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RATIONALE P < 0.001). An increased steroid-sensitive nephrotic syndrome PRS was observed in those with high-risk APOL1 genotypes and uKF, partly due to differences at HLA-DQB1∗03:19. LIMITATIONS: Potential limitations include the small sizes of subgroups and use of short-read WGS. CONCLUSIONS: WGS yielded a monogenic diagnosis in 17% of patients with uKF, with no additional solved cases arising from the case-control analysis. These findings underscore APOL1's role in those with recent African ancestry and suggest a genetic architecture distinct from common chronic kidney disease. PLAIN-LANGUAGE SUMMARY: Our study was motivated by the difficulty in understanding why some people experience kidney failure (KF) without a clear cause. Many patients face uncertainty about their future health and treatment because doctors cannot always find an explanation for their condition. To address this challenge, we examined the complete genetic blueprint of individuals with unexplained KF. We looked for genetic clues that might reveal hidden risks. Our work uncovered specific genetic factors that appear to contribute to KF, especially among people with African heritage. These insights are important because they may help explain why KF happens in some cases and inform personalized diagnosis and treatment.
Sadeghi‐Alavijeh et al. (Wed,) studied this question.