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

This article comments on Varatharajan et al 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.