PubMed · 5011388
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V F Guinee. 1972. Lead poisoning.. https://doi.org/10.1016/0002-9343(72)90015-0
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BACKGROUND: Glomerular filtration rate (GFR) is a heritable trait, and hyperfiltration (GFR increment in remnant nephrons) may accelerate renal functional decline in chronic kidney disease (CKD). Mesangial and vascular smooth myocytes control GFR by contraction, dependent on voltage-gated Ca(2+) influx, which is controlled by the regulatory β₁-subunit (KCNMB1) of large-conductance heteromeric K+ ('BK') channels. KCNMB1 gain-of-function variant Glu65Lys results in generalized vasorelaxation and thus protection against systemic hypertension. Here we asked whether the Glu65Lys variant influences GFR, in the basal state or during progressive renal decline. METHODS: We explored Glu65Lys effects on GFR in three populations spanning two ethnicities and two diseases (hypertension and nephrosclerosis). GFR was either estimated (eGFR from serum creatinine) or directly measured (iothalamate clearance). RESULTS: The 65Lys variant was relatively common, occurring on ∼5-10% of chromosomes in different biogeographic ancestry groups, and 65Lys carriers exhibited higher eGFR in two primary care populations: extreme BP values in Kaiser clinics (p = 0.029, accounting for ∼0.2% of trait variance), or treated hypertensives in VA clinics (p = 0.017, accounting for ∼0.9% of trait variance). In blacks with progressive renal disease (NIDDK AASK), 65Lys carriers displayed a steeper slope in GFR chronic decline (p = 0.030, accounting for ∼0.4% of trait variance), and Glu65Lys genotype also predicted time of onset of renal failure (log rank p = 0.019). CONCLUSIONS: Common KCNMB1 gain-of-function variant Glu65Lys influences GFR, and 65Lys carriers exhibit not only elevated baseline GFR, but also more rapid GFR decline (and consequent development of renal failure) in CKD. The results suggest that profiling patients at Glu65Lys can assist in gauging renal prognosis as well as selection of rational therapy in hypertension with progressive renal disease.
OBJECTIVE: To examine the relationship between level of education and childhood rural residence as possible risk factors for AD in African Americans in Indianapolis. BACKGROUND: Low level of education has been a risk factor for AD in some studies, but childhood rural residence has not been addressed in most of these studies. METHODS: A two-stage community-based prevalence study of AD was conducted in a random sample of 2,212 African Americans > or =65 years of age. A subsample of clinically assessed normal individuals (180) and individuals diagnosed with AD (43) were compared on the variables of rural/urban residence in childhood and low (< or =6 years) or high (> or =7 years) education. A logistic regression model was used with interaction between rural residence and low education to estimate odds ratios for the two risk factors combined, adjusting for age and gender. RESULTS: Odds ratios for AD: 6.5 (95% CI: 2.6 to 16.7) low education/rural residence; 0.5 (95% CI: 0.1 to 2.9) low education/urban residence; 1.5 (95% CI: 0.4 to 5.2) high education/rural residence, comparing with the group of high education/urban residence. CONCLUSION: Childhood rural residence, combined with < or =6 years of school, was associated with an increased risk of AD in this sample. It is possible that low education by itself is not a major risk factor for AD, but, rather, is a marker for other accompanying deleterious socioeconomic or environmental influences in childhood.
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