Therefore, it is impossible to obtain a temporal change of gene profiles in patients over the entire course of the disease. Due to these factors, the clinical utility of current human transcriptomic data is limited. Some of these limitations, however, could be overcome by studying animal models of kidney disease. Here, we examined the temporal profile of gene expression over the course of disease progression by serial sampling of the kidney. Many animal models have been used to study the pathogenesis and progression of kidney disease. However, most animal models develop only mild kidney disease without progression to renal failure, which is the case for almost all experimental models of diabetic nephropathy. HIV-1 transgenic mouse model has been used extensively to study the pathogenesis of HIVAN because these mice develop renal disease mimicking human HIVAN. Tg26 mice develop proteinuria as early as 4 weeks of age and proteinuria peaks at 8 weeks of age. Tg26 mice develop mild glomerulosclerosis at 4 weeks of age, moderate GS and mild tubulointerstitial injury at 8 weeks of age, and advanced GS and tubulointerstitial fibrosis, tubular atrophy and dilatation at 12 weeks of age. Tg26 mice have rapid progression of kidney disease to renal failure and usually die from uremia between the ages of 2 to 6 months. Variability in disease progression is thought to be due to genetic penetrance. Therefore, Tg26 mouse is a robust model to study the progression of kidney disease. In the current study, we performed serial kidney biopsies in Tg26 mice and age and gender-matched control littermates at 4 weeks and 8 weeks of age and mice were sacrificed at 12 weeks of age. Gene expression profiles in the kidney cortices of Tg26 and their control littermates at these three time points were assessed by next-generation sequencing of mRNA extracted from the kidney cortex. Transcriptomic data were analyzed to identify temporal pattern of gene expression during disease progression. To determine cellular processes and genes that could be drivers of disease progression, we NVP-BKM120 msds focused on the genes that are differentially regulated during the early stage of disease. Mechanisms underlying CKD development and progression remain largely unknown. Treatment options that effectively prevent disease development or stop disease progression are lacking. Transcriptomics is a powerful tool for identifying potential new biomarkers and drug targets. However, the application of transcriptomics in kidney disease is limited because most renal transcriptome datasets were derived from kidney biopsies of patients with advanced kidney disease at a single point in time. Here, we evaluated the profile of gene expression changes over time in an animal model of kidney disease by serial sampling of the kidney. These data from animal models provided information that is not available for human kidney diseases, as protocol serial renal biopsies are not routinely performed. Our data suggest that findings from animal studies could help us to understand human kidney disease.