PubMed · 5079295
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L H Lipsius. 1972. Reaching black professionals.. https://doi.org/10.1176/ajp.129.5.631
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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.
PURPOSE: This study examines geographic variation in reporting of Parkinson's disease mortality in the U.S. METHODS: National Center for Health Statistics and Bureau of the Census data were used to map age-adjusted, race- and race-gender-specific Parkinson's disease mortality rates in the U.S. for 1988. RESULTS: Among whites, high underlying-cause rates predominated in the North and low rates predominated in the South, whereas high contributing and all-cause rates were concentrated in the northeastern U.S. Strong north-to-south decreasing gradients were present for both underlying- and all-cause rates for whites, regardless of gender, whereas a clear west-to-east gradient could not be demonstrated. Geographic variation in contributing- and all-cause rates was partially explained by variation in tendency to report contributing causes of death. Reported rates among blacks were significantly lower than among whites. There was no latitudinal or longitudinal gradient of underlying-cause rates for blacks, but there was a relatively weak north-to-south decreasing gradient of all-cause rates for blacks, regardless of gender. CONCLUSIONS: The large-scale pattern of underlying-cause Parkinson's disease mortality among whites has persisted for over three decades.
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