In humans, nephrogenesis is completed by 32-36 weeks gestation, with a highly variable total number of nephrons, ranging from 200,000 to over 2 million. Premature birth disrupts the development and maturation of the kidneys, leading to a reduction in the final number of nephrons. Due to significant genetic variability in the number of nephrons among individuals, it is crucial to identify premature infants with fewer nephrons at birth as early as possible. These infants are more susceptible to developing renal failure with advancing age compared to those with a higher nephron endowment. Bedside ultrasound, an effective and non-invasive tool, is practical for identifying newborns with a lower nephron count. However, renal volume alone cannot reliably indicate the number of nephrons due to substantial variability at birth, influenced by gestational age when nephron maturation is incomplete. This variability in kidney volumes persists as newborns grow. In this observational study we hypothesize that the relationship between renal volume and birth weight may serve as an indicator of nephron endowment in premature infants with birth weight less than 1000 g. This finding could represent the basis for defining appropriate surveillance protocols and developing targeted therapeutic approaches.
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http://dx.doi.org/10.1038/s41598-024-64897-6 | DOI Listing |
Introduction: Metabolic syndrome (MetS) and chronic kidney disease are both important risk factors for cardiovascular disease and are closely related to each other. We retrospectively investigated whether MetS or its components increase the risk of development of impaired kidney function in the Japanese general population.
Methods: This is a retrospective cohort study which enrolled 14917 participants who visited our hospital for physical checkups from 2008 to 2018 and had normal estimated glomerular filtration rate (eGFR≥60 mL/min/1.
Cell Death Dis
December 2024
Department of Nephrology, Children's Hospital of Nanjing Medical University, Guangzhou Road 72, Nanjing, 210008, China.
Acute kidney injury (AKI) is a significant global health issue, which is often caused by cisplatin therapy and characterized by mitochondrial dysfunction. Restoring mitochondrial homeostasis in tubular cells could exert therapeutic effects. Here, we investigated Slc25a21, a mitochondrial carrier, as a potential target for AKI intervention.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Katz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Mitochondrial dysfunction is a critical factor in the pathogenesis of Alport syndrome (AS), contributing to podocyte injury and disease progression. Ezetimibe, a lipid-lowering drug, is known to inhibit cholesterol and fatty acid uptake and to reduce triglyceride content in the kidney cortex of mice with AS. However, its effects on lipid droplet (LD) utilization by mitochondria have not been explored.
View Article and Find Full Text PDFBJU Int
December 2024
Department of Urology, UC San Diego School of Medicine, La Jolla, California, USA.
Cell Mol Biol Lett
December 2024
Experimental Animal Center, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Background: The role of proximal tubular autophagy in repairing kidney injury following ischemia remains unclear.
Methods: In this study, we utilized mice with conditional deletion of the Atg5 gene in proximal tubules and monitored the long-term dynamic regulation of autophagy following ischemic acute kidney injury (AKI).
Results: The results showed that Atg5-deficient proximal tubule epithelial cells exhibited damaged mitochondria, concentric membranes, and lysosomal accumulation 24 h after ischemia/reperfusion.
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