Crosstalk between Podocytes and Tubular Epithelial Cells

Podocytes hold a strategic position in the regulation of the trafficking between the glomerular and tubular compartments. Defects in the expression of podocytic proteins or injury to podocytes may result in heavy proteinuria, glomerulosclerosis, and loss of kidney function. The process is associated with the infiltration to the tubulointerstitium by inflammatory cells. Previous findings suggest that soluble mediators from renal tubular epithelial cells (TEC) stimulate the proliferation of mesangial cells, which involves a bi-directional tubuloglomerular ‘crosstalk' mechanism, and is likely to operate in different glomerular and interstitial nephritis. While increasing evidence has demonstrated the pathogenic role of glomerulopodocytic communication in podocytic injury from various forms of glomerulonephritides, research into the implication of podocyte-TEC crosstalk in the progression of tubulointerstitial injury is still limited. We review in this article how podocyte pathology leads to subsequent tubulointerstitial atrophy and fibrosis and explore whether tubulointerstitial injury affects the development or progression of podocytic injury. A cytokine crosstalk network between TEC and podocyte with the participation of interstitial immunocompetent cells can be envisaged as the driving force of tubulointerstitial injury, which is a strong predictor of renal failure. An in-depth understanding of the interaction between podocyte and TEC in acute or chronic injury may lead to better design of potential therapeutic options.