There is insufficient to low strength of evidence that any non-pharmacologic intervention improves sleep quality or quantity of general inpatients. Further studies are needed in this area to guide clinicians.

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BackgroundThe degree to which genetic or environmental factors are associated with early kidney damage among African Americans (AAs) is unknown.MethodsAmong 462 AAs in the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study, we examined the cross-sectional association between apolipoprotein L1 (APOL1) risk variants and income with: 1) mildly reduced eGFR (<75 mL/min/1.73 m2, creatinine-cystatin C equation) and 2) elevated urine albumin-to-creatinine ratio (ACR) (≥17 in men and ≥25 mg/g in women). High risk APOL1 status was defined by 2 copies of high-risk variants; low risk if 0 or 1 copy. Income groups were dichotomized as < $14,000/year (lowest income group) or ≥ $14,000/year. Logistic regression models were adjusted for age, sex, and % European ancestry.ResultsOverall, participants’ mean age was 47 years and 16% (n = 73) had high risk APOL1 status. Mean eGFR was 99 mL/min/1.73 m2. Mildly reduced eGFR was prevalent among 11% (n = 51). The lowest income group had higher adjusted odds (aOR) of mildly reduced eGFR than the higher income group (aOR 1.8, 95% CI 1.2-2.7). High-risk APOL1 was not significantly associated with reduced eGFR (aOR 1.5, 95% CI 0.9-2.5). Among 301 participants with ACR data, 7% (n = 21) had elevated ACR. Compared to low-risk, persons with high-risk APOL1 had higher odds of elevated ACR (aOR 3.8, 95% CI 2.0-7.3). Income was not significantly associated with elevated ACR (aOR 1.8, 95% CI 0.7-4.5). There were no significant interactions between APOL1 and income.ConclusionsBoth genetic and socioeconomic factors may be important determinants of early kidney damage among AAs.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-015-0008-6) contains supplementary material, which is available to authorized users.

We report a case series of six women with peripartum cardiomyopathy (PPCM) who incidentally underwent echocardiography prior to the clinical presentation of PPCM. For comparison, we identified controls, matched 2:1 on age, race, body mass index, gestational age, and hypertensive disorder. Among the six cases, all were diagnosed with PPCM during the post-partum period. Pre-PPCM echocardiograms were performed between 17.7 weeks of gestation and 13 days post-partum. Baseline left ventricular ejection fraction and size were normal and similar to the 12 matched controls (60% ± 6.6% vs. 61.4% ± 6.3%, P = 0.63) or left ventricular end-diastolic dimension (4.6 cm ± 0.2 cm vs. 4.5 cm ± 0.4 cm, P = 0.689). There was a trend towards a less negative (more abnormal) mean global longitudinal strain in cases compared with controls (À14% ± 4% vs. À18.3% ± 4.5%, P = 0.0658). Mean global circumferential strain was significantly less negative (more abnormal) in cases compared with controls (À21.5% ± 5% vs. À29.3% ± 7.6%, P = 0.0329). We conclude that women who develop PPCM have normal left ventricular ejection fraction during gestation preceding PPCM, indicating that the disease develops acutely in the peripartum period. Abnormal strain can be detected, however, suggesting that strain imaging could represent a screening method in populations at high risk for PPCM if confirmed in future studies.