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U.S. Department of Health and Human Services
Robert Star
 

 Contact Info

 
Tel: 301-496-6325
Email: starr@mail.nih.gov
 

 Select Experience

 
  • M.D.Harvard Medical School-MIT1980
  • B.A.Harvard University1976
 

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Research Summary/In Plain Language

Research in Plain Language

Acute kidney Injury (AKI) leads to high levels of illness and death. In AKI, the kidneys suddenly stop working and no longer remove waste products from the blood. Researchers continue to develop new treatments, however, these have not helped people despite showing promise in tests with animals. We need to detect AKI early to treat it effectively. Scientists need to understand better AKI’s underlying disease processes in people. Our research has several long-term goals. We aim to find markers (biological indicators) to detect AKI. We are also developing therapies to treat and prevent AKI. Our research also generates new tools to study AKI.

Our recent findings suggest a potential therapy for AKI. Many experimental agents can prevent kidney damage in animal models of AKI. However, these must start before the initial injury. Only a few agents can treat AKI. We found that two inflammation fighters inhibit kidney damage in mice with two different kinds of kidney injury. The inflammation-fighting agents are called alpha-melanocyte stimulating hormone (MSH) and interleukin-10 (IL-10). MSH decreases kidney injury, even when given 6 hours after restriction of blood supply (ischemia). IL-10 works when started 1 hour after chemically induced injury. We are now testing an agent that is chemically similar to MSH in studies with people.

Our recent research has also produced an animal model that mimics sepsis. Sepsis occurs when inflammation takes over the entire body. Sepsis is one of the leading causes of AKI. Half of patients with sepsis develop AKI. Scientists understand very little about how sepsis leads to AKI. There are no drugs to treat sepsis-induced AKI. Researchers might improve the situation with animal models that mimic the human disease. Therefore, we developed a new mouse model. This model features phases typically seen in human sepsis. The model is similar in biochemistry and histology to human AKI. We are now describing this model. We are also testing treatment strategies with this model. Our tests have determined that several agents are effective, even when started 6 to 12 hours after sepsis begins.