New study offers insights into how infections can cause treatment-limiting damage in peritoneal dialysis
Research published in The Journal of Immunology has highlighted the biological pathways that can lead to scarring and damage (known as ‘fibrosis’) in patients who have infections during peritoneal dialysis (PD). Lead by Professor Simon Jones from the University of Cardiff, this study offers hope of identifying individuals most at risk of this complication.
Preventing treatment failure for PD patients
PD is a form of dialysis where a membrane within the abdomen (known as the ‘peritoneum’) is used to help clean the blood in patients with kidney failure. With appropriate support and training, PD can be performed at home. Complications, including infections, are common and can lead to damage to the peritoneal membrane. In serious cases these complications may lead to PD treatment failure.
Professor Jones and his team at Cardiff University, with support from a Kidney Research UK Research project grant, investigated how the relationship between the immune system and the peritoneum can change from protection against infection to damage using laboratory models.
Meet the researcher
Professor Simon Jones works at Cardiff University, focusing on infection and the immune system. For the past 20 years, his laboratory has investigated the role of inflammation in chronic conditions, such as kidney disease. He aims to improve diagnosis, look for ways to identify patients most at risk of certain diseases early and find new ways to predict response to any available treatments.
His investigations into peritoneal dialysis in kidney failure patients have shown several ways that inflammation could cause damage to the lining of the abdomen, leading to treatment failure. Professor Jones and his team also use the ideas and concepts from these studies to support new approaches in rheumatoid arthritis.
Pathways to peritoneal damage
Previous research by the team has shown an important role for immune system signalling proteins called cytokines in tissue damage following infection. To understand this process further, Professor Jones looked at the impact of cytokines, and related proteins, on inflammation markers and pathways, and gene expression, in models of peritoneal infection, and compared their findings with genetic studies performed in other diseases.
Working with colleagues in Bristol and collaborators in Australia, the Cardiff-based team found a new pathway to explain how repeated immune responses to infection can lead to damage to the peritoneum.
Professor Jones noted “It may be that certain groups of patients are more likely to suffer damage to their peritoneum following infection, which in serious cases may mean that PD is no longer possible. Our research has found a new mechanism for peritoneal fibrosis involving parts of the immune system called cytokines and T-cells, and a DNA sequence that is known to be involved in inflammatory diseases. Although this work needs to be confirmed in human studies, we hope it will offer hope to those patients impacted by infections during PD”.
What might this mean for the future?
This research offers an important step forward in our understanding of how and why infections cause damage to the peritoneal membrane. Building on these new insights, Professor Jones and colleagues hope to undertake further studies to help identify high-risk patients before the problems occur and look at targeted ways to block the inflammatory mechanisms.
Emily Surridge, research communications manager at Kidney Research UK added “Research like Simon’s is crucial to build up the knowledge needed for future treatment breakthroughs and an important reminder of the impact that early-stage studies can have. We look forward to the next steps in this work.”
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