ReviewInternational journal of molecular sciences2026
Low Nephron Number and Kidney Disease.
Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 authors.
Funding
Abstract
Reduced nephron endowment and acquired nephron loss increase susceptibility to hypertension and chronic kidney disease (CKD). Low birth weight, prematurity, genetic factors, and adverse prenatal exposures can limit nephron development, whereas aging and kidney injury reduce the number of functioning nephrons after birth. Compensatory glomerular hypertrophy and increased single-nephron filtration can initially preserve overall glomerular filtration rate, but sustained glomerular stress may promote podocyte injury, proteinuria, and glomerulosclerosis. These changes can accelerate nephron loss and create a cycle of progressive kidney damage. Disease susceptibility depends on genetic background and additional metabolic, environmental, and hemodynamic stresses. This review examines the determinants of nephron number, the adaptive and potentially harmful consequences of nephron reduction, and approaches to preserving kidney function. Improving maternal health, reducing harmful exposures, and controlling hypertension and metabolic disease may reduce the long-term consequences of low nephron number.
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