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Study highlights potential new approach for early intervention for diabetic patients at risk of kidney disease

Press release issued: 27 March 2024

Researchers at the University of Bristol have uncovered a mechanism by which a hormone can protect the blood vessels in the kidneys from the damage caused by diabetes. In doing so, the team has identified a potential early treatment strategy to prevent or slow progression of kidney disease in people with diabetes.

Diabetes is the leading cause of kidney failure in the UK. One in five people with diabetes will need treatment for kidney disease during their lifetime and almost one in three people who need dialysis or a transplant have diabetes. As well as these treatments being incredibly gruelling for patients, they come at a cost. It is estimated that in 2023, the direct cost to the NHS of dialysis and kidney transplant surgery with follow up care was £1.05 billion (not including the £225 million spent on transport for patients on in-centre dialysis) and £293 million, respectively. 

Kidney damage from diabetes usually happens slowly over many years. One of the ways damage can be caused is by disruption of the glycocalyx – a thin gel-like layer lining the surface of the blood vessels forming part of the tiny filters of the kidney (‘glomeruli’) – due to high blood sugar levels over a long period of time. This layer plays a crucial role in kidney function; it has a barrier function, preventing larger molecules like proteins from leaving the body in the urine. One of the first signs of kidney disease in patients with diabetes is the presence of a protein called albumin in the urine. 

Adiponectin, a hormone produced by fat cells in the body, plays a protective role: helping the body use sugar more efficiently, reducing inflammation and preventing blood vessel damage. Previous studies have shown that adiponectin levels are lower in people with diabetes and that adiponectin can prevent signs of kidney damage, such as preventing albumin from being lost in the urine in laboratory models of diabetic kidney disease (DKD).  Using several laboratory-based models of DKD, the team were able to show that adiponectin both reduced glycocalyx damage, and increased its thickness, which reduced the leakiness of the vessels. 

Read the full University of Bristol news item

'Adiponectin reduces glomerular endothelial glycocalyx disruption and restores glomerular barrier function in a mouse model of type 2 diabetes' by Rebecca R. Foster et al. in Diabetes

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