{"title":"Development of necrotizing enterocolitis in term newborns with critical congenital heart disease and affecting factors.","authors":"Berra Zumrut Tan Recep, Erkut Öztürk","doi":"10.1016/j.pedneo.2024.09.006","DOIUrl":"https://doi.org/10.1016/j.pedneo.2024.09.006","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to investigate the frequency of necrotizing enterocolitis (NEC) and its influencing factors in term newborns diagnosed with critical congenital heart disease.</p><p><strong>Methods: </strong>The study was conducted retrospectively on term neonates diagnosed with critical congenital heart disease who were admitted to the pediatric cardiac intensive care unit between January 1, 2022, and January 1, 2024. The frequency of NEC and the risk factors contributing to its development were evaluated in the cases. The results were analyzed statistically.</p><p><strong>Results: </strong>There were 400 cases during the study period, with 52% being male. The median weight was 2900 g (IQR 2800-3000 g). NEC development was observed in 12 cases (3%). Ten cases were ductus-dependent (10/320), and two cases were diagnosed with other critical congenital heart diseases (2/80). The median age at diagnosis was 7 days (IQR 5-10 days). According to the modified Bell criteria, six patients had NEC stage IIA, four had stage IIB, one had stage IIIA, and one had stage IIIB. Surgical treatment was administered to three cases (25%). Independent risk factors for NEC included gestational age <38 weeks (OR 5.9, p = 0.004), birth weight <2500 g (OR 3.2, p = 0.02), mechanical ventilation dependency (OR 6.4, p = 0.01), >6 packed red blood cells (OR 6.4, p = 0.01), parenteral nutrition (OR 9, p < 0.001), and presence of functional single ventricle (OR 6.8, p = 0.008). The mortality rate was higher in cases with NEC compared to those without (50% vs. 7.7%, p < 0.001).</p><p><strong>Conclusion: </strong>NEC is a common complication in term neonates diagnosed with critical congenital heart disease. Low birth weight and gestational age, single ventricle physiology, mechanical ventilation dependency, excessive blood product usage, and parenteral nutrition increase the risk of NEC development in these cases.</p>","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143558865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Alport syndrome: Expanding diagnosis and treatment","authors":"Hou-Xuan Huang , I-Jung Tsai , Larry A. Greenbaum","doi":"10.1016/j.pedneo.2024.10.005","DOIUrl":"10.1016/j.pedneo.2024.10.005","url":null,"abstract":"<div><div>Alport syndrome (AS) is the second common monogenic cause of end-stage kidney disease (ESKD) worldwide and is caused by defective type 4 collagen due to pathogenic variants of <em>COL4A3, COL4A4,</em> or <em>COL4A5</em>. Type 4 collagen also exists in the eyes and ears, and thus ocular defects and hearing loss occur in AS. The understanding of AS has expanded over the past two decades due to greater availability of genetic testing and research on genotype-phenotype correlation. Patients previously diagnosed with idiopathic steroid resistant nephrotic syndrome or ESKD of unknown etiology may now be diagnosed as AS if pathogenic <em>COL4A3-5</em> variants are identified. Some carriers of heterozygous <em>COL4A3-5</em> variants may now be classified into females with X-linked AS or autosomal dominant AS, if there are typical pathologic changes in the glomerular basement membrane or if there is proteinuria and progression of kidney disease. Lastly, it has been recommended that renin-angiotensin-aldosterone system inhibition be started as soon as possible for selected AS patients for its long-term protective effect against kidney function deterioration. The purpose of this review is to introduce these important concepts to general pediatricians and pediatric nephrologists.</div></div>","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":"66 ","pages":"Pages S13-S17"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Advocacy for DOHaD research optimizing child kidney health","authors":"You-Lin Tain","doi":"10.1016/j.pedneo.2024.10.006","DOIUrl":"10.1016/j.pedneo.2024.10.006","url":null,"abstract":"<div><div>Emerging antenatal risk factors have been associated with an increased risk of kidney disease throughout the offspring's life course. However, the intricate kidney programming mechanisms underlying these risks remain complex and are incompletely understood, but they are rooted in structural and functional alterations within the kidneys. The Developmental Origins of Health and Disease (DOHaD) theory underscores the significance of elucidating core mechanisms initiated through the maternal-fetal interface, which trigger kidney programming. Furthermore, it offers a promising avenue for preventing kidney disease at its earliest stages through a process known as reprogramming. This concise review aims to synthesize existing knowledge regarding the impact of kidney programming on offspring kidney disease and to provide an overview of documented reprogramming strategies as observed in animal models of kidney programming. By consolidating this information, we aim to expedite the translation of research breakthroughs into practical clinical solutions, ultimately resulting in enhanced outcomes for children facing kidney-related issues.