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Introduction: Glomerular filtration rate (GFR) is routinely used for clinical assessment of kidney function. However, the accuracy of estimating equations in older adults is uncertain., Methods: In 66 adults with ≥50 years type 1 diabetes (T1D) duration and 73 nondiabetic controls from age/sex-matched subgroups (65 ± 8 years old and 77[55%] were women) we evaluated the performance of estimated GFR (eGFR) by creatinine (Modification of Diet and Renal Disease [MDRD], Chronic Kidney Disease-Epidemiology [CKD-EPI] cr ), cystatin C (CKD-EPI cys , CKD-EPI cr-cys ), and β 2 -microglobulin (β2M) compared with measured GFR by inulin clearance (mGFR). Performance was evaluated using metrics of bias (mean difference), precision (SD), and accuracy (proportion of eGFR that differed by >20% of mGFR)., Results: Mean mGFR was 104 ± 18 ml/min per 1.73 m 2 (range: 70-154 ml/min per 1.73 m 2 ) and was not different between T1D and controls (103 ± 17 vs. 105 ± 19 ml/min per 1.73 m 2 , P = 0.39). All equations significantly underestimated mGFR (bias: -15 to -30 ml/min per 1.73 m 2 , P  < 0.001 for all comparisons) except for β2M, which had bias of 1.9 ml/min per 1.73 m 2 ( P = 0.61). Bias was greatest in cystatin C-based equations. Precision was lowest for β2M (SD: 43.5 ml/min per 1.73 m 2 , P  < 0.001 for each comparison). Accuracy was lowest for CKD-EPI cysC (69.1%, P  < 0.001 for each comparison). Cystatin C-based equations demonstrated greater bias and lower accuracy in older age subgroups (<60, 60-69, ≥70 years). All equations demonstrated greater bias across higher ranges of mGFR (60-89, 90-119, ≥120 ml/min per 1.73 m 2 ). Results were similar between T1D and controls except that β2M had lower performance in T1D., Conclusion: Better estimates of GFR in older adults are needed for research and clinical practice, as this subgroup of the population has an amplified risk for the development of chronic kidney disease (CKD) that requires accurate GFR estimation methods.

Objective: Individual propensity to chronic, low-grade inflammation--a determinant of atherosclerosis-is in part under the control of genetic factors. To identify genes involved in this modulation, we performed a 10cM genome screen for linkage with plasma C-reactive protein in 38 extended families including 317 non-diabetic and 177 type 2 diabetic family members (2547 relative pairs)., Methods and Results: In a variance component analysis, heritability of CRP values was significant (h(2)=0.39, p<0.0001). This effect was independent of BMI and was present in both diabetic (h(2)=0.42, p=0.003) and non-diabetic (h(2)=0.34, p=0.0015) relatives. The strongest evidence of linkage with CRP was on chromosome 5p15, where the LOD score reached genome-wide significance (LOD=3.41, genome-wide p=0.013). Both diabetic and non-diabetic family members contributed to linkage at this location. Smaller linkage peaks were detected on chromosomes 5q35 (LOD=1.35) and 17p11 (LOD=1.33). When the analysis was restricted to diabetic family members, another peak of moderate intensity (LOD=2.17) was evident at 3p21., Conclusions: A major gene influencing CRP levels appears to be located on chromosome 5p15, with an effect that is independent of diabetes. Another gene on 3p21 may control CRP variation but only in the presence of a diabetic or insulin-resistant environment.