Dr. Jonathan Barrett

So I do clinics, so I see patients with glomerular disease.

I run clinical trials, and I have my research work at the university in the laboratory.

So most of my career, no one was really interested in IgA nephropathy apart from a few people.

Now it is, you can't move at a kidney meeting without people talking about IgA nephropathy.

Normally, the patients I see have no idea why they're coming to see a kidney doctor.

Perhaps you've joined a new gym, you get a physical, you want to get a mortgage, you might have a job that requires you to have a physical, and someone dips your urine and they say, oh, wait a minute, there's blood and protein in here.

So each kidney contains about a million filters and they are continually filtering the blood to generate the urine.

And in IgA nephropathy, this protein called IgA starts sludging up those filters and stopping them from working properly.

And if the filters don't work very well, they become leaky and blood and protein can appear in the urine.

Some patients do really well with IgA nephropathy, and others end up on dialysis relatively quickly.

And that's the bit we haven't quite worked out yet.

But what we think is the major driver for this disease is the type of IgA we normally produce in our gut and in our respiratory tract.

It normally gets into our sputum, into our tears, into our saliva.

It's there to stop bugs entering the body.

And it does a very, very good job.

But in IgA nephropathy, some of that IgA actually gets into the bloodstream.

But when it's in the bloodstream, it's a bit out of place and it tends to stick to itself, to stick to other proteins.

There are antibodies in the circulation it sticks to.

And that forms these large, what we call immune complexes, which are essentially big aggregates of protein.

If you've got big globs of protein, it's completely reasonable to think that those globs of protein are going to start clogging up the filter, which is exactly what happens.