A/Prof Melinda Coughlan wins Diabetes Australia grant

Associate Professor Melinda Coughlan (left) receiving the DARP
award from Chris Jose, President of Diabetes Australia - Victoria
Photo: Jorge de Araujo artificialstudios.com.au

Congratulations to Associate Professor Melinda Coughlan on the Diabetes Australia Research Program (DARP) grant!

A/Prof Coughlan has received a grant for $53,000 from DARP to pursue research investigating a blockade of a major driver of inflammation, which contributes to the development of kidney disease, potentially leading to kidney failure.


The problem

More than 1.7 million Australians have diabetes which is the sixth-highest cause of death by disease category in Australia. The annual costs of diabetes exceed A$10 billion, and a major proportion of these costs are incurred due to the development of complications including diabetic kidney disease (DKD).

DKD, which affects more than 30% of patients with diabetes, is the most common cause of end stage renal disease (ESRD) in Western societies. Patients with DKD carry a higher risk for comorbidities such as cardiovascular disease, with renal dysfunction a major predictor of all cause mortality.

Currently there is no treatment to cure diabetes or deal effectively with its complications. Although inhibitors of the renin angiotensin system (RAS) remain the mainstay for treatment of DKD, a significant proportion of diabetic patients with renal disease still progress over time to renal failure.

A potential solution

A/Prof Coughlan said, "We're looking for new targets, as people can still go into renal failure despite the current best medication available, the RAS blockers.

"We're looking at what's called the complement system, the innate immune system's response to infection or damage, which works through increasing inflammation. In normal conditions, the complement system is tightly regulated to avoid tissue injury. However, we have found complement to be hyperactivated in diabetes and in the kidney of patients with DKD. The complement system involves about forty proteins. One particular protein, called C5a, which comes into action towards the end of the pathway, has the biggest effect in the inflammatory response. So what we're doing is testing a specific inhibitor of C5a, called PMX-53.

"If we can block the actions of C5a, then we can protect the kidneys from damage. So our study is checking out whether that particular pathway is going to be a valid therapeutic target."

See more about Melinda's group at:
www.monash.edu/medicine/ccs/diabetes/research/coughlan-group