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ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

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Kidney Week

Abstract: PO0251

Whole-Transcriptome Sequencing of Proximal Tubule Cells Exposed to Free Light Chains

Session Information

  • AKI Mechanisms - 3
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Upadhyay, Rohit, Tulane University School of Medicine, New Orleans, Louisiana, United States
  • Batuman, Vecihi, Tulane University School of Medicine, New Orleans, Louisiana, United States

Despite medical advancements, molecular markers for early detection of kidney injury (KI) are limited. Serum creatinine, the only functional marker for KI, has poor predictive accuracy, particularly in the early stages of acute KI due to free light chains in multiple myeloma (MM) patients. Identification of new markers would be highly useful in a select group of MM patients who do not present initially with a detectable rise in creatinine level.


Human kidney proximal tubule cells (PTCs; RPTEC cell line) were exposed to κ or λ FLCs. Control/ treated cells were harvested, and total RNA (mRNA+miRNA) was isolated following standard procedures for whole transcriptome analysis. After checking RNA quality by Bioanalyzer (Agilent Bioanalyzer 2100), RNA sequencing for whole transcriptome was performed by using Illumina NextSeq 500 to generate >60M paired-end 75bp reads per sample. After initial data quality checking by FastQC and RSeQC, bioinformatics analysis was performed using TopHat, Samtools, and Picard. Further classification, annotation, and visualization were facilitated by Partek and R statistical packages. RNA sequencing data were validated through qPCR.


Whole transcriptome RNA-Seq data suggested role of several genes involved in innate immunity (VNN1, MX1, OAS2, TLRs, IFI6, IFI27, IFIT1, ISG15, BST2), ERK signaling (KCTD12, IFI6, MAP3K, ERK1/2, JNK,p38), and inflammation (CXCL6, TNFA, IL6, CXCL8, IL8, IRAK1, IRAK4, TRAF6, NFKB, IKBA, IKK) as well as miRNAs (hsa-146a-5p, hsa-miR-574-3p, hsa-miR-331-3p, hsa-miR-125a-5p) in FLC induced tubular injury in MM patients. We also found a KI mechanism involving cross-talk among innate immunity, ERK signaling, and the inflammatory pathway by different FLCs types.


Our results show differentially expressed genes and a mechanism of injury involving cross-talk between innate immunity and inflammatory pathways in PTCs exposed to FLCs.


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