Low Nephron Number and Kidney Disease

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.

Authors

Institutions

Publication Details

Journal
International Journal of Molecular Sciences
Published
2026-10-07
DOI
https://doi.org/10.3390/ijms27198888
Primary Topic
Chronic Kidney Disease and Diabetes
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Low Nephron Number and Kidney Disease

John D. Imig, Samaneh Goorani
International Journal of Molecular Sciences
Chronic Kidney Disease and Diabetes
article

Low Nephron Number and Kidney Disease

John D. Imig, Samaneh Goorani
article en

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.

International Journal of Molecular SciencesVol. 27(19)
University of Arkansas for Medical Sciences (US)
Openalex Percentile: Top 12%
Chronic Kidney Disease and Diabetes
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.

Low Nephron Number and Kidney Disease — John D. Imig, Samaneh Goorani · International Journal of Molecular Sciences (2026) | TGRS Research Map | TGRS