Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavik, Iceland.
Internal Medicine and Rehabilitation Services, Landspitali-The National University Hospital, Reykjavik, Iceland.
Eur J Hum Genet. 2021 Jul;29(7):1061-1070. doi: 10.1038/s41431-020-00805-6. Epub 2021 Mar 11.
Adenine phosphoribosyltransferase deficiency is a rare, autosomal recessive disorder of purine metabolism that causes nephrolithiasis and progressive chronic kidney disease. The small number of reported cases indicates an extremely low prevalence, although it has been suggested that missed diagnoses may play a role. We assessed the prevalence of APRT deficiency based on the frequency of causally-related APRT sequence variants in a diverse set of large genomic databases. A thorough search was carried out for all APRT variants that have been confirmed as pathogenic under recessive mode of inheritance, and the frequency of the identified variants examined in six population genomic databases: the deCODE genetics database, the UK Biobank, the 100,000 Genomes Project, the Genome Aggregation Database, the Human Genetic Variation Database and the Korean Variant Archive. The estimated frequency of homozygous genotypes was calculated using the Hardy-Weinberg equation. Sixty-two pathogenic APRT variants were identified, including six novel variants. Most common were the missense variants c.407T>C (p.(Met136Thr)) in Japan and c.194A>T (p.(Asp65Val)) in Iceland, as well as the splice-site variant c.400 + 2dup (p.(Ala108Glufs*3)) in the European population. Twenty-nine variants were detected in at least one of the six genomic databases. The highest cumulative minor allele frequency (cMAF) of pathogenic variants outside of Japan and Iceland was observed in the Irish population (0.2%), though no APRT deficiency cases have been reported in Ireland. The large number of cases in Japan and Iceland is consistent with a founder effect in these populations. There is no evidence for widespread underdiagnosis based on the current analysis.
腺嘌呤磷酸核糖基转移酶缺乏症是一种罕见的常染色体隐性嘌呤代谢紊乱疾病,可导致肾结石和进行性慢性肾病。少数报道的病例表明其患病率极低,尽管有人认为漏诊可能起了一定作用。我们根据在各种大型基因组数据库中与 APRT 相关的序列变异的频率,评估了 APRT 缺乏症的患病率。我们彻底搜索了所有已被确认为隐性遗传模式下致病性的 APRT 变异,并在六个人群基因组数据库中检查了已鉴定变异的频率:deCODE 遗传学数据库、英国生物银行、十万基因组计划、基因组聚合数据库、人类遗传变异数据库和韩国变异档案。使用 Hardy-Weinberg 方程计算纯合基因型的估计频率。共鉴定出 62 种致病性 APRT 变异,包括 6 种新变异。最常见的是日本的错义变异 c.407T>C(p.(Met136Thr))和冰岛的 c.194A>T(p.(Asp65Val)),以及欧洲人群中的剪接位点变异 c.400 + 2dup(p.(Ala108Glufs*3))。在六个基因组数据库中的至少一个数据库中检测到 29 种变异。在日本和冰岛以外,致病性变异的累积最小等位基因频率(cMAF)最高的是爱尔兰人群(0.2%),尽管爱尔兰没有报道过 APRT 缺乏症病例。日本和冰岛的大量病例表明,这些人群中存在着一个奠基者效应。根据目前的分析,没有证据表明存在广泛的漏诊情况。