There is evidence that treatment with m-TOR inhibitors can be beneficial in cases of chronic renal allograft dysfunction. However, some authors have reported poor outcomes of renal function if the switch to m-TOR inhibitors is made in the presence
proteinuria > 0.8 g/d. The present study sought to provide a retrospective analysis of the clinical outcome of 63 kidney recipients diagnosed with chronic allograft dysfunction whose
therapy was converted to
rapamycin including 35 subjects with renal biopsy-proven chronic allograft nephropathy. At the time of conversion, patients were divided into three groups: group I (negative
proteinuria), group II (
proteinuria between 0.3 and 0.8 g/d), and group III (
proteinuria > 0.8 g/d). On conversion, 21 recipients had no
proteinuria (group I). After a follow-up of 24.6 +/- 12.8 months, they showed a significant improvement in renal function (previous MDRD4 = 39.9 +/- 11.5 mL/m/1.73 m(2), current MDRD4 50.3 +/- 13.3 mL/m/1.73 m(2), P < .05). Fifteen patients (71.4%) developed
proteinuria, which was generally mild (0.8 +/- 0.7 g/d) and controlled with
angiotensin-converting enzyme inhibitors (42.8%). In group II (n = 18), renal function clearly stabilized after a follow-up of 23.2 +/- 14.4 months (previous MDRD4 = 30 +/- 8.8 mL/m/1.73 m(2), current MDRD4 = 37 +/- 12.2 mL/m/1.73 m(2), NS), although there was a progressive deterioration of previous
proteinuria levels (previous
proteinuria 0.4 +/- 0.15 g/d, current
proteinuria 1.2 +/- 2 g/d, P < .05), which was more frequent and intense in patients whose treatment with
calcineurin inhibitors (CNIs) was suspended (with CNI 0.9 +/- 1.7 g/d, without CNI 1.6 +/- 2.2 g/d, P < .05). Group III (n = 24) had a greater degree of
renal insufficiency and a worse outcome after 25.9 +/- 18 months of follow-up, with a frank and progressive deterioration in renal function (previous MDRD4 = 38 +/- 17 mL/m/1.73 m(2), current MDRD4 = 32.5 +/- 19.2 mL/m/1.73 m(2), P < .05) and
proteinuria (previous
proteinuria = 1.5 +/- 0.7 g/d, current
proteinuria = 2.5 +/- 2.2 g/d, P < .05) after conversion. Again, the deterioration in
proteinuria was more intense in the patients whose previous CNIs were suspended (with CNI = 1.1 +/- 0.9 g/d, without CNI = 4.2 +/- 2.3 g/d, P < .05). In conclusion, for patients with chronic allograft dysfunction who do not present with
proteinuria or whose
proteinuria is less than 0.8 mg/d, switching to
rapamycin is useful, since it clearly improves or stabilizes renal function, although there may be a discrete increase in
proteinuria in the second case. However, among patients with
proteinuria greater than 0.8 mg/d accompanied by a greater degree of
renal insufficiency, conversion to
rapamycin leads to deterioration of
proteinuria levels and renal function. These data show that conversion to
rapamycin in cases of chronic allograft dysfunction must be made early when there is no
proteinuria or it is minimal, and that
proteinuria is a predictor of the outcome of allograft function.