Artificial Antibody Knocks Out Kidney Inflammation Interview with:

Michael P. Madaio, MD Sydenstricker Professor and Chairman Department of Medicine Medical College of Georgia at  Augusta University

Dr. Madaio

Michael P. Madaio, MD
Sydenstricker Professor and Chairman
Department of Medicine
Medical College of Georgia at
Augusta University What is the background for this study?

Response: Glomerulonephritis is a inflammatory disease of the kidney.  Glomeruli are the filtering units in the kidney. This is most often immunologically mediated and are autoimmune.

Most therapies are directed at inhibiting the Immune/autoimmune process (immunotherapy) systemically. What are the main findings?

Response: Protein kinase C is an important mediator of the glomerulitis inflammatory response.

Inhibiting protein kinase C during the course of disease enhances resolution of nephritis.

Targeting the inhibitor to a human antibody that binds to glomeruli, allows for efficient delivery of drug, thereby enhancing efficacy while limiting the potential of systemic toxicity (I.e. Associated with higher amounts of drug administered orally or intravenously).

Protein kinase C inhibition may be a potential strategy to alter the course of glomerulonephritis.

Targeted drug delivery is an efficient means of therapy that has application to other glomerular diseases (e.g. Nephritis, diabetes. etc.). What recommendations do you have for future research as a result of this work? 

Response: For human application developing novel means of kidney delivery has the potential for application to common kidneys diseases such as diabetes and hypertension, to alter disease progression.  


Nino Kvirkvelia, Malgorzata McMenamin, Marie Warren, Ravirajsinh N. Jadeja, Sai Karthik Kodeboyina, Ashok Sharma, Wenbo Zhi, Paul M. O’Connor, Raghavan Raju, Rudolf Lucas, Michael P. Madaio. Kidney-targeted inhibition of protein kinase C-α ameliorates nephrotoxic nephritis with restoration of mitochondrial dysfunction. Kidney International, 2018; 94 (2): 280 DOI: 10.1016/j.kint.2018.01.032

Jul 31, 2018 @ 11:20 am 

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