Table 1.
Characteristics/Findings | Allograft Injury Group (n=103) | Normal Control Group (n=20) |
---|---|---|
Donor age, yr, median (IQR) | 51 (43–56) | 50 (45–52) |
Donor sex, male, n (%) | 40 (39) | 10 (50) |
Recipient age, yr, mean (±SD) | 38±10 | 35±9 |
Recipient sex, male, n (%) | 73 (71) | 16 (80) |
Causes of ESKD | ||
Unknown, n (%) | 74 (72) | 15 (75) |
Glomerulonephritides, n (%) | 21 (20) | 4 (20) |
Other, n (%) | 8 (8) | 1 (5) |
Transplant type | ||
Living donor kidney transplant, n (%) | 44 (43) | 9 (45) |
Deceased donor kidney transplant, n (%) | 59 (57) | 11 (55) |
Immunosuppressive regimens | ||
Pre+MMF+FK506, n (%) | 74 (72) | 17 (85) |
Pre+MMF+CsA, n (%) | 13 (13) | 2 (10) |
Other, n (%) | 16 (15) | 1 (5) |
Serum creatinine, mg/dl, median (IQR) | 1.9 (1.4–2.6) | 1.2 (1.0–1.3) |
eGFR, ml/min per 1.73 m2, median (IQR) | 47 (21–61) | 81 (71–85) |
Proteinuria, g/24 h, median (IQR) | 0.5 (0.3–1.5) | 0.2 (0.1–0.3) |
Hemoglobin level, g/dl, mean (±SD) | 11.5±2.2 | 13.9±2.5 |
Concomitant antihypertensives | ||
Renin-angiotensin blockers, n (%) | 34 (33) | 3 (15) |
Calcium channel blockers, n (%) | 58 (56) | 10 (50) |
β-Blockers, n (%) | 31 (30) | 9 (45) |
Diuretics, n (%) | 4 (4) | 0 (0) |
α-Receptor antagonists, n (%) | 9 (9) | 2 (10) |
Main pathologic diagnoses in the allograft injury group | IgA nephropathy (n=22); chronic active AMR (n=17); IF/TA (n=10); acute AMR (n=6); BK virus nephropathy (n=6); CNI toxicity (n=6); acute mixed rejection (n=5); FSGS (n=5); donor-derived changes (n=5); idiopathic thrombotic microangiopathy (n=5); T cell–mediated rejection (n=5); glomerulosclerosis (n=3); transplant glomerulopathy suspicious for chronic AMR (n=3)a; MN (n=3); PGNMID (n=1); MPGN (n=1) |
IQR, interquartile range; Pre, prednisone; MMF, mycophenolate mofetil; FK506, tacrolimus; CsA, cyclosporine A; AMR, antibody-mediated rejection; IF/TA, interstitial fibrosis/tubular atrophy; CNI, calcineurin inhibitor; MN, membranous nephropathy; PGNMID, proliferative GN with monoclonal IgG deposits; MPGN, membranoproliferative glomerulonephritis.
In these three cases, both glomerulitis (g) and peritubular capillaritis (ptc) were present and g+ptc≥2, in addition to the histologic finding of glomerular capillary duplication. However, panel reactive antibody screening was negative, making the diagnosis of antibody-mediated rejection likely but not definitive according to the criteria outlined in the 2015 Banff Schema.