Predictive value of biomarkers for tubulointerstitial and glomerular interactions in diabetic nephropathy

This article comments on Varatharajan <i>et al</i> recent article, highlighting the role of tubulointerstitial damage mechanisms in diabetic nephropathy progression. Evidence suggests a bidirectional interaction between the interstitium, tubular cells, and glomeruli. Renal tubules are highly susceptible to proteinuria, metabolic disorders, and toxins. Since diabetic nephropathy persistently activates inflammatory and fibrotic pathways, epithelial-to-mesenchymal transition mechanisms present promising targets for risk assessment. Periostin, a cellular matrix protein, plays a key role in modulating extracellular interactions. Increased periostin expression in tissue, serum, and urine correlates with type 2 diabetes, making it a valuable biomarker alongside neutrophil gelatinase-associated lipocalin and kidney injury molecule-1. While periostin and neutrophil gelatinase-associated lipocalin reflect distal tubular damage, kidney injury molecule-1 serves as a marker for proximal tubular injury. Combining these biomarkers enhances diagnostic precision.