In this study, we have first demonstrated that both homozygous (TauT-/-) and heterozygous deletion of the TauT gene (TauT+/-) cause C57BL/6 mice to be highly susceptible to diabetic nephropathy and to display classic characteristics of end-stage renal disease in humans, such as microalbuminuria, azotemia and significant kidney hypertrophy. The gene discussed is SLC6A6; the disease is stage 5 chronic kidney disease.