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Articles by B. I. Freedman
Total Records ( 4 ) for B. I. Freedman
  B. I. Freedman , D. W. Bowden , S. S. Rich , J. Xu , L. E. Wagenknecht , J. Ziegler , P. J. Hicks and C. D. Langefeld
  Aims/hypothesis  Glomerular filtration rate (GFR), end-stage renal disease and albuminuria are highly heritable. We performed a genome-wide linkage scan in 416 Diabetes Heart Study (DHS) families to detect loci that contributed to renal function and albuminuria.

Materials and methods  A total of 1067 individuals (900 with Type 2 diabetes mellitus) from 348 European American and 68 African American DHS families had measures of urine albumin : creatinine ratio (ACR), serum creatinine concentration and Modification of Diet in Renal Disease estimated GFR (eGFR). Variance components quantitative trait linkage analysis (using SOLAR) was computed.

Results  Participants had mean ± sd age 61.4 ± 9.4 years; diabetes duration 10.5 ± 7.4 years; eGFR 1.15 ± 0.32 ml/sec; and urine ACR 15.8 ± 67.2 mmol/l (median 1.4). In all families, significant evidence for linkage of GFR was observed on chromosome 2p16 (log of the odds; LOD = 4.31 at 72.0 cM, ATA47C04P/D2S1352) and 1p36 (LOD = 3.81 at 45.0 cM, D1S3669/D1S3720), with suggestive evidence on 7q21 (LOD = 2.42 at 99.0 cM, D7S820/D7S821) and 13q13 (LOD = 2.28 at 28.0 cM, D13S1493/D13S894). The evidence for linkage to ACR was far weaker, on 13q21-q22 (LOD = 1.84 at 50 cM, D13S1807/D13S800), 3p24-p23 (LOD = 1.81 at 58 cM, D3S3038/D3S2432) and 10p11 (LOD = 1.78 at 71.0 cM, D10S1208/D10S1221).

Conclusions/interpretations  The eGFR linkage peaks on 2p16, 7q21 and 13q13 closely overlap with nephropathy peaks identified in family studies enriched for severe kidney disease. These diabetes-enriched families provide an opportunity to map genes regulating renal function, potentially leading to the identification of genes producing nephropathy susceptibility in subjects with Type 2 diabetes.

  A. J. Bleyer , D. Hire , G. B. Russell , J. Xu , J. Divers , Z. Shihabi , D. W. Bowden and B. I. Freedman
  Aims  To determine if the relationship between serum glucose concentration and glycated haemoglobin is different between African-Americans and whites.

Methods  Retrospective cross-sectional study comparing the association between glycated haemoglobin and serum glucose levels, based upon ethnicity. Two databases were evaluated: (i) 4215 African-American and 6359 white outpatients who had simultaneous glycated haemoglobin, random serum glucose and creatinine concentration measurements between 2000 and 2007 at the North Carolina Baptist Hospital and (ii) 1021 white and 312 African-American Diabetes Heart Study (DHS) participants.

Results  In North Carolina Baptist Hospital clinic attendees, a given glycated haemoglobin was associated with higher serum glucose concentrations in African-Americans compared with whites. In a multivariate model with glycated haemoglobin as the outcome variable, racial differences remained significant after adjustment for serum glucose, age, gender and kidney function. For individuals with a serum glucose between 5.6 and 8.3 mmol/l, the glucose : glycated haemoglobin ratio was 1.03 ± 0.16 mmol/l/% in white individuals and 0.99 ± 0.17 mmol/l/% in African-Americans (P < 0.0001). For a glycated haemoglobin value of 7.0%, there was a 0.98-mmol/l difference in predicted serum glucose concentration in 50-year-old African-American men, relative to white. Results were replicated in the DHS, where in a best-fit linear model, after adjustment for glucose, African-American race was a significant predictor of glycated haemoglobin (P < 0.0001).

Conclusions  African-Americans have higher glycated haemoglobin values at given serum glucose concentrations relative to whites. This finding may contribute to the observed difference in glycated haemoglobin values reported between these race groups.

  A. J. Bleyer , S. Vidya , L. Sujata , G. B. Russell , D. Akinnifesi , D. Hire , Z. Shihabi , M. A. Knovich , P. Daeihagh , J. Calles and B. I. Freedman
  Aims  To determine the effect of sickle cell trait on measurement of glycated haemoglobin (HbA1c) in African American patients with diabetes mellitus.

Methods  This is a retrospective study including 885 outpatients who underwent HbA1c testing. Medical record review and sickle cell trait determinations based on the HbA1c assay were performed in African American participants. The relationship between HbA1c and serum glucose measurements was analysed.

Results  Data were obtained from 385 AA (109 with SCT, 22 with haemoglobin C trait and 254 without haemoglobinopathy) and 500 European American patients. In a model created through multivariate repeated-effects regression, the relationship between HbA1c and simultaneous serum glucose did not differ between African American subjects with and without the sickle cell trait, but differed between African American subjects without the sickle cell trait and European Americans (P = 0.0002).

Conclusions  Sickle cell trait does not impact the relationship between HbA1c and serum glucose concentration. In addition, it does not appear to account for ethnic difference in this relationship between African Americans and whites.

  A. J. Cox , S. Agarwal , D. M Herrington , J. J. Carr , B. I. Freedman and D. W. Bowden
  Aims  Although current American Heart Association guidelines address C-reactive protein concentration and cardiovascular disease risk, it remains unclear whether this paradigm is consistent across populations with differing disease burdens. Individuals with Type 2 diabetes mellitus represent one group at increased risk of cardiovascular disease and subsequent mortality. This study aimed to examine the relationship between C-reactive protein concentrations and risk for all-cause mortality in European Americans with Type 2 diabetes from the Diabetes Heart Study.

Methods  A total of 846 European Americans with Type 2 diabetes and baseline measures of C-reactive protein were evaluated. Vital status was determined after a follow-up period of 7.3 ± 2.1 years (mean ± SD). C-reactive protein concentrations were compared between living and deceased subgroups along with other known risk factors for cardiovascular disease, including blood lipids. Logistic regression was performed to determine risk for mortality associated with increasing C-reactive protein concentrations.

Results  At follow-up 160 individuals (18.7%) were deceased. No significant differences in baseline serum glucose or lipid measures were observed between living and deceased subgroups. Baseline C-reactive protein concentrations were significantly higher in the deceased subgroup (9.37 ± 15.94) compared with the living subgroup (5.36 ± 7.91 mg/l; P < 0.0001). Participants with C-reactive protein concentrations of 3-10 mg/l were approximately two times more likely to be deceased at follow-up (OR 2.06; 95% CI 1.17-3.62); those with C-reactive protein >10 mg/l were more than five times more likely to be deceased (OR 5.24; CI 2.80-9.38).

Conclusions  This study documents the utility of C-reactive protein in predicting risk for all-cause mortality in European Americans with Type 2 diabetes and supports its use as a screening tool in risk prediction models.

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