7 research outputs found

    Association between serum resistin levels and low eGFR (<60ml/min/1.73m<sup>2</sup>).

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    <p>SGR: San Giovanni Rotondo;</p><p>OR (95% CI) are given for SD increase of resistin levels.</p><p>Model 1: unadjusted (Boston sample adjusted by coronary artery disease status-yes/no).</p><p>Model 2: adjusted by smoking habits, BMI, waist circumference, diabetes duration, HbA1c, insulin treatment, hypertension and lipid-lowering therapy (Boston sample adjusted by coronary artery disease status-yes/no).</p><p>*Since the effect in SGR was different than that in Boston sample (p for OR values heterogeneity being = 0.014), individual data meta-analysis was carried out by using random effects</p><p>Association between serum resistin levels and low eGFR (<60ml/min/1.73m<sup>2</sup>).</p

    Clinical characteristics of patients from SGR and Boston studies.

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    <p>Continuous variables were reported as mean ± SD whereas categorical variables were reported as total frequency and percentages. SGR: San Giovanni Rotondo; BMI: Body Mass Index; HbA1c: glycated haemoglobin;, eGFR: estimated glomerular filtration rate.</p><p>Clinical characteristics of patients from SGR and Boston studies.</p

    Association between serum resistin levels and eGFR (continuous trait).

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    <p>SGR: San Giovanni Rotondo.</p><p>The β linear coefficients represent the change in eGFR level for 1SD increase in resistin. SE: standard error.</p><p>Model 1 = unadjusted (Boston sample was adjusted by coronary artery disease status-yes/no).</p><p>Model 2 = adjusted by smoking habits, BMI, waist circumference, diabetes duration, HbA1c, insulin treatment, hypertension and lipid-lowering therapy (Boston sample was adjusted by coronary artery disease status-yes/no).</p><p>*Since the effect in SGR was different than that in Boston sample (p for beta values heterogeneity being = 3.3*10<sup>−6</sup>), individual data meta-analysis was carried out by using random effects.</p><p>Association between serum resistin levels and eGFR (continuous trait).</p

    <strong>Cardiovascular autonomic neuropathy and risk of kidney function decline in type 1 and type 2 diabetes: findings from the PERL and ACCORD cohorts </strong>

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    Previous studies have suggested that cardiovascular autonomic neuropathy (CAN) may predict rapid kidney function decline among persons with diabetes. We analyzed the association between baseline CAN and subsequent glomerular filtration rate (GFR) decline among individuals with type 1 diabetes (T1D) from the Preventing Early Renal Loss in Diabetes (PERL) study (N=469) and with type 2 diabetes (T2D) from the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study (N=7,973). Baseline CAN was ascertained using ECG-derived heart rate variability indices. Its association with GFR slopes, rapid kidney function decline (GFR loss ≥-5 ml/min/1.73 m2/year), and ≥40% GFR loss was evaluated by linear mixed effect, logistic, and Cox regression, respectively. Participants with CAN experienced more rapid GFR decline, by an excess 1.15 (95%CI [-1.93, -0.37], P= 4.0x10-3) ml/min/1.73m2/year in PERL and 0.34 (95%CI [-0.49, -0.19], P= 6.3x10-6) ml/min/1.73m2/year in ACCORD. This translated in 2.11 (95% CI [1.23-3.63], P=6.9x10-3) and 1.39 (95% CI [1.20-1.61], P=1.1x10-5) odds ratios of rapid kidney function decline in PERL and ACCORD, respectively. Baseline CAN was also associated with a greater risk of ≥40% GFR loss events during follow-up (HR=2.60, 95%CI [1.15-5.45], p=0.02 in PERL and HR=1.54, 95%CI [1.28-1.84], P=3.8×10-6 in ACCORD). These associations remained significant after adjustment for potential confounders, including baseline GFR and albuminuria. Our findings indicate that CAN is a strong, independent predictor of rapid kidney function decline in both T1D and T2D. Further studies of the link between these two complications may help develop new therapies to prevent kidney function decline in patients with diabetes.  </p

    Clinical characteristics of study participants of the GFS (635 non-diabetic individuals from 218 families).

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    <p>Data are expressed as Mean ± SD or %.</p><p>BMI: Body Mass Index; SBP: Systolic Blood Pressure; DBP: Diastolic Blood Pressure; FBG: Fasting Blood Glucose; HOMA<sub>IR</sub>: homeostasis model assessment of insulin-resistance; HDL-Cholesterol: high-density lipoprotein cholesterol; eGFR: estimated Glomerular Filtration Rate by CKD-EPI formula; ACR: Albumin Creatinine Ratio.</p><p>Obese: BMI ≥30.</p><p>Overweight: BMI ≥25≤29.9.</p><p>Hypertensive: (i.e. systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg).</p

    The reproducibility of the allele frequency estimates is shown by the scatter plot of repeated estimates of allele frequency inferred from pooled DNA samples (left)

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    <p><b>Copyright information:</b></p><p>Taken from "A hierarchical and modular approach to the discovery of robust associations in genome-wide association studies from pooled DNA samples"</p><p>http://www.biomedcentral.com/1471-2156/9/6</p><p>BMC Genetics 2008;9():6-6.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2248205.</p><p></p> The labels "run 1" and "run 2" in the x- and y-axis specify each replication. The accuracy of the allele frequency estimates is shown by the scatter plot of the estimates of allele frequency inferred from pooled DNA samples (y-axis in the right plots) and those computed from individually genotyped samples (x-axis). The analysis of the other chromosomes shows similar results

    Relation between the pattern of LD (x-axis) and the global measure of association (y-axis) in the regional filter

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    <p><b>Copyright information:</b></p><p>Taken from "A hierarchical and modular approach to the discovery of robust associations in genome-wide association studies from pooled DNA samples"</p><p>http://www.biomedcentral.com/1471-2156/9/6</p><p>BMC Genetics 2008;9():6-6.</p><p>Published online 14 Jan 2008</p><p>PMCID:PMC2248205.</p><p></p> The pattern of LD is measured by the average of the Bayes D' between consecutive SNPs in the region, and the global measure of association is the joint probability of association in the region. The two figures in the top half show the relation using data from the study of fetal hemoglobin in the sickle cell anemia subjects. The two figure in the bottom half show the relation using data from the longevity study. The different extent of LD reflect the fact that sickle cell anemia subjects are all African American while centenarians in the longevity study are all Caucasians The correlations in the four sets are 0.03, 0.18, 0.018, -0.10
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