ASN's Mission

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.

learn more

Contact ASN

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


The Latest on Twitter

Kidney Week

Abstract: PO0225

Regulation of Renal Calbindin Expression During Cisplatin-Induced Kidney Injury

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


  • George, Blessy, Rutgers The State University of New Jersey, Piscataway, New Jersey, United States
  • Szilagyi, John T., Rutgers The State University of New Jersey, Piscataway, New Jersey, United States
  • Joy, Melanie S., University of Colorado Denver - Anschutz Medical Campus, Aurora, Colorado, United States
  • Aleksunes, Lauren, Rutgers The State University of New Jersey, Piscataway, New Jersey, United States

Since the discovery of calbindin release into urine during renal injury, there has been growing interest in the utility of this calcium-binding protein as a biomarker of nephrotoxicity. However, little is known about the intrarenal regulation of calbindin during acute kidney injury. We sought to characterize the time-dependent expression and excretion of the distal tubule protein calbindin in comparison to the proximal tubule protein Kim-1 in a mouse model of cisplatin nephrotoxicity.


Male C57BL/6 mice were administered saline vehicle or 20 mg/kg of cisplatin i.p. Urine was collected in metabolic cages for 24 h periods on days 0 – 4. Blood and kidneys were collected between days 2 and 4. Kim-1 and calbindin proteins were measured in urine, kidneys, and blood. Kim-1 and calbindin (Calb1) mRNAs were quantified in kidneys by qPCR.


SCr and BUN levels increased in cisplatin-treated mice by day 3, confirming development of acute kidney injury. Urinary concentrations of calbindin and Kim-1 were elevated by 11.6-fold and 2.5-fold, respectively by day 2. Time-dependent decreases in intrarenal calbindin protein to levels 60% of control were observed on days 3 and 4. A 200-fold up-regulation of Calb1 and Kim-1 mRNAs was seen on day 3. These data suggest that early loss of calbindin protein into the urine along with declines in renal calbindin protein initiates a compensatory induction of mRNA expression at later time points (days 3 and 4).


Understanding the regulation of calbindin during cisplatin nephrotoxicity further enhances its utility as a urinary biomarker of kidney damage. The results of the current study support the combined use of a proximal (Kim-1) and distal tubule (calbindin) marker to phenotype acute kidney injury secondary to cisplatin administration.


  • Other NIH Support