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Kidney disease ends here.

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Getting results

Getting results.

Every piece of research brings us one step closer to transforming treatments and freeing lives from kidney disease. The clinical trials we fund can improve the care kidney patients receive today. The laboratory science we support makes discoveries that will fuel the advances of tomorrow. Here are just a few of the important discoveries that your donations made possible last year.

Professor Will Herrington, pictured right, and his colleagues at the University of Oxford, used genetics to show obesity can increase the chances of someone developing kidney disease. Their work was funded by a joint David Kerr fellowship.

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No kidney left behind

The demand for kidney transplants outweighs the supply of donated organs. Worse still, some donated kidneys are wasted because they’re not in perfect condition. In July, the results of research we funded revealed a way to revive donated kidneys that might otherwise be discarded. Dr Emily Thompson and colleagues at Newcastle University pumped blood and stem cells through kidneys in the lab. This improved the condition of the organs; the first time that a pre-treatment has been shown to do this. The next step is to find out if pre-treated kidneys result in better and longer lasting transplants.

This research could increase the number of donated kidneys that can be used for transplant in the future, and make more transplants successful.

Tackling high blood pressure

High blood pressure is a major cause of kidney disease. It’s very common, and we urgently need to find better ways to tackle it. High blood pressure often develops because our arteries have stiffened up as we age. Kidney Research UK Senior Fellow at the University of Edinburgh, Dr Laura Denby, has been investigating this problem. In April she was part of a team who published research identifying a tiny piece of genetic material, known as a micro-RNA, as key to the process.

They showed that a micro-RNA called miR-214 causes T-cells from the immune system to invade the tissue around arteries. Here, the T-cells trigger the production of tough collagen fibres that make arteries less elastic. They also kick off a damaging process called ‘oxidative stress’, which compounds the problem. Next steps include finding drugs that can control the actions of miR-214, and seeing if this could be a safe and effective way to combat artery stiffening and high blood pressure.

An unexpected discovery

Healthy kidneys filter out waste products in our blood to make urine, while stopping essential proteins from escaping. Cells called podocytes are key components of the filter, and when they begin to fail, proteins leak out. An early sign of kidney disease is detecting protein in the urine.

Dr Abigail Lay and colleagues at the University of Bristol have been funded by us to understand how podocytes fail. They have discovered that a molecule called Neuropeptide Y is involved; too much of it causes podocyte damage. It’s exciting because Neuropeptide Y is normally found in the brain and spinal cord – no-one suspected it had a role in the kidneys. The researchers would now like to investigate whether blocking Neuropeptide Y could prevent the loss of protein, and even interrupt the early stages of kidney disease.

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