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Sickle cell trait linked to end-stage renal disease


 

DNA helix Image by Spencer Phillips Image by Spencer Phillips

DNA helix

Black individuals with sickle cell trait (SCT) have an increased risk of developing end-stage renal disease (ESRD), according to new research.

The study indicates that having SCT actually doubles the risk of ESRD.

And the trait confers a similar degree of risk as APOL1 gene variants, which are currently the most widely recognized genetic contributors to kidney disease in blacks.

Researchers believe this finding may have important public policy implications for genetic counseling for individuals with SCT.

Rakhi P. Naik, MD, of Johns Hopkins University School of Medicine in Baltimore, Maryland, and her colleagues reported this finding in the Journal of the American Society of Nephrology.

Previous research suggested there is an association between SCT and chronic kidney disease, but it hasn’t been clear if that extends to ESRD. Studies have also suggested a possible association between kidney disease and hemoglobin C trait, but the link has not been confirmed.

So Dr Naik and her colleagues decided to investigate these potential links. To do so, the researchers analyzed data from a large, population-based study, the REasons for Geographic and Racial Differences in Stroke (REGARDS) study.

The team evaluated information on 9909 black individuals, 739 of whom had SCT and 243 of whom had hemoglobin C trait.

The data indicate that individuals with SCT have a 2-fold higher risk of developing ESRD when compared to those without SCT. But there is no association between hemoglobin C trait and ESRD.

At a median follow-up of 6.5 years, the incidence of ESRD was 5.4% (40/739) in participants with SCT, 2.5% (6/243) in subjects with hemoglobin C trait, and 2.6% (234/8927) in individuals without either trait.

The incidence rate for ESRD was 8.5 per 1000 person-years for participants with SCT, 3.9 per 1000 person-years for subjects with hemoglobin C trait, and 4.0 per 1000 person-years for individuals without either trait.

The researchers noted that SCT conferred a similar degree of ESRD risk as APOL1 gene variants. The hazard ratio for subjects with SCT was 2.03, and the hazard ratio for those with APOL1 high-risk genotypes was 1.77.

“Although you cannot change the genes you are born with, doctors can use this information to start screening for kidney disease earlier and to aggressively treat any other risk factors you may have, such as diabetes or high blood pressure,” Dr Naik said.

“We still need more studies to determine if there are other treatments that can be used to slow the progression of kidney disease, specifically in individuals with sickle cell trait.”

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