Apolipoprotein L1 genotype may not be a major factor for kidney disease risk
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Key takeaways:
- White participants had lower eGFRcr based on creatinine and cystatin C.
- At the last follow-up, less than 5% of participants developed end-stage kidney disease.
Apolipoprotein L1 genotype may not be a major factor for future risk of kidney disease in middle-aged adults, according to data from a longitudinal cohort study.
“Currently it is unclear if kidney donation is the instigating event for some [living kidney donor] LKD carrying high-risk APOL1 genotype to progress to [chronic kidney disease] CKD or end-stage kidney disease (ESKD),” Mona D. Doshi, MD, of the University of Michigan, Ann Arbor, and colleagues wrote. “To fully appreciate the impact of the high-risk [apolipoprotein L1] APOL1 genotype on post-donation outcomes, it is important to first establish baseline risk of kidney disease in healthy individuals carrying two APOL1 kidney risk variants.”
Researchers studied 5,886 healthy individuals, aged 45 to 64 years, who were enrolled in the Atherosclerosis Risk in Communities study. The goal of their research was to examine the demographic impact on kidney risk variants and long-term kidney function. The cohort was grouped based on race and APOL1 genotype. Participants had eGFR based on creatinine (eGFRcr), and rates of at least 80 mL/min were considered suitable kidney donors.
Outcomes were based on creatinine and cystatin C (eGFRcr-cys), urine albumin-to-creatinine ratio, proportion with CKD 3a or worse, ESKD and death.
Overall, there were 5,075 white participants, 701 Black participants who carried a low-risk APOL1 genotype and 110 Black participants who carried a high-risk APOL1 genotype.
Data showed white participants had lower eGFRcr-cys than low-risk and high-risk groups at 10 years (89±16 mL/min/1.73 m2 vs. 91±16 mL/min/1.73 m2 and 92±15 mL/min/1.73 m2, respectively. At 25 years, white participants still had lower eGFRcr-cys than the low-risk group (70±18 mL/min/1.73 m2 vs. 72±19 mL/min/1.73 m2) but not compared with participants with the high-risk APOL1 genotype (67±23 mL/min/1.73 m2).
There was no significant difference in uACR among the groups at 10 or 25 years. The odds of developing CKD stage 3a or worse were similar between the low-risk and high-risk APOL1 groups in both unadjusted and adjusted models. Additionally, at the last follow-up, less than 5% of participants developed ESKD, and 45% either died or reached ESKD, with no significant differences in outcomes between the groups.
“Given the data we have so far, despite its limitations, we recommend that Black middle-aged and older individuals considering kidney donation or are unaffected family members of patients with CKD attributed to APOL1 should be educated about APOL1 kidney risk variants, availability of APOL1 testing [and] counseled that APOL1 kidney risk variants are not major driver of their future risk of kidney disease,” the researchers wrote.
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