Purpose: High renal resistance (RR) and low flow of donor kidney on hypothermic machine perfusion (HMP) may not be accepted for transplant. High doses of tacrolimus may induce acute high RR and low flow of renal graft. This kind of graft could be utilized for transplant. Here, we report 2 kidney transplants using grafts with high RR and low flow which came from a donation after circulatory death (DCD) donor who was a previous bilateral lung recipient.
Methods: A 34-y female had a bilateral lung transplant 1.5 years ago. High doses of tacrolimus were administered for uncontrolled rejection recently. Once end-of-life decisions were made, DCD donation was coordinated following authorization from the legal next of kin. No abnormal results (K 3.6-3.9, BUN 21-27, Creatinine (Cr) 0.83-1.14, Cr Clearance 60.9-83.68) were observed except urine output (UO) decreased from 107 mL/h to 8.8mL/h in 3 days. KDPI was 59%. 2 DCD kidneys were procured with 56 mins of warm ischemia time (WIT). Both kidneys were connected to HMP for 8 hours.  The RR were right (R) 0.76-1.20 and  left (L) 0.63-0.78 mmHg/mL/min; the flows of were 11-45 (R) and 32-38 (L) mL/min. Both kidneys were accepted for transplant.
Results: Both kidneys were transplanted successfully. The cold ischemia time (CIT) were (R) 47.2 and (L) 42.8 hours. Both recipients had delayed graft function (DGF). Patients were discharged home with functioning grafts at 4 and 5-days post-transplant. Pre-transplant creatinine (Cr) of recipients were 4.4 and 7.2 mg/dL (with dialysis). Cr of recipients at discharge were 3.6 and 7.6 mg/dL (with dialysis due to DGF). At 1-week following-up post-transplant, Cr were 5.9 and 9.4 mg/dL (without dialysis). At 4-month following-up, Cr were 3.0 and 4.2 mg/dL. Both kidneys had a good quantity of UO daily, and dialysis was not required after discharge. Longer CIT (due to allocation) might have contributed to the DGF in these 2 patients. Reducing CIT may decrease the risk of DGF. For most renal allografts experiencing CIT >40 h, urine production usually preceeds creatinine filtration by several days to weeks. Tacrolimus decreases glomerular filtration rate by promoting angiotensin II, decreasing production of vasodilating prostaglandin E2 and nitric oxide, specific vasoconstriction in afferent arterioles, which may result in a high RR and low flow of kidney during HMP. The terminal elimination half-life of tacrolimus is approximately 12 hours (with a range of 3.5 to 40.5). We believe this donor’s kidneys exhibited high RR because of tacrolimus, which was reversible “acute tacrolimus-induced vasoconstriction”, not from irreversible chronic tacrolimus-induced nephrotoxicity of kidney.
Conclusions: Transplantation of kidneys with high RR and low flow on HMP from donors with previous non-kidney solid organ transplants may be utilized for transplantation and may represent an underutilized organ source. A larger study should be considered.