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Kidney Week

Abstract: TH-PO820

Inflammasome Activation in Primary Hyperoxaluria

Session Information

Category: Genetic Diseases of the Kidneys

  • 1002 Genetic Diseases of the Kidneys: Non-Cystic


  • Hoppe, Bernd, University Hospital Bonn, Bonn, Germany
  • Mehring, Julia, University of Bonn, Germany, Bonn, Germany
  • Latz, Eicke, Institute of Innate Immunity , Bonn, Germany

In the primary hyperoxalurias (type I - III), increased production of oxalate in the liver consecutively leads to hyperoxaluria, urolithiasis and/or nephrocalcinosis. Hyperoxaluria causes deposition and internalization of calcium oxalate (CaOx) crystals in the epithelial cells of the proximal tubule. As a result, it activates the inflammasome pathway, which is a protein complex in the cytosol of macrophages. In a mouse model of CaOx induced inflammasome activation, the progression of renal damage was delayed by administration of a specific NLRP3 inflammasome pathway inhibitor. The aim of our present study was to investigate inflammasome activation in PH patients.


Serum samples from 50 PH patients (39 PH I, 6 PH II, 5 PHII) were collected. Thirtyfive patients had preserved renal function, 14 PH I an d1 PH II patient were on maintenance hemodialysis (HD). In addition, samples from 8 healthy controls and from 9 non PH HD patients were collected. So far, results from 9/6 PH patients with good renal function/HD and from 4 controls are available. Samples were examined for inflammation and organ damage markers by use of a proximity extension assay (PEA) (n=184). In PEA antibody pairs bind to the desired target structure and, if in close proximity to another, form a new PCR target sequence, which can be quantified using real-time PCR.


The preliminary findings have shown no differences in inflammatory/organ damage markes among the three types of PH patients with preserved kidney function. However, there were signficiant reactions in dialysis dependent PH I patients. So far it is not yet clear whether these differences are caused by the advanced kidney disease or the dialysis therapy per se.


Our current results might allow the following conclusions: 1) the activation of the inflammasome described in the mouse model is only detectable late, e.g. in ESRD, 2) there is no inflammatory reaction to oxalate at all, 3) the response is below the detection limit, or 4) all three forms have a comparable inflammation and therefore no difference can be seen. The latter might suggest protective factors in type III or predisposing factors in types I and II.


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