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Abstract: TH-PO722

Endogenous Pentraxin 3 Inhibits Nephrocalcinosis and Protects from Hyperoxaluria-Induced CKD

Session Information

Category: Genetic Diseases of the Kidney

  • 1002 Genetic Diseases of the Kidney: Non-Cystic


  • Marschner, Julian A., Klinikum der Universität München, LMU München, Munich, Germany
  • Mulay, Shrikant R., Klinikum der Universität München, LMU München, Munich, Germany
  • Anguiano, Lidia, Klinikum der Universität München, LMU München, Munich, Germany
  • Steiger, Stefanie, Klinikum der Universität München, LMU München, Munich, Germany
  • Inforzato, Antonio, Humanitas Clinical and Research Center, Pieve Emanuele, Italy
  • Anders, Hans J., Klinikum der Universität München, LMU München, Munich, Germany

Patients with primary hyperoxaluria type 1 have an elevated oxalate production leading to intrarenal calcium oxalate crystal deposition (nephrocalcinosis) and CKD progressing to ESRD. Pentraxin 3 (PTX3) exerts a variety of regulatory functions in acute and chronic tissue inflammation. Also, PTX3 acts as an opsonin for a variety of pathogens and endogenous particles. We hypothesized, that PTX3 would exhibit opsonin-like functions on calcium oxalate crystals and inhibiting crystal growth and nephrocalcinosis.


Direct effects of PTX3 on calcium oxalate crystals were investigated in chemico using standard imaging techniques. To study the role of PTX3 in vivo, we used a murine model of hyperoxaluria induced nephrocalcinosis where Ptx3-deficient B6;129- mice or their PTX3-competent littermates were fed with a high-oxalate diet for 21 days. PTX3 expression was assessed by Western blot and immunohistochemistry. Phenotype analysis included histochemistry, flow cytometry and GFR measurement.


Adding PTX3 to supersaturated calcium and oxalate in-chemico dose-dependently inhibited crystal growth, while an isomolar albumin control did not (A). PTX3 protein was undetectable in the urine of healthy wildtype mice but increased within 3 weeks of oxalate feeding. Immunhistochemistry of kidney sections indicated that urinary PTX3 originated from tubular epithelial cells. Testing the role of PTX3 in vivo we induced hyperoxaluria in Ptx3-deficient mice and their wildtype littermates. In this particular background, lack of PTX3 induced profound nephrocalcinosis associated with interstitial inflammation and fibrosis as well as a linear decline in GFR, whereas Ptx3+/+ littermates where protected (B-D).


Thus, PTX3 is an endogenous inhibitor of calcium oxalate crystallization even in profound hyperoxaluria. It will be interesting to look into the precise mechanism of action and to develop therapeutic strategies to exploit this novel found function of PTX3 to prevent nephrocalcinosis in primary hyperoxaluria, a disease with currently very few treatment options.


  • Government Support - Non-U.S.