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. 2018 Nov 29;34(7):1232–1239. doi: 10.1093/ndt/gfy350

Table 2.

Recipient, donor and transplant characteristics

Recipient
 Age (years), mean ± SD 48.2 ± 14.8 (range 18–75)
 Race
  Non-AA 106 (84.8)
  AA 19 (14.6)
 Males 79 (63.2)
 BMI (kg/m2), mean ± SD 29.0 ± 5.4
 BSA (kg/m2), mean ± SD 1.98 ± 0.26
 Cause of renal disease
  Congenital/familial 8 (6.4)
  PKD 14 (11.2)
  Glomerular 28 (22.4)
  Hypertension 17 (13.6)
  Diabetes 39 (31.2)
  Other 19 (15.2)
 Dialysis vintage
  Preemptive 28 (22.4)
  Dialysis 0–2 years 60 (48.0)
  Dialysis >2 years 37 (29.6)
 Calculated panel reactive antibody >20 22 (17.6)
 Previous transplantation 6 (4.8)
 Induction (thymoglobulin) 106 (85)
 No induction 19 (15)
 Maintenance immunosuppression
  Tacrolimus, mycophenolate mofetil, steroid 121 (96.8)
  Tacrolimus, mycophenolate mofetil 1(0.8)
  Tacrolimus, everolimus, steroid 2(1.6)
  Cyclosporine, mycophenolate, steroid 1(0.8)
Transplantation
  Living donor 84 (67.2)
  Cold ischemia time, median (IQR) 3.0 (1.7–10.0)
  HLA mismatch
   0–2 30 (24.0)
   3–4 53 (42.0)
   5–6 42 (33.6)
Donor
 Age (years), mean ± SD 40.2 ± 12.4 (range 7–64)
 Race
  Non-AA 111 (88.8)
  AA 14 (11.2)
 Males 53 (42.4)
 BMI (kg/m2), mean ± SD 26.9 ± 5.4
 BSA (kg/m2), mean ± SD 1.86 ± 0.28

Values presented as n (%) unless stated otherwise. Diseases included congenital/familial (prune belly, renal hypoplasia, medullary cystic disease, renal agenesis, congenital obstructive uropathy), glomerular (IgA, FSGS, membranous, SLE, Wegner’s granulomatosis, Alport’s, chronic glomerulonephritis, Henoch–Schöenlein purpura) and other (lithium toxicity, pyelonephritis, obstructive uropathy, interstitial nephropathy, unknown).

AA, African American; BMI, body mass index; PKD, polycystic kidney disease; HLA, human leukocyte antigen; FSGS, focal segmental glomerulosclerosis; SLE, systemic lupus erythematosus.