Genetic causes of diabetic kidney disease
Official title: Genetic risk and molecular characterization of Diabetic Kidney Disease
Funded at Icahn School of Medicine at Mount Sinai · NIH-11295460 · Data updated 2026-11-12
This research looks at how genetic differences, especially in the Xor gene, change kidney damage risk in people with diabetes so new treatments can be developed.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Icahn School of Medicine at Mount Sinai NIH-funded |
| Lab location | 1 site (New York, United States) |
| Project start | April 5, 2024 |
| Project end | January 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $331,100 |
| NIH project number | 5R01DK139395-03 |
| Project ID | NIH-11295460 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with diabetes who have early signs of kidney damage, such as albumin in the urine, or who are at high risk for diabetic kidney disease would be most relevant to future clinical work from this project.
✕Less likely to help
People without diabetes or with kidney disease from other causes, and patients whose kidney damage is not driven by Xor-related pathways, are less likely to benefit from these findings.
What this research studies
Researchers compare mouse strains that are prone or resistant to diabetic kidney damage to find the genes that make a difference. They map genetic regions linked to loss of podocytes, the kidney cells that help filter blood, and identified the Xor gene as a key source of damaging oxidative stress. The team tests whether blocking Xor or editing the gene with CRISPR reduces protein in the urine (albuminuria) and protects kidney cells. If findings hold up, the work could guide later studies that include human samples or patients to see who might benefit from Xor-targeted approaches.
Why it matters
Potential benefit: Could identify a genetic target (Xor) that, if blocked, might prevent or reduce kidney damage in people with diabetes.
How similar studies have gone: Similar mouse studies showed that inhibiting Xor reduced albuminuria and protected podocytes, but translation to human treatments has not yet been established.
Where this research is happening
-
Icahn School of Medicine at Mount Sinai
New York, United States Active
Researchers
- Principal investigator: Daehn, Ilse Sofia — Icahn School of Medicine at Mount Sinai
- Study coordinator: Daehn, Ilse Sofia
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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.