PDF(Pubmed)
Abstract：
In single-center studies, both preterm birth and low birth weight (LBW) are associated with worse outcomes in childhood nephrotic syndrome. Using the Nephrotic Syndrome Study Network (NEPTUNE) observational cohort, we tested the hypothesis that in patients with nephrotic syndrome, hypertension, proteinuria status, and disease progression would be more prevalent and more severe in subjects with LBW and prematurity singly or in combination (LBW/prematurity).
Three hundred fifty-nine adults and children with focal segmental glomerulosclerosis (FSGS) or minimal change disease (MCD) and available birth history were included. Estimated glomerular filtration rate (eGFR) decline and remission status were primary outcomes, and secondary outcomes were kidney histopathology, kidney gene expression, and urinary biomarkers. Logistic regression was used to identify associations with LBW/prematurity and these outcomes.
We did not find an association between LBW/prematurity and remission of proteinuria. However, LBW/prematurity was associated with greater decline in eGFR. This decline in eGFR was partially explained by the association of LBW/prematurity with APOL1 high-risk alleles, but the association remained after adjustment. There were no differences in kidney histopathology or gene expression in the LBW/prematurity group compared to normal birth weight/term birth.
LBW and premature babies who develop nephrotic syndrome have a more rapid decline in kidney function. We did not identify clinical or laboratory features that distinguished the groups. Additional studies in larger groups are needed to fully ascertain the effects of (LBW) and prematurity alone or in combination on kidney function in the setting of nephrotic syndrome.
Three hundred fifty-nine adults and children with focal segmental glomerulosclerosis (FSGS) or minimal change disease (MCD) and available birth history were included. Estimated glomerular filtration rate (eGFR) decline and remission status were primary outcomes, and secondary outcomes were kidney histopathology, kidney gene expression, and urinary biomarkers. Logistic regression was used to identify associations with LBW/prematurity and these outcomes.
We did not find an association between LBW/prematurity and remission of proteinuria. However, LBW/prematurity was associated with greater decline in eGFR. This decline in eGFR was partially explained by the association of LBW/prematurity with APOL1 high-risk alleles, but the association remained after adjustment. There were no differences in kidney histopathology or gene expression in the LBW/prematurity group compared to normal birth weight/term birth.
LBW and premature babies who develop nephrotic syndrome have a more rapid decline in kidney function. We did not identify clinical or laboratory features that distinguished the groups. Additional studies in larger groups are needed to fully ascertain the effects of (LBW) and prematurity alone or in combination on kidney function in the setting of nephrotic syndrome.
摘要：
背景：在单中心研究中，早产和低出生体重(LBW)均与儿童肾病综合征的不良结局相关.使用肾病综合征研究网络(NEPTUNE)观察队列，我们检验了肾病综合征患者的假设，高血压,蛋白尿状态，和疾病进展在患有单独或组合的LBW和早产(LBW/早产)的受试者中更普遍和更严重。
方法：纳入了三百五十九名患有局灶性节段性肾小球硬化（FSGS）或微小病变（MCD）且有出生史的成人和儿童。估计的肾小球滤过率（eGFR）下降和缓解状态是主要结果，次要结果是肾脏组织病理学，肾脏基因表达，和尿生物标志物。Logistic回归用于确定与LBW/早产和这些结果的关联。
结果：我们未发现LBW/早产与蛋白尿缓解之间存在关联。然而,LBW/早产与eGFR下降幅度较大相关。eGFR的下降部分解释为LBW/早产与APOL1高风险等位基因的关联。但经过调整后，协会仍然存在。与正常出生体重/足月出生相比，LBW/早产组的肾脏组织病理学或基因表达没有差异。
结论：LBW和发展为肾病综合征的早产儿肾功能下降更快。我们没有确定区分这些群体的临床或实验室特征。需要在更大的群体中进行更多的研究，以充分确定单独或联合使用（LBW）和早产对肾病综合征患者肾功能的影响。
方法：纳入了三百五十九名患有局灶性节段性肾小球硬化（FSGS）或微小病变（MCD）且有出生史的成人和儿童。估计的肾小球滤过率（eGFR）下降和缓解状态是主要结果，次要结果是肾脏组织病理学，肾脏基因表达，和尿生物标志物。Logistic回归用于确定与LBW/早产和这些结果的关联。
结果：我们未发现LBW/早产与蛋白尿缓解之间存在关联。然而,LBW/早产与eGFR下降幅度较大相关。eGFR的下降部分解释为LBW/早产与APOL1高风险等位基因的关联。但经过调整后，协会仍然存在。与正常出生体重/足月出生相比，LBW/早产组的肾脏组织病理学或基因表达没有差异。
结论：LBW和发展为肾病综合征的早产儿肾功能下降更快。我们没有确定区分这些群体的临床或实验室特征。需要在更大的群体中进行更多的研究，以充分确定单独或联合使用（LBW）和早产对肾病综合征患者肾功能的影响。
