肾毒性PCR芯片可用于研究的84个关键基因的表达，这些基因可以作为肾毒性的潜在的分子标志物。减小肾毒性仍然是新药上市最大的障碍之一。肾脏是药物排泄的重要器官，因此它是毒理学试验的重要研究对象。在动物模型的毒性反应中表达出现持续上升或者下降的基因能够作为预测不良临床反应的潜在标识物。肾脏的排泄过程是从血液经过肾小球过滤开始，然后将滤液通过近端小管，亨勒环路，远端肾小管，并最终到达收集管。药物引起的肾毒性研究主要集中在近端小管的毒性，大多数药物在这个区域重吸收。该芯片包含已知肾毒性药物引起的差异表达的基因。利用实时定量PCR，研究者可以方便并且可信地对与肾毒性反应相关的基因进行同时检测。
Up-Regulated: Apoptosis: ANGPTL4, ANXA5, BTG2, CD24, CD44, CDKN1A, CLU, GADD45A, GSTP1, HMOX1, NQO1, RTN4, SOCS3, TNFRSF12A. Cell Cycle: CCND1, CCNG1, CDKN1A, GADD45A, MCM6. Metal Ion Binding: BMP1, CCS, CP, CTSS, HMOX1, HMOX2, MT1A. Oxidative Stress: CLU, G6PD, GPX2, GPX8, HMOX1, HMOX2, NQO1. Proliferation: ATF3, BTG2, CCND1, CD24, CDKN1A (p21CIP1/WAF1), CLU, CXCL1, CXCL10 (INP10), GLUL, GPNMB, HMOX1, HSP90AA1, TIMP1, UCHL1, VCAM1. Tissue Remodeling: CST3, FN1, HAVCR1 (KIM-1), SPP1 (Osteopontin), TIMP1. Transporters: ABCB1 (MDR1), ABCC2 (MRP2). Xenobiotic Metabolism: CYP2C19, GSTP1. Extracellular Matrix: ANGPTL4, CCL3 (MIP-1A), CD44, CST3, FGB, LGALS3, MGP, TIMP1. Cytoskeleton: CCL3, G6PD, SPRR1A, TMSB10, VIM. Others: A2M, GC, IGFBP1, LCN2 (NGAL), UGT1A1. Down-Regulated: Apoptosis: BMP4, CAT, GHR, IGFBP3, SOD2. Cell Cycle: BMP4, EGF. Metal Ion Binding: BHMT, IDH1, RGN, SCD, SOD2, SOD3. Oxidative Stress: CAT, GATM, IDH1, SOD2, SOD3. Proliferation: BMP4, EGF, IGFBP3, NOX4, ODC1, SOD2. Transporters: SLC22A1, SLC22A5, SLC22A6. Xenobiotic Metabolism: CYP2D6, FMO2, GSTK1. Extracellular Matrix: BMP4, CYR61, SOD3. Others: AASS, ALDH1A1, CALB1, G6PC, GAMT, IPMK, KLK1, NPHS2, OAT