erm.A novel finding from this study is that adults born preterm were more likely to have an apolipoprotein L1 high-risk genotype. Background While some studies of children with nephrotic syndrome have demonstrated worse outcomes in those born preterm compared with term, little data exist on associations of preterm birth with outcomes in adult-onset glomerular disease. Cardiovascular outcomes in those born preterm with glomerular disease are unknown. Methods We performed a cross-sectional and longitudinal analysis of participants in the Cure Glomerulonephropathy cohort. Preterm (<37 weeks' gestation) was compared with term (≥37 weeks' gestation). A survival analysis and adjusted Cox proportional hazards model were used to examine a composite outcome of 40% decline in eGFR or progression to kidney failure. An adjusted logistic regression model was used to examine remission of proteinuria. Results There were 2205 term and 235 preterm participants. Apolipoprotein L1 (APOL1) risk alleles were more common in those born preterm. More pediatric than adult participants in Cure Glomerulonephropathy were born preterm: 12.8% versus 7.69% (P < 0.001). Adults born preterm compared with term had a higher prevalence of FSGS (35% versus 25%, P = 0.01) and APOL1 high-risk genotype (9.4% versus 4.2%, P = 0.01). Participants born preterm had a shorter time interval to a 40% eGFR decline/kidney failure after biopsy (P = 0.001). In adjusted analysis, preterm participants were 28% more likely to develop 40% eGFR decline/kidney failure (hazard ratio: 1.28 [1.07 to 1.54], P = 0.008) and 38% less likely to attain complete remission of proteinuria (odds ratio: 0.62 [0.45 to 0.87], P = 0.006). There was no significant difference in cardiovascular events. Conclusions Preterm birth was a risk factor for adverse outcomes in this heterogeneous cohort of children and adults with glomerular disease. Adults born preterm were more likely to have an APOL1 high-risk genotype and FSGS. In analyses adjusted for FSGS and APOL1 risk status, there was less remission and faster progression of kidney disease in those born preterm....

中文翻译：

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早产与儿童和成人肾小球疾病不良后果的关系


呃。这项研究的一个新发现是，早产成年人更有可能具有载脂蛋白 L1 高风险基因型。背景 虽然一些肾病综合征儿童的研究表明，与足月出生的早产儿相比，早产儿的结局更差，但关于早产与成人发病的肾小球疾病结局之间关系的数据却很少。患有肾小球疾病的早产儿的心血管结局尚不清楚。方法 我们对治愈肾小球肾病队列的参与者进行了横断面和纵向分析。将早产（<37 周妊娠）与足月（≥37 周妊娠）进行比较。使用生存分析和调整后的 Cox 比例风险模型来检查 eGFR 下降 40% 或进展为肾衰竭的复合结果。使用调整后的逻辑回归模型来检查蛋白尿的缓解情况。结果 共有 2205 名足月参与者和 235 名早产参与者。载脂蛋白 L1 (APOL1) 风险等位基因在早产儿中更为常见。 Cure 肾小球肾病的儿童参与者早产率高于成人参与者：12.8% 对比 7.69% (P < 0.001)。与足月出生的成年人相比，早产儿的 FSGS 患病率更高（35% 对比 25%，P = 0.01），APOL1 高危基因型患病率更高（9.4% 对比 4.2%，P = 0.01）。早产参与者在活检后 eGFR 下降 40%/肾衰竭的时间间隔较短 (P = 0.001)。在调整分析中，早产参与者出现 40% eGFR 下降/肾衰竭的可能性高出 28%（风险比：1.28 [1.07 至 1.54]，P = 0.008），而蛋白尿完全缓解的可能性低 38%（比值比： 0.62 [0.45 至 0.87]，P = 0.006）。心血管事件没有显着差异。 结论 早产是肾小球疾病儿童和成人异质队列中不良结局的危险因素。早产成年人更有可能具有 APOL1 高危基因型和 FSGS。在针对 FSGS 和 APOL1 风险状态进行调整的分析中，早产儿的肾脏疾病缓解较少且进展较快。