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Updated: Feb 19, 2026

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A Switch in Iron Delivery Is Critical for Postnatal Kidney Development.

Andong Qiu1,2, Melanie Viltard1,3, Rong Deng1

  • 1Division of Nephrology, Department of Medicine, Columbia University, New York, New York.

Kidney360
|February 17, 2026
PubMed
Summary
This summary is machine-generated.

Maternal iron deficiency impacts kidney development. While transferrin receptor 1 (TfR1) is key postnatally, alternative iron sources are vital during embryonic development. Iron-deficient kidney disease is treatable after birth.

Keywords:
epithelialkidney developmentkidney failuremalnutritionmineral metabolismnutrition

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Area of Science:

  • Developmental Biology
  • Iron Metabolism
  • Renal Physiology

Background:

  • Periconceptual maternal iron deficiency (FeD) is a global cause of adverse pregnancy outcomes.
  • The differential impact of FeD on developing tissues and the roles of specific iron species (transferrin-bound vs. non-transferrin-bound iron - NTBI) in organogenesis remain unclear.

Purpose of the Study:

  • To investigate the role of transferrin receptor 1 (TfR1) in kidney development.
  • To differentiate the contributions of transferrin-bound and NTBI to embryonic kidney organogenesis.
  • To explore the reversibility of iron deficiency-induced kidney disease.

Main Methods:

  • Generated TfR1-deficient mice and cell lines.
  • Utilized global iron deficiency models via iron-poor diets.
  • Examined cell-autonomous TfR1 deletions in specific kidney cell lineages.
  • Assessed kidney development at mid-gestation and postnatal stages.

Main Results:

  • TfR1 deletion alone had minimal impact on embryonic kidney development.
  • Nutritional iron deficiency severely impaired kidney development.
  • Postnatal TfR1 function became critical, with its absence leading to polycystic kidney disease.
  • Iron supplementation reversed kidney malformations and restored function.

Conclusions:

  • TfR1 is essential for postnatal kidney tubulogenesis.
  • Alternative iron species (NTBI) are crucial for embryonic kidney development, complementing TfR1.
  • Iron deficiency-induced kidney disease is reversible with postnatal iron treatment.