In a significant leap forward, researchers from the United States and Canada have shed light on a critical factor that could raise the risk of acute kidney injury (AKI), a condition affecting more than 20% of hospitalized adults worldwide.
Their findings, published in the prestigious journal Nature Medicine, reveal that common changes in our blood as we age, specifically related to a condition called CHIP, might play a key role in this increased risk.
This discovery opens up new pathways for developing treatments for AKI and potentially preventing its progression to more severe kidney disease.
CHIP, or clonal hematopoiesis of indeterminate potential, involves mutations in blood stem cells that aren’t inherited but acquired over time. These mutations can cause the abnormal cells to multiply rapidly.
It’s a condition that becomes more common as we get older, affecting between 10 to 20% of people over 65. Besides being linked to a heightened risk of death from various diseases, CHIP now appears to also make individuals more susceptible to AKI, especially as they age.
The study’s co-leading researchers, Raymond Harris, MD, and Alexander Bick, MD, PhD, from Vanderbilt University Medical Center, along with their team, were intrigued by how CHIP could influence the occurrence of AKI.
Their research showed that people with CHIP faced a tougher time recovering from AKI, highlighting a strong connection between this genetic condition and kidney health.
The study involved analyzing health data from over 440,000 individuals across three large cohorts, including the UK Biobank and two long-term studies from the U.S.
This large-scale analysis helped the researchers pinpoint the association between CHIP and AKI, noting it was even more evident in patients needing dialysis and those with specific mutations.
To dive deeper into the mechanisms at play, the team developed mouse models with CHIP, specifically with mutations in the Tet2 and Jak2 genes.
They discovered these mice experienced more severe AKI, had higher levels of inflammation in their kidneys, and showed slower recovery and more scarring post-AKI.
These findings suggest that CHIP might hinder AKI recovery by promoting an inflammatory response, offering a potential target for future treatments by focusing on the immune system’s role in kidney inflammation.
This collaborative research not only highlights the impact of genetic and environmental factors on kidney health but also emphasizes the need for a deeper understanding of how conditions like CHIP influence our body’s response to diseases and injuries.
By pinpointing specific genetic mutations and their effects, scientists can pave the way for targeted therapies that could prevent AKI or lessen its severity, marking a significant step forward in kidney disease treatment and management.
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The research findings can be found in Nature Medicine.
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