{"title":"多囊发育不良肾与局部肾素-血管紧张素-醛固酮系统之间的关系:一种新的生物标志物的初步研究。","authors":"Shingo Ishimori, Shinya Ishiko, Junya Fujimura, Asahi Yamamoto, Shuhei Aoyama, Yuka Kimura, Yuta Inoki, Atsushi Kondo, Tomoko Horinouchi, Tomohiko Yamamura, Nana Sakakibara, China Nagano, Kazumichi Fujioka, Masafumi Oka, Wataru Shimabukuro, Koichi Nakanishi, Kandai Nozu","doi":"10.1111/nep.70132","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>To examine the relationship between children with multicystic dysplastic kidney (MCDK) that persists or spontaneously regresses over time and local renin-angiotensin-aldosterone system (RAAS) activity in children.</p><p><strong>Methods: </strong>We conducted a multicentre, cross-sectional study of patients who were diagnosed with unilateral MCDK or a solitary kidney. The controls were age- and sex-matched children who underwent evaluation for short stature without any clinical kidney symptoms. We evaluated urinary angiotensinogen (AGT) as a biomarker of local RAAS activity, which acts specifically within the kidneys and differs from systemic RAAS.</p><p><strong>Results: </strong>We included 52 children who were divided into the following four groups: 11 children with residual MCDK (MCDK persisted), 11 with regressed MCDK (MCDK spontaneously regressed), 12 with a solitary kidney and 18 were controls. Hypertension was identified in six patients, all of whom were in the residual or regressed MCDK groups. The urinary AGT/creatinine ratio was significantly higher in children in the residual MCDK group than in those in the regressed MCDK, solitary and control groups (p = 0.02, p < 0.01, p < 0.01, respectively). A logistic regression model showed that the only significant independent factor for regression of MCDK was urinary AGT/creatinine (odds ratio: 16.0, p < 0.01).</p><p><strong>Conclusion: </strong>Our data suggest that local RAAS activation could be associated with persistence of MCDK, but causality cannot be inferred because of the cross-sectional study design. Whether RAAS activation in residual MCDK is involved in the pathogenesis of MCDK or AGT is secreted from the MCDK kidney itself remains unknown.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"30 10","pages":"e70132"},"PeriodicalIF":1.9000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Association Between Multicystic Dysplastic Kidney and the Local Renin-Angiotensin-Aldosterone System: A Pilot Study of a New Biomarker.\",\"authors\":\"Shingo Ishimori, Shinya Ishiko, Junya Fujimura, Asahi Yamamoto, Shuhei Aoyama, Yuka Kimura, Yuta Inoki, Atsushi Kondo, Tomoko Horinouchi, Tomohiko Yamamura, Nana Sakakibara, China Nagano, Kazumichi Fujioka, Masafumi Oka, Wataru Shimabukuro, Koichi Nakanishi, Kandai Nozu\",\"doi\":\"10.1111/nep.70132\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aim: </strong>To examine the relationship between children with multicystic dysplastic kidney (MCDK) that persists or spontaneously regresses over time and local renin-angiotensin-aldosterone system (RAAS) activity in children.</p><p><strong>Methods: </strong>We conducted a multicentre, cross-sectional study of patients who were diagnosed with unilateral MCDK or a solitary kidney. The controls were age- and sex-matched children who underwent evaluation for short stature without any clinical kidney symptoms. We evaluated urinary angiotensinogen (AGT) as a biomarker of local RAAS activity, which acts specifically within the kidneys and differs from systemic RAAS.</p><p><strong>Results: </strong>We included 52 children who were divided into the following four groups: 11 children with residual MCDK (MCDK persisted), 11 with regressed MCDK (MCDK spontaneously regressed), 12 with a solitary kidney and 18 were controls. Hypertension was identified in six patients, all of whom were in the residual or regressed MCDK groups. The urinary AGT/creatinine ratio was significantly higher in children in the residual MCDK group than in those in the regressed MCDK, solitary and control groups (p = 0.02, p < 0.01, p < 0.01, respectively). A logistic regression model showed that the only significant independent factor for regression of MCDK was urinary AGT/creatinine (odds ratio: 16.0, p < 0.01).</p><p><strong>Conclusion: </strong>Our data suggest that local RAAS activation could be associated with persistence of MCDK, but causality cannot be inferred because of the cross-sectional study design. Whether RAAS activation in residual MCDK is involved in the pathogenesis of MCDK or AGT is secreted from the MCDK kidney itself remains unknown.</p>\",\"PeriodicalId\":520716,\"journal\":{\"name\":\"Nephrology (Carlton, Vic.)\",\"volume\":\"30 10\",\"pages\":\"e70132\"},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2025-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nephrology (Carlton, Vic.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1111/nep.70132\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nephrology (Carlton, Vic.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1111/nep.70132","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Association Between Multicystic Dysplastic Kidney and the Local Renin-Angiotensin-Aldosterone System: A Pilot Study of a New Biomarker.
Aim: To examine the relationship between children with multicystic dysplastic kidney (MCDK) that persists or spontaneously regresses over time and local renin-angiotensin-aldosterone system (RAAS) activity in children.
Methods: We conducted a multicentre, cross-sectional study of patients who were diagnosed with unilateral MCDK or a solitary kidney. The controls were age- and sex-matched children who underwent evaluation for short stature without any clinical kidney symptoms. We evaluated urinary angiotensinogen (AGT) as a biomarker of local RAAS activity, which acts specifically within the kidneys and differs from systemic RAAS.
Results: We included 52 children who were divided into the following four groups: 11 children with residual MCDK (MCDK persisted), 11 with regressed MCDK (MCDK spontaneously regressed), 12 with a solitary kidney and 18 were controls. Hypertension was identified in six patients, all of whom were in the residual or regressed MCDK groups. The urinary AGT/creatinine ratio was significantly higher in children in the residual MCDK group than in those in the regressed MCDK, solitary and control groups (p = 0.02, p < 0.01, p < 0.01, respectively). A logistic regression model showed that the only significant independent factor for regression of MCDK was urinary AGT/creatinine (odds ratio: 16.0, p < 0.01).
Conclusion: Our data suggest that local RAAS activation could be associated with persistence of MCDK, but causality cannot be inferred because of the cross-sectional study design. Whether RAAS activation in residual MCDK is involved in the pathogenesis of MCDK or AGT is secreted from the MCDK kidney itself remains unknown.