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Medical Science Monitor Basic Research


eISSN: 2329-0358

Comparing graft function for tacrolimus- and cyclosporine-treated patients. A long-term comparative study involving nephrotoxicity markers

Z. Marchewka, J. Kuźniar, K. Falkiewicz, B. Szymańska, M. Zynek-Litwin, D. Patrzałek, A. Długosz, M. Klinger

Ann Transplant 2008; 13(1): 43-43

ID: 880211

Available online:


Background: The study compares the effect of cyclosporine and tacrolimus treatment on the transplanted kidney.
Material/Methods: This is done by examining nephrotoxicity markers in urine: lysosomal enzymes of proximal tubular cells (NAG, NAG-B, GAL, b-Gr) and brush border enzymes (AAP, GGT). The study involved 120 CsA-treated and 99 TAC-treated patients. Patients groups were identified depending on the time since transplantation (I - up to 1 year after transplantation; II - 1-2 years; III - 2-3 years; IV - more than 3 years). The control group consisted of 31 healthy people. Urine marker levels for CsA- and TAC-patients were examined in each group. For each group the study focused on correlation between markers' density and graft function as well as between CsA and TAC whole blood levels and the enzymes activity.
Results: In TAC group the time from transplantation was found to correlate negatively with creatinine level. No such association was found for CsA-treated group. NAG and NAG-B urine activity was significantly lower in control group. Peak enzyme activity for both CsA- and TAC-treated patients occurred in group I. As for groups III and IV, NAG-B excretion was found higher for the CsA group. NAG activity in urine and serum creatinine level were correlated significantly in CsA group (p<0.05). Similar correlation was found in TAC-group, but it was not significant. NAG urine activity was shown to correlate negatively with the time after transplantation (p<0.001) in TAC group.
Conclusions: The study favours tacrolimus-based treatment.
NAG and NAG-B appear to be the best CsA and TAC nephrotoxicity markers.

Keywords: Cyclosporine, Tacrolimus, Cerebral Palsy, Factor V Leiden mutation, Prothrombin G20210A mutation,