Sickle cell trait, APOL1 risk allele status and chronic kidney disease among ART-experienced adults living with HIV in northern Nigeria.

Autor:	Abdulhamid A; Department of Statistics, School of Technology, Kano State Polytechnic, Kano, Nigeria.; Department of Mathematical Sciences, Bayero University, Kano, Nigeria., Shepherd BE; Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA., Wudil UJ; Vanderbilt Institute for Global Health, Vanderbilt University Medical Center, Nashville, TN, USA., Van Wyk C; Vanderbilt Institute for Global Health, Vanderbilt University Medical Center, Nashville, TN, USA., Dankishiya FS; Aminu Kano Teaching Hospital, Kano, Nigeria., Hussaini N; Department of Mathematical Sciences, Bayero University, Kano, Nigeria., Wester CW; Vanderbilt Institute for Global Health, Vanderbilt University Medical Center, Nashville, TN, USA.; Department of Medicine, Division of Infectious Diseases, Vanderbilt University Medical Center, Nashville, TN, USA., Aliyu MH; Vanderbilt Institute for Global Health, Vanderbilt University Medical Center, Nashville, TN, USA.; Department of Health Policy, Vanderbilt University Medical Center, Nashville, TN, USA.
Jazyk:	angličtina
Zdroj:	International journal of STD & AIDS [Int J STD AIDS] 2024 Jun 24, pp. 9564624241262397. Date of Electronic Publication: 2024 Jun 24.
DOI:	10.1177/09564624241262397
Abstrakt:	Background: We sought to determine the prevalence of sickle cell trait (SCT) and apolipoprotein-1 ( APOL1) risk variants in people living with HIV (PLWH) in Nigeria, and to establish if SCT and APOL1 high-risk status correlate with estimated glomerular filtration rate (eGFR) and/or prevalent chronic kidney disease (CKD). Methods: Baseline demographic and clinical data were obtained during three cross-sectional visits. CKD was defined as having an eGFR<60 mL/min/1.73 m 2 . We collected urine specimens to determine urine albumin-creatine ratio and blood samples for sickle cell genotyping, APOL1 testing, and for creatinine/cystatin C assessment. The associations between SCT, APOL1 genotype, and eGFR/CKD stages/CKD were investigated using linear/ordinal logistic/logistic regression models, respectively. Results: Of 2443 participants, 599 (24.5%) had SCT, and 2291 (93.8%) had a low-risk APOL1 genotype (0 or 1 risk variant), while 152 (6.2%) had high-risk genotype (2 allele copies). In total, 108 participants (4.4%) were diagnosed with CKD. In adjusted analyses, SCT was associated with lower eGFR (adjusted mean difference [aMD]= -2.33, 95% CI -4.25, -0.42), but not with worse CKD stages, or increased odds of developing CKD. Participants with the APOL1 high risk genotype were more likely to have lower eGFR (aMD= -5.45, 95% CI -8.87, -2.03), to develop CKD (adjusted odds ratio [aOR] = 1.97, 95% CI: 1.03, 3.75), and to be in worse CKD stages (aOR = 1.60, 95% CI: 1.12, 2.29) than those with the low-risk genotype. There was no evidence of interaction between SCT and APOL1 genotype on eGFR or risk of CKD. Conclusion: Our findings highlight the multifaceted interplay of genetic factors in the pathogenesis of CKD in PLWH. Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Databáze:	MEDLINE
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