This study investigated the expression of genes that were turned on or off in renal cells of chicks as a result of different exposure times to ochratoxin A (OTA). One hundred and 80 d-old male broiler chicks (Ross 308) were randomly assigned to a 3 × 3 factorial arrangement of treatments (3 levels of OTA: 0, 1 and 2 mg OTA/kg diet and 3 time periods: 7, 14 and 21 d) with 4 replicate pens of 5 birds each per treatment. For RNA-Sequencing analysis (RNA-Seq), kidney samples were collected weekly from 3 controls and 3 chicks fed 1 mg OTA/kg. Birds fed 2 mg OTA/kg diet were not used because their reduced feed intake could affect gene expression. The libraries were constructed by Illumina’s TruSeq RNA protocol. NextGENe software was used for alignment and transcript quantification. Reads per kilobase of target per million tiled reads (RPKM) were used in the Binary test analysis (P < 0.05). A total of 27,638,976 50-bp RNA-Seq reads were produced over the 3 time periods. Transcripts (40,782) were assembled de novo and annotated by homology to either G. gallus or H. sapiens. The interleukin 9 (IL9) and tubby like protein 1 (TULP1) genes were activated at 7 d, the growth hormone secretagogue receptor (GHSR) gene was activated at 14 d, and the G protein-coupled receptor kinase 6 (GRK6) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) genes were activated at 21 d. The preprogastrin (LOC396365) was activated during all time periods. The sperm associated antigen 4 (SPAG4), sperm-associated antigen 4 protein-like (LOC100857131) and V-region-like B-G antigen, and MHC class IV antigen (B-G) were deactivated at 7 d, the zinc finger B-box domain-containing protein 1-like (LOC771469), NK2 homeobox 1, variant 2, and NK2 homeobox 8 (NKX2–1 and NKX2–8), forkhead box O1 (FOXO1), myosin heavy chain (MyHC) and claudin 18 (CLDN18) genes were deactivated at 14 d and finally, the V-region-like B-G antigen (B-G) and xeroderma pigmentosum, complementation group C (XPC) genes were deactivated at 21 d. The turning on and off of the genes may be a response to the carcinogenic and tumorigenic effects of OTA in birds.