Protein contributes to the failure of arteriovenous fistulae

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A protein implicated in the development of vascular diseases may also contribute to the failure of arteriovenous fistulae created for vascular access in dialysis patients, according to a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN).

“Our findings raise the possibility that monocyte chemoattractant protein-1 (MCP-1) may contribute to the relatively poor outcomes regarding the function and longevity of human haemodialysis arteriovenous fistulae,” said Karl A Nath, Mayo Clinic, Rochester, USA.

 

Arteriovenous fistulae are the preferred form of access to the circulatory system in dialysis patients. They are created by a surgical procedure to connect a vein to an artery, usually in the lower arm. The use of arteriovenous fistulas, compared to other types of dialysis access, leads to fewer complications such as infections, less hospitalisation of dialysis patients, and overall, a better outcome for the dialysis patient.

 

However, arteriovenous fistulae are prone to certain problems. About half of arteriovenous fistulae never become functional for use in dialysis, while those that do become functional have a significant failure rate. “We thus need to understand why arteriovenous fistulae do not develop, or fail to function after a relatively short period of use,” says Nath.

 

In a series of experiments in mice, the researchers found that MCP-1 – an inflammation-promoting chemokine protein – was a “critical contributor” to arteriovenous fistula failure. The failing fistulae showed increased levels of MCP-1, and of the gene that encodes it. In contrast, arteriovenous fistulae functioned much better in genetically altered mice that lacked MCP-1. In the absence of MCP-1, arteriovenous fistulae had less vein wall thickening, and the number of functional arteriovenous fistulae was substantially higher.

 

“The present study […] is the first to directly demonstrate that MCP-1 critically contributes to failure of an arteriovenous fistula,” the researchers wrote. The results are timely, because drugs that act as MCP-1 blockers are currently under development. “Such agents, when clinically available, may be considered as a possible therapeutic approach to promote the maturation of arteriovenous fistulae, and/or extend their duration of function,” said Nath.

 

The researchers emphasised that more research will be needed to confirm whether the results of these animal experiments are relevant to arteriovenous fistulae in humans.

 

Source: American Society of Nephrology

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