36 research outputs found

    Virologic failure and immune suppression over study visits.

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    a<p>Number of virologic failures is indicated by x, number of available VL measurements are indicated by n.</p>b<p>Number of CD4 counts defining suppressed immune function indicated by x, number of available CD4 counts indicated by n.</p

    Effect of depressive symptoms on nonadherence and clinical outcomes.

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    a<p>Adjusted for baseline measurement of age, gender, marital status, education, and household assets.</p>b<p>Any self-reported deviation from perfect ART adherence was used as indicator for nonadherence.</p>c<p>Failure/suppression at any point after baseline measurement, adjusted for baseline measure of failure/suppression.</p

    <i>APOL1</i> risk alleles among individuals with CKD in Northern Tanzania: A pilot study

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    <div><p>Introduction</p><p>In sub-Saharan Africa, approximately 100 million people have CKD, yet genetic risk factors are not well-understood. Despite the potential importance of understanding <i>APOL1</i> risk allele status among individuals with CKD, little genetic research has been conducted. Therefore, we conducted a pilot study evaluating the feasibility of and willingness to participate in genetic research on kidney disease, and we estimated <i>APOL1</i> risk allele frequencies among individuals with CKD.</p><p>Methods</p><p>In 2014, we conducted a community-based field study evaluating CKD epidemiology in northern Tanzania. We assessed for CKD using urine albumin and serum creatinine to estimate GFR. We invited participants with CKD to enroll in an additional genetic study. We obtained dried-blood spots on filter cards, from which we extracted DNA using sterile punch biopsies. We genotyped for two single nucleotide polymorphisms (SNPs) defining the <i>APOL1</i> G1 risk allele and an insertion/deletion polymorphism defining the G2 risk allele. Genotyping was performed in duplicate.</p><p>Results</p><p>We enrolled 481 participant, 57 (12%) of whom had CKD. Among these, enrollment for genotyping was high (n = 48; 84%). We extracted a median of 19.4 ng of DNA from each dried-blood spot sample, and we genotyped the two <i>APOL1</i> G1 SNPs and the <i>APOL1</i> G2 polymorphism. Genotyping quality was high, with all duplicated samples showing perfect concordance. The frequency of <i>APOL1</i> risk variants ranged from 7.0% to 11.0%, which was similar to previously-reported frequencies from the general population of northern Tanzania (p>0.2).</p><p>Discussion</p><p>In individuals with CKD from northern Tanzania, we demonstrated feasibility of genotyping <i>APOL1</i> risk alleles. We successfully genotyped three risk variants from DNA extracted from filter cards, and we demonstrated a high enrollment for participation. In this population, more extensive genetic studies of kidney disease may be well-received and will be feasible.</p></div
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