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

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: TH-PO791

Urinary Podocin Cell Count in Relation to Glomerular and Tubular Damage Markers in Patients with Primary Nephrotic Syndrome

Session Information

Category: Glomerular Diseases

  • 1403 Podocyte Biology

Authors

  • van den Berge, Bartholomeus Tideman, RadboudUMC Department of Nephrology, Nijmegen, Netherlands
  • van de Logt, Anne-Els, RadboudUMC Department of Nephrology, Nijmegen, Netherlands
  • Jansen, Jitske, RWTH Aachen Institute of Experimental Medicine and Systems Biology, Aachen, Germany
  • Smeets, Bart, RadboudUMC Department of Pathology, Nijmegen, Netherlands
  • Wetzels, Jack F., RadboudUMC Department of Nephrology, Nijmegen, Netherlands
  • Maas, Rutger J., RadboudUMC Department of Nephrology, Nijmegen, Netherlands
Background

Progressive renal failure in patients with glomerular disease is driven by podocyte depletion. Several methods have been proposed to monitor urinary podocyte loss. Here, we investigated the process of podocyte depletion in patients with primary membranous nephropathy (MN) by flow cytometric detection of Podocin-positive cells in urine.

Methods

We included 27 patients with MN. Urinary cell pellets were processed and stained for Podocin and subsequently counted using FACS. Urinary protein and creatinine levels were determined from the same portion of urine. Normal values of urinary Podocin-positive cells were obtained in urine samples of 13 healthy controls.

Results

Mean urinary podocyte count (Podocin-positive cells) was significantly higher in patients compared to healthy controls. Podocyte excretion showed significant correlations with urinary protein (r = 0.71), glomerular damage marker IgG (r = 0.75) and the tubular damage markers α1-microglobulin (r = 0.66) and β2-microglobulin (r = 0.43), all corrected for creatinine.

Conclusion

Urinary excretion of Podocin-positive podocytes was significantly increased in patients with MN, and correlated significantly with protein/creatinine ratios and glomerular and tubular damage markers. We conclude that this method can be used to monitor the process of podocyte depletion, and potentially the impact of treatment. We are planning prospective studies to evaluate the prognostic value of urinary Podocin+ podocyte excretion in patients with PNS.

Funding

  • Government Support – Non-U.S.