Abstract
Chronic kidney disease (CKD) is a highly prevalent and potential progressive condition with life-threatening consequences. Glomerular diseases (glomerulopathies) are causes of CKD that are potentially amenable by specific therapies. Significant resources have been invested in the identification of novel biomarkers of CKD progression and new targets for treatment. By using experimental models of kidney diseases, periostin has been identified amongst the most represented matricellular proteins that are commonly involved in the inflammation and fibrosis that characterize progressive kidney diseases. Periostin is highly expressed during organogenesis, with scarce expression in mature healthy tissues, but it is upregulated in multiple disease settings characterized by tissue injury and remodeling. Periostin was the most highly expressed matriceal protein in both animal models and in patients with glomerulopathies. Given that periostin is readily secreted from injury sites, and the variations in its humoral levels compared to the normal state were easily detectable, its potential role as a biomarker is suggested. Moreover, periostin expression was correlated with the degree of histological damage and with kidney function decline in patients with CKD secondary to both inflammatory (IgA nephropathy) and non-inflammatory (membranous nephropathy) glomerulopathies, while also displaying variability secondary to treatment response. The scope of this review is to summarize the existing evidence that supports the role of periostin as a novel biomarker in glomerulopathies.