#5393 INFLUENCE OF CELLULAR INFLAMMATION ON THE OUTCOME OF KIDNEY TRANSPLANTATION AFTER RECURRENCE OF IGA NEPHROPATHY

Abstract

Abstract Background and Aims The recurrence of IgA nephropathy (rIgAN) worsens the prognosis of renal transplantation, representing the third cause of loss in these recipients. Several variables at the time of recurrence, such as worse renal function, greater proteinuria, previous steroid withdrawal, and MEST-C histological findings have been associated with a higher risk of graft loss after recurrence. The presence of clinical or subclinical inflammation has been associated with a higher risk of kidney graft loss, but it is not precisely known how it influences the outcome of patients with rIgAN. Method A multicenter retrospective study was carried out including renal transplant recipients with biopsy-proven IgA nephropathy as the underlying disease in which the recurrence of the primary disease had been verified by means of graft biopsy and in which the Banff criteria were available or could be reviewed. Cellular inflammation was defined according to Banff scores as “t” or “i” ≥2. The main endpoint was progression to CKD stage 5 or death censored-graft loss (DCGL). Results 118 kidney transplant recipients were included with an age of 47 ± 14 years at recurrence, 80% male, with a mean time to biopsy of 65 ± 69 months and a post-transplant follow-up of 118 ± 70 months. After recurrence, 34 (28.8%) transplants were lost after 35 ± 28 months, excluding death. Using univariate Cox regression, the factors related to CKD stage 5 or graft loss were systolic blood pressure (HR 1.039, 95%CI 1.016-1.064, p = 0.001), glomerular filtration rate (HR 0.948, 95%CI 0.922-0.974, p <0.001), the logarithm of proteinuria (HR 15.836, 95% CI 5.504-45.565, p < 0.001), Oxford-C score (HR 3.490, 95% CI 2.137-5.699, p <0.001), interstitial fibrosis (HR 2.173, 95% CI 1.362-3.468, p = 0.001) and cellular inflammation (HR 2.458, 95% CI 1.237-4.884, p = 0.010). After multivariate analysis, cellular inflammation remained significantly related to CKD stage 5 or DCGL (HR 2.338, 95% CI 1.077-5.075, p = 0.032). independently of systolic blood pressure, glomerular filtration rate, the logarithm of proteinuria and Oxford-C score. Conclusion In addition to the previously described factors usually related to worse evolution of IgA nephropathy in the native kidney and after post-transplant recurrence, we observed that cellular inflammation influences worse evolution after rIgAN. We suggest to considering the Banff criteria for acute cellular inflammation to better understand the subsequent evolution of patients with rIgAN.