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NDT Advance Access first published online on September 5, 2006
This version published online on September 19, 2006
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfl447
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received June 21, 2006
Accepted June 28, 2006

Original Article

Increase of proteinuria after conversion from calcineurin inhibitor to sirolimus-based treatment in kidney transplant patients with chronic allograft dysfunction

Juan Carlos Ruiz 1 *, Josep M. Campistol 2, Ana Sánchez-Fructuoso 3, Constantino Rivera 4, Juan Oliver 4, David Ramos 5, Begoña Campos 6, Manuel Arias 1, and Fritz Diekmann 7

1 Department of Nephrology, Hospital Universitario Marqués de Valdecilla, Santander, Spain
2 Department of Nephrology, Hospital Clínic, Barcelona, Spain
3 Department of Nephrology, Hospital Clínico Universitario, Madrid, Spain
4 Department of Nephrology, Hospital Juan Canalejo, A Coruña, Spain
5 Department of Nephrology, Hospital La Fé, Valencia, Spain
6 Department of Biostatistics, Universidad de Barcelona, Barcelona, Spain
7 Department of Nephrology, Hospital Clínic, Barcelona, Spain; Department of Nephrology, Charite Campus Mitte, Berlin, Germany

* To whom correspondence should be addressed.
Juan Carlos Ruiz, E-mail: ruizjc{at}humv.es



  Abstract

Background. Conversion from calcineurin inhibitor to sirolimus, rapamycin has become an option in patients with chronic allograft dysfunction (CAD). However, in many cases an increase of proteinuria has been observed. The aim was to characterize the course of this so far unexplained proteinuria after conversion.

Methods. In 149 renal transplant patients from various Spanish centres, proteinuria and renal function were analysed 6 months before until 6 months after conversion. Patients were divided into three groups according to mean proteinuria before conversion (1: ≤300 mg/day; 2: >300-3500 mg/day; 3: >3.5 g/day).

Results. Generally patients showed an increase of proteinuria from 864 ± 1441 (0-12125) to 1541 ± 1878 (0-10976) mg/day after conversion; P < 0.001. Group 1: 145 ± 92 vs 669 ± 868 mg/day, P < 0.001; group 2: 1041 ± 799 vs 1995 ± 2021 mg/day, P < 0.001; group 3: 6205 ± 3184 vs 4859 ± 2122 mg/day, P = NS. Patients with an increase of proteinuria of >500 mg/day (n = 60; 40%) had a higher serum creatinine before conversion compared with patients with no or moderate increase (2.5 ± 0.8 vs 2.15 ± 0.72 mg/dl; P = 0.002). The group that experienced an increase >500 mg/day had a higher serum creatinine after conversion compared with the patients with no or moderate increase (2.8 ± 1.0 vs 2.1 ± 1.2; P < 0.001). Of 64 patients, 19 in group 1 showed an increase >500 mg/day.

Conclusion. Conversion for CAD can be associated with an increase of proteinuria in patients with pre-existing renal damage; however, it preserves renal function in patients with better creatinine and proteinuria before conversion, and might not be of benefit if advanced loss of renal function and high proteinuria are already present before conversion.

Keywords: calcineurin inhibitor; chronic allograft dysfunction; conversion; mTOR inhibitor; proteinuria; sirolimus.

This version contains the corrected last author name.


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