PubMed · 10131071
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T C Dolan. 1993. Appreciating diversity.. https://pubmed.ncbi.nlm.nih.gov/10131071/
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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.
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Between 2 and 11 months of age, the risk of sudden infant death syndrome (SIDS) declines more slowly in black infants than in infants of other races. This phenomenon might also be a feature of certain non-SIDS causes of death. Identifying these causes may through analogy provide support for the theory that SIDS is a disease of the central nervous system, an unusual consequence of respiratory infection, or a form of suffocation. We used logistic regression analysis on details of infant deaths in the United States, 1985-1991, to examine the difference between the rates of decline with increasing age in the mortality rates of black infants and infants of other races. We defined slower rate of decline in black infants as a positive difference. The magnitude and direction (positive) of the difference for deaths due to respiratory infection were similar to those for SIDS. It is unlikely that this difference in the rates of decline for respiratory infection can be explained by diagnostic cross-misclassification between respiratory infection and SIDS. SIDS appears to be a disease of the respiratory system caused by infection that affects that system's control centers.