Back
Recurrent IgA nephropathy (IgAN) following renal transplantation might be asymptomatic, and not detected without protocol biopsies to demonstrate glomerular IgA deposits. There is widespread variation in the reported incidence of recurrent IgAN and associated graft loss.
The use of corticosteroids has been identified as being protective, but the association of steroids and graft loss is conflicting. There are no studies comparing basiliximab and alemtuzumab induction.
In this single centre study we aimed to identify incidence of recurrent IgAN and graft loss, and their associated factors.
Search of our electronic database for ‘recurrent IgAN’ in transplant biopsies identified 40 cases between 2010 and 2021.
We looked at time from transplant to biopsy-proven disease recurrence, and transplant to death-censored graft loss.
Electronic patient records were examined to determine donor type, HLA mismatch, induction immunosuppression, maintenance immunosuppression, steroid therapy and duration (up to 3 months versus greater than 3 months). These variables were correlated with time from transplant to biopsy-proven disease recurrence, and transplant to death-censored graft loss.
There were 21 living and 19 cadaveric donors. 23 patients received basiliximab induction and 16 received alemtuzumab. One patient did not receive induction as they received the transplant from an identical twin.
24 patients had steroid exposure, 10 of whom received steroids for <3 months and 14 for >3 months.
Our centre incidence of recurrent IgAN was 21% in a 11-year-period.
The average time to recurrence was 6.7 years. Recurrence at 1, 5 and 10 years was 22%, 52%, 87% respectively.
Steroid use was associated with a delay in recurrence of 4.6 years. Duration of steroid use was not associated with time to recurrence (graph 2).
There was a significant difference in time to recurrence according to induction immunosuppression (p< 0.005). Mean time to recurrence was 9.7 years with basiliximab versus 2.8 years with alemtuzumab (graph 3).
55% patients lost their graft with an average time to graft loss of 8.2 years. Graft loss at 1, 5 and 10 years was 2%, 18% and 38% respectively.
The use of steroids was associated with a trend to delayed graft loss, although this was statistically insignificant (graph 4). There is no association between duration of steroid therapy and time to graft loss (graph 5)
Basiliximab was associated with a delayed graft loss compared to alemtuzumab (p=0.01). Mean graft loss in the basiliximab group was 12 years versus 4.7 years with alemtuzumab (graph 6)
Our retrospective single centre study demonstrates that patients receiving basiliximab induction have a significantly lower incidence of IgAN recurrence and graft loss post transplantation compared to those receiving alemtuzumab induction. A potential confounding factor is the increased use of steroids in patients receiving basiliximab which might explain the apparent protective effect of steroids on IgAN recurrence in our cohort. Steroid use as part of a maintenance regimen was associated with lower incidence of IgAN recurrence however duration of steroid treatment beyond a total of 3 months showed no protective benefit. These data suggest choice of induction agent may be the dominant factor in risk of IgAN recurrence and further analysis is required to investigate this.