Myoglobin Cast Nephropathy as an Incidental Finding in Kidney Biopsy for Slow Graft Function (SGF)

Introduction: Slow graft function (SGF) is a common complication following kidney transplantation and is associated with poorer long-term graft outcomes. While multiple donor and recipient factors are known contributors, we report an unexpected and rare etiology of SGF identified on post-transplant biopsy. Case Description: A 62-year-old male with stage 5 CKD due to lithium toxicity underwent a preemptive deceased donor kidney transplant. The donor was a 35-year-old woman at 32 weeks’ gestation who suffered brain death following a witnessed seizure, raising concern for eclampsia, and experienced prolonged cardiac arrest (downtime >30 minutes). She developed oligo-anuric kidney failure requiring continuous renal replacement therapy. Her creatinine rose from 1.3 to a peak of 2.5 mg/dL, with a terminal value of 1.4 mg/dL. Biopsy showed 24 glomeruli without hyalinosis, necrosis, thrombi, or vascular disease during intraoperative frozen section evaluation. Immunohistochemical stain for myoglobin was not performed. Cold and warm ischemia times were 1204 and 48 minutes, respectively. The recipient received alemtuzumab induction and maintenance immunosuppression with tacrolimus, mycophenolate mofetil, and prednisone. Postoperatively, the recipient developed SGF. Allograft biopsy on post-transplant day 8 revealed acute tubular injury with intratubular myoglobin casts. The recipient was chronically on atorvastatin, but serum creatine kinase (CK) levels remained normal. Donor CK and urinalysis were unavailable due to oligoanuria. The recipient’s kidney function gradually improved, with a creatinine of 1.58 mg/dL at four months post-transplant. Discussion: This case highlights a rare, donor-derived cause of SGF: myoglobin cast nephropathy. The donor’s prolonged cardiac arrest and suspected eclampsia likely led to skeletal muscle breakdown, myoglobin release, and nephrotoxicity. Unlike prior reports where rhabdomyolysis-related AKI was known in the donor, this diagnosis emerged unexpectedly on post-transplantation biopsy. The absence of recipient rhabdomyolysis supports a donor-origin process.