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Is sirolimus responsible for proteinuria?

T Dervaux1, S Caillard, C Meyer

  • 1Service de Néphrologie et Transplantation, CHU Strasbourg, France. thomas.dervaux@chru-strasbourg.fr

Transplantation Proceedings
|September 27, 2005
PubMed
Summary
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Sirolimus (SRL) did not cause proteinuria in liver transplant recipients. In kidney transplant patients, a slight increase in proteinuria was linked to calcineurin inhibitor withdrawal, not SRL.

Area of Science:

  • Nephrology
  • Transplantation
  • Pharmacology

Background:

  • Sirolimus (SRL) is a mammalian target of rapamycin (mTOR) inhibitor used in transplantation.
  • Proteinuria is a potential adverse effect of immunosuppressive agents.

Purpose of the Study:

  • To investigate the incidence and evolution of proteinuria in liver and kidney transplant recipients switched to SRL.
  • To determine the association between SRL, calcineurin inhibitors (CNI), and proteinuria.

Main Methods:

  • Retrospective study of 59 liver and kidney transplant recipients.
  • Data collected on proteinuria, estimated glomerular filtration rate (eGFR), antiproteinuric drug use, and SRL, cyclosporine (CsA), and tacrolimus (FK) serum concentrations.
  • Analysis of changes in proteinuria correlated with SRL and CNI levels.

Related Experiment Videos

Main Results:

  • No new proteinuria was detected in liver transplant recipients; proteinuria remained stable in others.
  • A slight increase in proteinuria occurred in 14 kidney transplant recipients (0.57 +/- 0.93 g/d to 1.83 +/- 1.26 g/d).
  • eGFR remained stable; proteinuria variation correlated with decreased CsA/FK levels, not SRL levels.

Conclusions:

  • SRL did not appear to induce proteinuria in liver transplant recipients without prior renal damage.
  • The observed increase in proteinuria in some kidney transplant patients was associated with CNI withdrawal, likely due to hemodynamic renal effects.