</div></div>","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":"66 ","pages":"Pages S18-S22"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142585255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Acid-base homeostasis in the neonate","authors":"Michael G. Michalopulos, Raymond Quigley","doi":"10.1016/j.pedneo.2024.10.004","DOIUrl":"10.1016/j.pedneo.2024.10.004","url":null,"abstract":"","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":"66 ","pages":"Pages S8-S12"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Emerging trends in pediatric nephrology: A new frontier in care and research","authors":"You-Lin Tain","doi":"10.1016/j.pedneo.2025.01.001","DOIUrl":"10.1016/j.pedneo.2025.01.001","url":null,"abstract":"","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":"66 ","pages":"Page S1"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142959165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gut dysbiosis as a susceptibility factor in childhood idiopathic nephrotic syndrome","authors":"Kazunari Kaneko","doi":"10.1016/j.pedneo.2024.10.003","DOIUrl":"10.1016/j.pedneo.2024.10.003","url":null,"abstract":"<div><div>Idiopathic nephrotic syndrome (INS) is a relatively common renal disorder of childhood characterized by severe proteinuria and associated hypoproteinemia and edema. Although the pathogenesis of INS remains unknown, the prevailing theory of its pathogenesis is as follows. Antigenic stimulation, such as viral infections or vaccines, in children with susceptibility factors for INS triggers abnormal immune responses, resulting in production of pathogenic substances that injure podocytes (renal glomerular epithelial cells). The injured podocytes then change their function and morphology, resulting in increased permeability of plasma proteins. Consequently, plasma proteins, especially albumin, are leaked into urine and massive proteinuria ensues. Research on susceptibility factors for INS has focused on polymorphisms in several genes including human leukocyte antigen class II genes. However, we propose that dysbiosis of the intestinal microbiota could be a susceptibility factor for relapse. This proposal is based on our research group finding that children with INS and frequent relapses have gut dysbiosis characterized by a decreased proportion of beneficial bacteria such as short-chain fatty acid-producing bacteria. Dysbiosis from the neonatal period to infancy may result from environmental factors, such as cesarean section delivery and antibiotic administration, which prevent the establishment of a normal intestinal microbiota. Dysbiosis leads to aberrant gut immunity and is characterized by a decreased ratio of T helper 1 cells/T helper 2 cells and an increased ratio of T helper 17 cells/regulatory T-cells. Therefore, relapse occurs when immunologically pathogenic factors that injure podocytes are produced in response to trigger events in children with INS and gut dysbiosis. Our recent clinical trial suggested that long-term oral administration of butyric acid-producing bacterium as a probiotic is promising for suppressing relapse. Therefore, studying the causal relationship between dysbiosis and relapses in patients with INS in a larger number of patients is necessary.</div></div>","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":"66 ","pages":"Pages S2-S7"},"PeriodicalIF":2.3,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142633302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of diagnostic renal arteriography in children with suspected secondary hypertension.","authors":"Hou-Xuan Huang, Chun-Ann Chen, Gwo-Tsann Chuang, I-Jung Tsai","doi":"10.1016/j.pedneo.2024.12.001","DOIUrl":"https://doi.org/10.1016/j.pedneo.2024.12.001","url":null,"abstract":"","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cutoff levels of serum 25-OH-D for defining vitamin D deficiency in early infancy.","authors":"Bharti Yadav, Neeraj Gupta, Pragya Kumar, Rohit Sasidharan, Purvi Purohit, Kuldeep Singh, Praveen Sharma, Arun Singh","doi":"10.1016/j.pedneo.2024.06.017","DOIUrl":"https://doi.org/10.1016/j.pedneo.2024.06.017","url":null,"abstract":"<p><strong>Background: </strong>Various organizations use different thresholds to define vitamin D deficiency (VDD), which complicates its diagnosis, particularly in infants, as these thresholds are often extrapolated from adult data. Routine vitamin D3 supplementation in infants based on these criteria may impose unnecessary economic costs without clear benefits. Recent evidence suggests that the Institute of Medicine's (IOM) current threshold of <12 ng/ml might overestimate VDD in infants.</p><p><strong>Method: </strong>This study is a secondary analysis of data derived from a randomized controlled trial that compared the effects of 800 IU/day versus 400 IU/day of oral vitamin D3 supplementation in healthy, term, breastfed infants from 48 hours after birth to 14 weeks of age. The primary goal was to determine the serum 25-hydroxyvitamin D (25-OH-D) inflection point at which parathyroid hormone (PTH) levels begin to rise, in order to establish a more accurate cutoff for VDD in early infancy.</p><p><strong>Result: </strong>Among the 99 infants analyzed, 16 (16.2%) exhibited both elevated PTH levels and VDD at 14 weeks. The optimal inflection point for serum 25-OH-D was identified as 6.83 ng/ml (95% CI, 5.02-8.64), with an adjusted R<sup>2</sup> of 39.4% (p < 0.001). Using a revised cutoff of 8.64 ng/ml based on the 95% CI, only 10 (10.1%) infants would be classified as VDD, compared to 16 (16.2%) (p = 0.18) under the current threshold.</p><p><strong>Conclusion: </strong>The lower inflection point of 6.83 ng/ml and a revised cutoff of 8.64 ng/ml, supported by limited existing literature, suggest the need to reassess the IOM's current threshold for defining VDD in infants.</p>","PeriodicalId":56095,"journal":{"name":"Pediatrics and Neonatology","volume":" ","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143392418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}