Background. The association between cyclosporine (CsA) and thrombotic micro
angiopathy (TMA) in renal allografts is well documented. However, predispos
ing factors and therapy guidelines are not adequately characterized.
Methods. We reviewed 188 patients with kidney or kidney-pancreas transplant
s who were treated between January 1994 and December 1996 with prednisone,
CsA, or tacrolimus, and azathioprine or mycophenolate. We analyzed 50 patie
nts who had graft biopsies: 26 with TMA and 24 with no TMA, as well as 19 p
atients with well-functioning grafts who never required biopsy.
Results. TMA was observed in 26 of 188 renal graft recipients (14%). TMA wa
s confined to the allograft kidney without any systemic evidence in 24 of t
he 26 patients. At the time of the diagnosis of TMA, 24 of the patients wer
e on CsA, with 19 on the microemulsion form. Conversely, 5 of 18 control pa
tients with no graft dysfunction were on the microemulsion form of CsA (P =
0.0026). Graft loss was seen in 8 of 26 patients with TMA. Conversion from
CsA to tacrolimus resulted in a one-year salvage of graft function in 13 o
f 16 (81%) patients.
Conclusions. TMA was the cause of renal graft dysfunction in 14% of renal g
raft recipients and was associated with the use of the microemulsion form o
f CsA. Systemic signs of TMA were rare, underscoring the importance of the
graft biopsy in making the diagnosis. The most successful strategy was swit
ching from CsA to tacrolimus, with good graft function in 81% of the recipi
ents one year after the TMA episode.