How kidney blood-vessel cells control tiny-vessel clots in the kidney
Official title: Transcriptional Regulation of Thrombotic Microangiopathy in the Renal Microvasculature
Funded at Northport VA Medical Center · NIH-11212768 · Data updated 2026-11-12
This project looks at whether a protein called KLF4 in kidney blood-vessel cells helps stop dangerous clotting and inflammation in people with thrombotic microangiopathy.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Northport VA Medical Center NIH-funded |
| Lab location | 1 site (Northport, United States) |
| Project start | October 1, 2021 |
| Project end | September 30, 2026 |
| Funding year | 2026 |
| NIH project number | 5IK2BX005380-05 |
| Project ID | NIH-11212768 on NIH RePORTER |
Who could benefit from this research
✓Could help
People whose kidney biopsies show thrombotic microangiopathy (including cases after anti-VEGF therapy, hemolytic uremic syndrome, malignant hypertension, or antibody-mediated transplant rejection) would be the most relevant candidates.
✕Less likely to help
People with kidney disease that is not caused by TMA or those seeking an immediate treatment benefit should not expect direct clinical benefit from this mechanistic research.
What this research studies
Researchers are examining gene activity from kidney biopsy samples taken from people with thrombotic microangiopathy (TMA) to see which genes change in sick blood-vessel cells. They focus on a protein called KLF4 that normally helps blood-vessel cells stay anti-clotting and anti-inflammatory, and they will study how changing KLF4 affects complement proteins and membrane complement regulators like DAF, CD59, and CD46. The team combines analysis of human RNA-sequencing data with laboratory experiments on kidney endothelial cells to trace whether KLF4 loss drives complement activation and microthrombi. The goal is to understand mechanisms that cause TMA so future treatments might stop progression to chronic kidney disease.
Why it matters
Potential benefit: If successful, this work could point to new ways to prevent or treat TMA and reduce progression to chronic kidney disease.
How similar studies have gone: KLF4 has been shown to protect systemic blood vessels from clotting and inflammation in other settings, but applying that finding specifically to renal microvessels and complement-driven TMA is a novel approach.
Where this research is happening
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Northport VA Medical Center
Northport, United States Active
Researchers
- Principal investigator: Estrada, Chelsea — Northport VA Medical Center
- Study coordinator: Estrada, Chelsea
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.