Could THIS lead to a cure for deadly kidney disease? Scientists discover it can be triggered by microscopic 'shuttles'

The microscopic exosomes are approximately 1,000 times thinner than hair
The tiny vesicles transport a damaging enzyme that leads to kidney fibrosis
This is the main cause of kidney disease - which strikes 2.6 million in the UK
There is no cure and thousands of patients rely on life-saving dialysis

A cure for kidney disease could be in the pipeline after scientists discovered the killer disease can be triggered by tiny 'shuttles'.

The microscopic exosomes - 1,000 times thinner than hair - transport a damaging enzyme that leads to fibrosis of the kidney.

Fibrosis, or kidney scarring, is the primary cause of kidney disease - which strikes roughly 2.6 million people in the UK.

There is currently no cure and patients whose organs go on to fail, the end-stage of the disease, need dialysis or a transplant to survive.

The new findings, led by Nottingham Trent University researchers, offer hope of a way of stopping the disease in its tracks.

The microscopic exosomes - 1,000 times thinner than hair - transport a damaging enzyme that leads to fibrosis of the kidney

Scientists hope they will be able to block the microscopic vessels, which are 100 nanometers wide and transmit transglutaminase-2 (TG2).

Dr Elisabetta Verderio, lead author, told MailOnline: 'This is a major marker for kidney disease development.

'To play a role in fibrosis, TG2 needs to get to the right location where fibrosis forms, outside the cells. We know that TG2 doesn't travel alone.

'We now need to look at how we can target these tiny vesicles as a means of controlling, or interrupting, fibrosis before serious problems occur.

'It is also possible that we could look at TG2 in these vesicles as a way of diagnosing the disease earlier. The more we know, the more avenues we have to intervene.'

Kidney disease costs the NHS £1.5 billion each year - but charities warn this could soar because it is becoming increasingly common.

Staggering figures show the number of people dying from kidney disease have roared by 31 per cent in the space of a decade.

The organs completely fail in around one in 50 patients, according to the NHS. This is when the sufferer can be listed for a transplant.

Others are given dialysis - a procedure that removes waste products and excess fluids from the blood when the kidneys stop functioning properly.

WHAT IS KIDNEY DISEASE?

Our kidneys filter out waste products from the blood before converting them into urine. They also help maintain blood pressure.

Chronic kidney disease (CKD) is a long-term condition where the kidneys do not work as well as normal.

CKD is very common and the risk increases as you age. It is also more common among south Asian and black people.

CKD does not usually cause any symptoms until it has reached an advanced stage. It can be detected early on via blood and urine tests.

The main symptoms of advanced kidney disease include tiredness, swollen ankles or hands, shortness of breath, nausea and blood in urine.

Those with the condition have a greater risk of having a stroke or heart attack. It can also cause kidney failure, when sufferers will need to have dialysis and possible transplant.

However, lifestyle changes and medication can stop it getting worse if it's diagnosed at an early stage. Kidney disease can be caused by other conditions that put a strain on the organs, such as high blood pressure and diabetes.

However, evidence shows fibrosis, which is deemed largely irreversible, plays a 'key' role in the onset of kidney disease.

Researchers from Sheffield University and the CNR Institute of Neuroscience in Milan also chipped in to the latest project to find a cure.

It delved into how an enzyme known to cause kidney scarring was transported from the cells to perform its damaging action.

Transglutaminase-2 (TG2) was first identified as a trigger of kidney scarring by the Trent and Sheffield researchers back in 1997.

Scientists used pioneering new technology to detect all TG2-associated proteins in simulated conditions of kidney disease.

They were then able to identify how TG2 left the kidney cells to cross-link proteins like collagen and fibronectin, leading to fibrosis.

This is when they discovered that the damaging enzyme is transported through the body via the nano-sized exosomes.

Researchers confirmed their findings by screening the urine of 10 kidney disease patients. Samples showed TG2 was being carried by the exosomes.

The results, published in the Journal of the American Society of Nephrology, have been welcomed by experts.

Elaine Davies, director of research operations at Kidney Research UK - which funded the study, is hopeful it could revolutionise treatment.

She said: 'Kidney failure is life-threatening and caused when the kidneys no longer function normally due to irreversible scarring within its structure.

'This biological mechanism research finding is helping us build our understanding about scarring.'

Ms Davies added that it will 'help us to find the tipping point where kidney scarring changes, from being reversible to irreversible'.