ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: FR-PO985

Testing the Relationship Between NBL1 and CKD in a Cisplatin-Induced Mouse Model

Session Information

  • CKD: Pathobiology - I
    November 04, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2203 CKD (Non-Dialysis): Mechanisms


  • Bufi, Rei, The Jackson Laboratory, Bar Harbor, Maine, United States
  • Sheehan, Susan Marie, The Jackson Laboratory, Bar Harbor, Maine, United States
  • Korstanje, Ron, The Jackson Laboratory, Bar Harbor, Maine, United States

Increased serum levels of neuroblastoma suppressor of tumorigenicity 1 (NBL1), a bone morphogenetic protein (BMP) inhibitor, have been associated with a faster decline in kidney function in patients with diabetes, and in vitro experiments have shown a linkage between increased NBL1 levels and podocyte apoptosis. We aim to discover the causality-effector relationship and the role of NBL1 in kidney disease.


We obtained a transgenic (TG) mouse model that has a cDNA copy of Nbl1 behind a chicken B-actin promoter in a DBA/2 and B6J mixed background. In addition, a knockout (KO) model was created using CRISPR technology in the B6J background. We induced chronic kidney disease (CKD) by following a low dose cisplatin protocol for 4 weeks. Wild type (WT), TG, and heterozygous KO mice received either cisplatin (treatment) or saline (control) for 4 weeks. Urine, serum, and kidneys were collected 3 days after the last treatment.


We observed substantial decrease in weight for all mice that received cisplatin with no significant differences between genotypes. In addition to podocyte number as measured by staining with a podocyte marker-specific, we will present our results including measurements of albuminuria, BUN, and histology to establish whether there is a causal relationship between NBL1 and CKD.


Previous literature suggest NBL1 has a damaging effect on podocytes, and we speculate that white blood cells expressing NBL1 drive the mechanism. Results from our measurements of changes in podocytes due to differences in serum NBL1 levels expressed in white blood cells from our WT, TG, and heterozygous KO mouse models could lead to identification of pathways useful for drug targets.


  • Other NIH Support