Premature birth may cause lifelong kidney damage, Israeli researchers find

A joint Israeli-Australian study identifies the cellular mechanism by which premature birth disrupts kidney development, leaving babies with a lifelong shortage of nephrons. The research, led by Hadassah Medical Center and Monash University, pinpoints a narrow therapeutic window for potential intervention.

A joint Israeli-Australian study has identified the cellular mechanism by which premature birth disrupts kidney development, potentially leaving babies with a lifelong shortage of vital filtration units. The research, led by Dr. Morris Nechama of Hadassah-University Medical Center and Monash University, used an advanced mouse model to observe that nephron progenitor cells enter distress within hours of premature birth, triggering an emergency molecular response that suppresses genes responsible for differentiation into mature nephrons. The cells focus on survival instead of building. Although the period of nephron building extends by about 24 hours, the compensation comes too late, resulting in a permanent nephron deficit measurable a month after birth. In adulthood, the kidneys show signs of chronic damage: enlarged glomeruli, protein in the urine, and markers of tubular damage. The study, published in iScience, also found a gender difference, with males more significantly affected. The researchers emphasize that the first days after birth are critical for setting the kidney's reserve for life, and that preemies should be monitored for kidney disease as they age.