According to a study published in the journal Kidney International, researchers have identified a gene that controls the cut-off switch for kidney inflammation. They noted that this discovery can pave the way for more precise disease diagnostics and personalized treatment for kidney diseases.

Acute kidney injury is defined as a sudden and rapid loss of kidney function caused by inflammation, which is an important risk factor for the progression of chronic kidney disease. At present, there are limited treatment options for acute kidney injury and insufficient tools to predict the risk of poor recovery or kidney failure in diagnosed patients.

The researchers found a common genetic variant of TNFAIP3, which increases inflammation in the body and can paradoxically protect the kidneys from damage in the short term. They observed that the TNFAIP3 gene produced a protein called A20, which acted as a ‘brake’ for inflammation. Therefore, in the study, they examined the different variants of TNFAIP3 and their influence on the function of the A20 protein.

The lead author of the study noted that TNFAIP3 variants can alter the outcome of kidney injury. She noted that the alteration in the disease progresses via complex effects on inflammation and cell survival. She also stated that the most important function of A20 observed in this study was preventing cells from self-destruction. 

(Source: https://www.ibtimes.co.in/this-new-inflammation-hot-gene-may-help-personalise-kidney-disease-treatment-858497 )