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Pediatric Nephrology

, Volume 29, Issue 12, pp 2411–2414 | Cite as

Serum suPAR levels are modulated by immunosuppressive therapy of minimal change nephrotic syndrome

  • Jutta Gellermann
  • Franz Schaefer
  • Uwe QuerfeldEmail author
Brief Report

Abstract

Background

Soluble urokinase-type plasminogen activator receptor (suPAR) could be a causative factor in idiopathic focal segmental glomerulosclerosis (FSGS). It is currently unknown to what extent suPAR levels could be affected by treatment with immunosuppressive drugs such as cyclosporin A (CsA) and mycophenolate mofetil (MMF). Treatment with CsA, but not MMF, is accompanied by nephrotoxicity, and since suPAR levels correlate with glomerular filtration rate (GFR), treatment with these drugs could indirectly modulate suPAR levels by their effect on renal function.

Methods

We measured suPAR levels in a recent prospective multicenter crossover trial comparing the efficacy of MMF and CsA in pediatric patients with minimal change disease (MCD) and frequently relapsing steroid-sensitive nephrotic syndrome (FR-SSNS). All patients had biopsy-proven MCD and normal renal function; they were treated with each drug for 1 year in a crossover study design. Serum suPAR levels were measured before and after 1 year of therapy with MMF (n = 40) and CsA (n = 35).

Results

The suPAR levels decreased after 1 year of treatment with MMF (p < 0.05). Conversely, suPAR levels increased after 1 year of treatment with CsA in the same patients (p = 0.01). These changes in suPAR levels were not correlated to the estimated glomerular filtration rate (eGFR) or changes in the GFR.

Conclusions

Data from this prospective randomized trial suggest that treatment with MMF and CsA is associated with different effects on suPAR levels in children with MCD and that these are independent of their effects on GFR.

Keywords

Nephrotic syndrome Cyclosporin A Mycophenolate mofetil Soluble urokinase-type plasminogen activator receptor (suPAR) Minimal change disease Children 

Notes

Acknowledgments

We thank all GPN members of the Nephrotic Syndrome Study Group and the local investigators of the Nephrotic Syndrome Study Group: I. Franke (Bonn), E.M. Rüth and W. Rascher (Erlangen), A.K. Büscher and P. Hoyer (Essen), M. Pohl (Freiburg), L. Pape (Hannover), R. Feneberg and B. Tönshoff (Heidelberg), J. Misselwitz (Jena), S. Wygoda (Leipzig), H. Fehrenbach (Memmingen), M. Benz, L. Weber (München), O. Schofer (Neunkirchen), M. Wigger (Rostock), A. Rudolph (Schwerin), O. Beringer (Tübingen). This work was supported by funding from the European Commission’s 7th Framework Programme (EURenOmics, grant 2012–305608).

Statement of competing financial interests

None.

Supplementary material

467_2014_2913_MOESM1_ESM.docx (63 kb)
ESM 1 (DOCX 62 kb)
467_2014_2913_MOESM2_ESM.docx (16 kb)
ESM 2 (DOCX 15 kb)

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Copyright information

© IPNA 2014

Authors and Affiliations

  • Jutta Gellermann
    • 1
  • Franz Schaefer
    • 2
  • Uwe Querfeld
    • 1
    Email author
  1. 1.Department of Pediatric Nephrology, Charité Universitätsmedizin BerlinCharité Children’s HospitalBerlinGermany
  2. 2.Division of Pediatric Nephrology, Center for Pediatrics and Adolescent MedicineUniversity of HeidelbergHeidelbergGermany

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