Westmead Hospital research finds inflammation ‘brake’ gene may help reveal outcomes of kidney disease

Researchers in the Westmead Health Precinct have found a gene that controls the cut-off switch for kidney inflammation could pave the way for more precise disease diagnostics and personalised treatments.

The discovery about gene variants of an inflammation ‘brake’ brings scientists a step closer to personalised treatment for patients at risk of kidney disease and kidney failure.

Researchers at Westmead Hospital in Western Sydney Local Health District (WSLHD), Garvan Institute of Medical Research and University of New South Wales, found that common genetic variants of TNFAIP3, which increase inflammation in the body, can paradoxically protect the kidneys from damage in the short term.

Professor Natasha Rogers, Senior Staff Specialist in Nephrology and Transplantation at Westmead Hospital in the Westmead Health Precinct co-led the study and said “Common variants of TNFAIP3 have been linked to autoimmune disease, but their role in kidney disease was unknown.

Our discovery that some genetic variants can be protective against inflammation could lead to a simple genetic test that helps predict the risk of kidney disease for patients.” 

The genetic test would allow doctors to determine whether an individual carries a ‘hot’ version of the inflammation control gene, giving families greater certainty about their risk factors.

Professor Shane Grey, senior author of the paper and Head of the Transplant Immunology Lab at Garvan said “We wanted to investigate whether inherited differences in how people regulate inflammation could lead to better or worse kidney health outcomes.

“We focused on the TNFAIP3 gene, which produces a protein that acts as a ‘brake’ on inflammation.”

The findings are published in the journal Kidney International.