Insulin Resistance (IR) in general population. Although the impaired homeostasis of vitamin D and IR are common conditions in chronic kidney disease (CKD), the underlying mechanisms of IR remain unclear and it is not known if vitamin D status is associated with IR in nondialyzed CKD patients. OBJECTIVE: To investigate if serum levels of 25 hidroxivitamin D [25(OH)D] are associated with IR in nondialyzed CKD patients. Methods: Cross-sectional study conducted in nondialyzed CKD outpatients under regular treatment, clinically stable, age≥18 years, estimated glomerular filtration rate (CKD-EPI) (eGFR)≤ 60 ml/min., not using vitamin D, corticosteroids and immunosuppressive drugs and without malignant diseases. Body adiposity: body mass index (BMI); total body adiposity by dual-energy X-ray absorptiometry-DXA; waist-to-height ratio (WheiR). Vitamin D was determined by analysing 25(OH)D by Passing-Bablok method; insulin by radioimmunoassay; Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Results: Patients included in this study were 158 (men:55%/n=87) nondialyzed CKD patients presenting age=66±13years; eGFR=29±13ml/min.; BMI=26±5kg/m2 (54%/n=86 overweight/obese: BMI>25). Total body adiposity-DXA=34±9% and central body adiposity-WheiR=0.6±0.08. Patients were grouped according to HOMA-IR as: Group 1 (HOMA-IR<2.7; n=110) and Group 2 (HOMA-IR ≥2.7; n=48). VitD levels (ng/ml) were not different (p≥0.05) between Group 1 (27±9) and Group 2 (28±9). Participants were also stratified as: VitD-deficient (<20ng/ml; 25%/n=40) and VitD-no-deficient (≥20 ng/ml; 75%/n=118). VitD-deficient patients compared to VitD-no-deficient presented, respectively, similar values (p≥0.05) of HOMA-IR (median; interquartil interval: 1.7; 1-3 vs. 1.6; 1-3.4), insulin (7; 5-12 vs. 6; 5-13 μU/mL); glucose (105±28 vs. 109±62 mg/dl), glycosylated hemoglobin (GHb=6±1 vs. 6±2 %). No correlation (adjusted for confounders) was observed between VitD with HOMA-IR (r=0.01,p=0.87), insulin (r=0.02,p=0.8), glucose (r=-0.05,p=0.5) and GHb (r=-0.1,p=0.6). Conclusion: The present study suggests that serum levels of 25(OH)D are not associated with IR in nondialyzed CKD patients.

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