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Antibody-mediated rejection (ABMR) is a significant cause of graft loss. The diagnosis of ABMR was historically made by three criteria: morphological evidence of acute tissue injury, presence of donor-specific antibodies (DSA), and C4d staining in peritubular capillaries (PTC) (Banff).
This study aims to analyze the clinical and histological characteristics of patients (ptes) with ABMR with and without of circulating donor-specific anti-human leukocyte antigen (HLA) DSA, and graft function.
This is a retrospective single-center study (Hospital Italiano de Buenos Aires, Argentina). We analyzed 218 kidney transplant recipients from 2017 to 2019. We included 52 ptes (23%) with ABMR (Banff 2021), during the first post-transplant year. Renal allograft biopsies were performed by cause. Pre and posttransplant anti-HLA antibodies were monitored by Luminex. A positive result was defined as a median fluorescence intensity (MFI) of the donor-specific bead above 1000. Graft function was assesed by serum creatinine (mg/dl), eGFR (CKD-EPI) and proteinuria (gr/24 hs) at 1, 3 and 5 years. Univariate analysis was performed with MedCalc® Statistical Software version 22.014 (MedCalc Software Ltd, Ostend, Belgium; https://www.medcalc.org; 2023).
Out of 218 ptes, we included 52 (23%) presented ABMR. Most of them (49 (90%)) within < 3 post tx months. Median recipient age was 57 years (range 25-82), 34 were males (65,4 %) and 26 (50 %) were sensitized. 35 ptes (67%) received kidneys from deceased donors. Re-transplant ptes were 14 (26,9%), mean cold ischemia time was 13.4 hs and mean missmatch was 4,3. 24 ptes (46%) developed DGF. 9 ptes had pre-formed or de novo donor-specific antibodies (17.3%), while 43 did not (82.7%). Rejection in all ptes were treated with corticosteroids and IVIG, 45 ptes (86%) with plasmapheresis and 44 (84%) with rituximab. The renal function at 1, 3 and 5 years are presented at Table 1, and histological characteristics in Table 2. Ptes without DSA had a higher percentage of polymorphonuclear cells in glomerulus (72% vs. 42%, p 0.18).
Table 1. Graft function over time
Entire cohort (n=52)
DSA ABMR
(n=9)
nDSA ABMR
(n=43)
p-value
GFR 1° year, mean (SD)
38.0 (15.9)
34.9 (19.3)
38.7 (15.3)
0.55
Creatinine, mean (SD)
2.2 (1.5)
2.87 (2.9)
2.0 (1.0)
Proteinuria 1° year, mean (SD)
336.5 (268.8)
326.4 (259.4)
338.7 (274.4)
0.91
GFR 3° year, mean (SD)
63.1 (148.7)
32.6 (16)
35 (17)
0.63
Creatinine 3° year, mean (SD)
2.1 (0.8)
2.2 (1.0)
2.0 (0.8)
Proteinuria 3° year, mean (SD)
403 (394)
390 (195)
405 (421)
0.94
GFR 5° year, mean (SD)
37.5 (17.3)
32.0 (15.6)
38.4 (17.7)
0.50
Creatinine 5° year, mean (SD)
2.2 (0.9)
2.34 (0.6)
2.1 (1.0)
0.71
Proteinuria 5° year, mean (SD)
559 (853)
725 (876)
530 (866)
0.68
Table 2 . Comparison of the histological appearance of the ABMRh on the index biopsies, according to HLA-DSA status.
Histology
g ≥ 1, n (%)
41 (78.9)
7 (77.8)
34 (79.1)
1.0
cpt ≥ 1, n (%)
48 (92.3)
8(88.9)
40 (93.0)
0.54
mvi score ≥ 2, n (%)
6 (66.7)
35 (81.4)
0.37
v score ≥ 2, n (%)
6 (11.5)
2 (22.2)
4 (9.3)
0.27
C4d focal, n (%)
37 (71.1)
5 (55.6)
32 (74.4)
0.41
C4d diffuse, n (%)
14 (26.9)
3 (33.3)
11 (25.6)
0.69
mat, n (%)
11 (21.1)
8 (18.6)
0.38
t ≥ 1, n (%)
13 (25.5)
10 (23.8)
i ≥ 1, n (%)
23 (44.2)
4 (44.4)
19 (44.2)
ct ≥ 1, n (%)
34 (65.4)
28 (65.1)
ci ≥ 1, n (%)
43 (82.7)
36 (83.7)
0.64
cv ≥ 1, n (%)
18 (41.9)
0.48
NTA ≥ 1, n (%)
39 (75.0)
g PMN, n (%)
27 (67.5)
3 (42)
24 (72)
0.18
cpt PMN, n (%)
29 (60.4)
4 (50)
25 (62.5)
We found no significant differences in histological characteristics and graft function between both groups. ABMR without HLA-DSA is not an unusual condition.