IMPORTANCE The association between sickle cell trait (SCT) and chronic kidney disease (CKD) is uncertain. OBJECTIVE To describe the relationship between SCT and CKD and albuminuria in self-identified African Americans. DESIGN, SETTING, AND PARTICIPANTS Using 5 large, prospective, US population-based studies (the Atherosclerosis Risk in Communities Study [ARIC, 1987–2013; n = 3402], Jackson Heart Study [JHS, 2000–2012; n = 2105], Coronary Artery Risk Development in Young Adults [CARDIA, 1985–2006; n = 848], Multi-Ethnic Study of Atherosclerosis [MESA, 2000–2012; n = 1620], and Women’s Health Initiative [WHI, 1993–2012; n = 8000]), we evaluated 15 975 self-identified African Americans (1248 participants with SCT [SCT carriers] and 14 727 participants without SCT [noncarriers]). MAIN OUTCOMES AND MEASURES Primary outcomes were CKD (defined as an estimated glomerular filtration rate [eGFR] of <60 mL/min/1.73 m2 at baseline or follow-up), incident CKD, albuminuria (defined as a spot urine albumin:creatinine ratio of >30 mg/g or albumin excretion rate >30 mg/24 hours), and decline in eGFR (defined as a decrease of >3 mL/min/1.73 m2 per year). Effect sizes were calculated separately for each cohort and were subsequently meta-analyzed using a random-effects model. RESULTS A total of 2233 individuals (239 of 1247 SCT carriers [19.2%] vs 1994 of 14 722 noncarriers [13.5%]) had CKD, 1298 (140 of 675 SCT carriers [20.7%] vs 1158 of 8481 noncarriers [13.7%]) experienced incident CKD, 1719 (150 of 665 SCT carriers [22.6%] vs 1569 of 8249 noncarriers [19.0%]) experienced decline in eGFR, and 1322 (154 of 485 SCT carriers [31.8%] vs 1168 of 5947 noncarriers [19.6%]) had albuminuria during the study period. Individuals with SCT had an increased risk of CKD (odds ratio [OR], 1.57 [95% CI, 1.34–1.84]; absolute risk difference [ARD], 7.6% [95% CI, 4.7%–10.8%]), incident CKD (OR, 1.79 [95% CI, 1.45–2.20]; ARD, 8.5% [95% CI, 5.1%–12.3%]), and decline in eGFR (OR, 1.32 [95% CI, 1.07–1.61]; ARD, 6.1% [95% CI, 1.4%–13.0%]) compared with noncarriers. Sickle cell trait was also associated with albuminuria (OR, 1.86 [95% CI, 1.49–2.31]; ARD, 12.6% [95% CI, 7.7%–17.7%]). CONCLUSIONS AND RELEVANCE Among African Americans in these cohorts, the presence of SCT was associated with an increased risk of CKD, decline in eGFR, and albuminuria, compared with noncarriers. These findings suggest that SCT may be associated with the higher risk of kidney disease in African Americans.

Cervical cancer is a leading cause of cancer death in women in developing countries. A key factor linked to the relatively high levels of cervical cancer in these populations is the lack of awareness and access to preventive methods. This study aimed to determine the level of awareness of cervical cancer and Papanicolaou test (Pap smear test) and factors associated with the utilization of Pap test among female civil servants in Jos. Data was obtained from female workers (n = 388) aged 18–65 years in a Nigerian Federal establishment. Participants were randomly approached and instructed to complete validated questionnaires. Data was analyzed using Chi-square, t-tests and logistic regression analysis to determine if there was an association between variables and identify any predictors of awareness and utilization of the Pap test. Cervical cancer and Pap smear test awareness was 50.9% and 38.6% respectively, with the media as the major source of information. Pap smear test utilization rate was 10.2%, with routine antenatal care (ANC) as the major reason for getting screened. Personal barriers to screening include the lack of awareness, and belief that cervical cancer is not preventable. Opportunistic screening, mass media campaigns and ANC education were suggested as ways of improving awareness and utilization of cervical cancer screening services.

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.

Finding a widely available cure for sickle cell anemia (HbSS) still remains a challenge one hundred years after its discovery as a genetically inherited disease. However, growing interest in the nutritional problems of the disease has created a body of literature from researchers seeking nutritional alternatives as a means of decreasing morbidity and improving quality of life among HbSS patients. This review demonstrates that over the past 30 years the role of protein/energy deficiency in HbSS has been more clearly defined via direct measurements, leading to the concept of a relative shortage of nutrients for growth and development, despite apparently adequate dietary intakes. Although there is still a paucity of data supporting the efficacy of macronutrient supplementation, it is becoming clearer that recommended dietary allowances (RDAs) for the general population are insufficient for the sickle cell patient. A similar shortage is likely to be true for micronutrient deficiencies, including recent findings of vitamin D deficiency that may be associated with incomplete ossification and bone disease, which are well known complications of HbSS disease. We conclude that there is need for more effort and resources to be dedicated to research (including supplementation studies of larger sample size) aimed at establishing specific RDAs for HbSS patients, much like the specific RDAs developed for pregnancy and growth within the general population.