Abstract
In the normal transition of the term infant from fetal to extrauterine life, nephrogenesis is complete and the number of functioning nephrons is not reduced. However, the range of nephron number in the human population varies by over tenfold, a function of normal inter-individual variation. Nephrogenesis may be impaired by fetal stress (malnutrition, ischemia, hypoxia, toxins, infection), maldevelopment, or preterm birth. Compensatory growth of remaining nephrons is maladaptive, leading to decreasing nephron function in adulthood. Serum creatinine concentration is a poor predictor of renal development or injury, and more accurate biomarkers are desperately needed. Contrast-enhanced magnetic resonance imaging is currently being developed to permit the identification of glomeruli in vivo, permitting serial measurement of glomerular number and size. Improved management of renal disease will depend on elucidation of factors mediating or modulating nephrogenesis and nephron loss, and on better tracking of individual nephrons throughout life.
Structure does not determine Function or vice versa, but both are simply different ways of regarding and describing the same thing.
—Jean R. Oliver, Nephrons and Kidneys 1968
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Chevalier, R.L., Charlton, J.R. (2014). The Human Kidney at Birth: Structure and Function in Transition. In: Faa, G., Fanos, V. (eds) Kidney Development in Renal Pathology. Current Clinical Pathology. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-0947-6_5
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DOI: https://doi.org/10.1007/978-1-4939-0947-6_5
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