Professor Tang is known for his contribution to both clinical and basic sciences in the field of nephrology. The research team has dissected some of the most important intracellular pathways through which excessive albumin, high glucose and glycated proteins induce toxicity to kidney tubule cells, the very cell type in the kidney that determines ultimate clinical outcomes in patients with chronic kidney disease. Albumin is a strong stimulus for tubular interleukin-8 overexpression through activation of nuclear factor-kappa B-dependent pathways, providing a mechanism for the occurrence of interstitial inflammatory cell infiltration that is observed in all forms of chronic proteinuric nephropathies. High glucose activates the Toll-like receptor that senses and reacts to diabetic injury in the kidney, and these observations are reproduced using gene knockout animal models, thus providing a novel therapeutic target for diabetic nephropathy which is currently the most prevalent disease leading to kidney failure in developed countries. In IgA nephropathy, a podocyte and glomerular-interstitial cross-talk pathway exists to mediate the occurrence of proteinuria and tubulointerstitial injury.