Laith Al-Rabadi
University of Utah, UT·Medicine & Clinical Research·Early-career
Membranous nephropathy (MN) is an autoimmune kidney disease and a major cause of nephrotic syndrome, a condition in which the kidneys leak protein into the urine. In MN, the immune system makes antibodies against the patient's own kidney proteins.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Biochemistry
- Topics
membranous nephropathy
serine protease
autoantigen
- Grants
- 1 known grant, through Mar 2028
What they work on
- Identify the HTRA1 epitopes, the protein regions bound by autoantibodies, in membranous nephropathy, and determine how antibody binding affects HTRA1's protein-cutting function, using proteomics and patient biospecimens.
- Test how HTRA1 autoantibodies and HTRA1 protein buildup drive kidney disease in newly developed animal models of membranous nephropathy.
- Use patient samples from the CureGN network, ARUP and Arkana laboratories to characterize HTRA1-associated membranous nephropathy.
More about the research
The resulting antibody–protein clumps (immune complexes) build up in the glomerular basement membrane, the kidney's filtering layer. It is still unclear what triggers these autoantibodies and how they damage the kidney. Better answers could lead to earlier diagnosis and better treatment.
Why it matters
Patients with HTRA1-associated membranous nephropathy currently lack targeted options. Knowing which HTRA1 regions the autoantibodies attack could improve diagnosis. It could also lay the groundwork for peptide-based therapies designed to block the harmful immune response against the kidney.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Rupali Avasare
Oregon Health & Science University, OR·Medicine & Clinical Research·Early-career
Determine whether circulating NELL1 antibodies, measured by Western blot, associate with and precede protein loss in the urine among 150 lipoic acid users followed over two years.
Jan Novak
University of Alabama at Birmingham, AL·Microbiology & Immunology
Test whether circulating IgA1 immune complexes from patients with progressive IgA nephropathy are larger and more active, measuring their ability to make kidney mesangial cells grow, signal and release cytokines, compared with non-progressive disease.
Kirk Campbell
University of Pennsylvania, PA·Physiology
Define how Hippo-YAP signaling regulates the calcium-activated potassium channel KCa3.1 in podocytes, including whether nuclear YAP protects the actin cytoskeleton by repressing the KCNN4 gene that encodes it.
The school
University of Utah: 58 labs on PI Pages, $789M a year on research, 366 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.