Antibody sugar patterns in lupus kidney disease
Official title: IgG glycosylation in lupus nephritis
Funded at Tulane University of Louisiana · NIH-11138781 · Data updated 2026-11-12
Researchers are seeing whether unusual sugar decorations on antibodies lead to kidney damage in people with lupus.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Tulane University of Louisiana NIH-funded |
| Lab location | 1 site (New Orleans, United States) |
| Project start | July 18, 2022 |
| Project end | June 30, 2027 |
| Funding year | 2025 |
| Award (this year) | $249,000 |
| NIH project number | 5R00AI162843-05 |
| Project ID | NIH-11138781 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are adults with systemic lupus erythematosus (SLE), especially those with current or prior lupus nephritis and SLE patients without kidney involvement who can provide blood samples for comparison.
✕Less likely to help
People without SLE or those whose kidney disease is due to other causes are unlikely to gain direct benefit from this study.
What this research studies
You would have a blood sample taken so researchers can map the sugar patterns on your IgG antibodies and compare people with and without lupus-related kidney inflammation. In the lab they will expose human kidney cells (podocytes) to these antibodies to see if they trigger a damaging signal involving the lectin CLEC7A and the enzyme CaMK4. They will also test whether blocking CaMK4 prevents the cell damage seen in earlier animal studies. The goal is to find markers that predict kidney risk and possible targets for treatments that could stop damage before kidneys are harmed.
Why it matters
Potential benefit: If successful, this work could lead to blood tests that identify lupus patients at high risk for kidney disease and to new ways to prevent kidney damage.
How similar studies have gone: Preliminary lab and mouse studies suggest abnormal IgG sugars and CaMK4 inhibition can affect kidney injury, but applying these findings in humans is still new.
Where this research is happening
-
Tulane University of Louisiana
New Orleans, United States Active
Researchers
- Principal investigator: Bhargava, Rhea — Tulane University of Louisiana
- Study coordinator: Bhargava, Rhea
Related research
Other NIH-funded projects on the same topics.
-
Glycoprotein urine markers that signal lupus nephritis treatment response
A novel test uses urine glycoprotein patterns to show how well lupus nephritis is responding to standard treatment.
-
PTPRS and lupus nephritis: a new target to reduce kidney damage in lupus
Aims to understand how PTPRS contributes to kidney inflammation and scarring in lupus nephritis and explore targeting it to help patients.
-
Sodium’s effect on kidney B cells in lupus kidney disease
This grant explores how high sodium in the kidneys affects B cells in lupus nephritis and whether blocking a key cellular pump could reduce kidney damage.
-
Oral CD11b Activator for Lupus Nephritis
A new oral CD11b activating drug is being explored to help people with lupus nephritis by targeting immune pathways that cause kidney inflammation.
-
Objective classification of lupus nephritis using computer vision
A new computer vision tool uses deep learning to classify lupus nephritis from kidney tissue images to help doctors predict outcomes for patients with lupus.
-
AI-powered look at lupus nephritis in humans and mice
Researchers will use artificial intelligence to compare kidney tissue from people with lupus nephritis to tissue from mouse models, aiming to understand why treatments work differently in humans.
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.