Regulation of nephron progenitor cell lifespan and nephron endowment.
Level 5 - mechanism / opinion, no new human data
Narrative review without systematic search or meta-analysis
PubMed 36104510 · doi:10.1038/s41581-022-00620-w
What was done
This narrative review summarizes literature on the environmental inputs and intrinsic molecular mechanisms regulating nephron progenitor cell lifespan, the timing of nephrogenesis cessation, and total nephron endowment.
What was found
The abstract reports no primary experimental metrics or quantitative effect estimates. It describes that nephron endowment varies up to tenfold in humans, that nephrogenesis ends permanently when nephron progenitor cells are exhausted in utero or shortly after birth, and that low nephron numbers increase the risk of hypertension, chronic kidney disease, and kidney failure.
Why it matters
Because new nephrons cannot form after developmental cessation, defining the molecular triggers of progenitor exhaustion is necessary to design interventions that could extend nephrogenesis in preterm infants.
Limits
As a narrative review, it presents no new human data, meta-analytic pooling, or systematic search criteria. Specific effect sizes, molecular pathways, and clinical trial outcomes are absent from the abstract.
Cited by
- supports Humans are born with roughly one million nephrons per kidney and destroyed nephrons cannot regenerate.