Acute Renal Failure in a Kidney Donor

A 34-year-old man was shocked by a Taser stun gun. The man became unresponsive and was transferred to the hospital. Past medical history is significant for depression, including clonazepam, zopiclone and concerta as medication. He is a known alcohol and drug addict. Laboratory parameters at admission: increased blood and urine levels for amphetamines (ethanol, cocaine, barbiturate and opiate screens were negative), troponin 3.5 μg/L (normal: < 0.15 μg/L), serum creatinine 1.60 mg/dL (normal: 0.56–1.3 mg/dL), urine output <30 cc/h, creatine phosphokinase 60,000 U/L (normal: <250), phosphorus level 2.87 mmol/L (normal: 0.80–1.45 mmol/L) and potassium 5.5 mmol/L (normal: 3.5–5.0 mmol/L). The patient was declared brain dead 2 days postadmission and was considered as an organ donor. Prior to organ procurement, a renal biopsy was done in the donor, who showed further decline in kidney function (urine output <10 cc/h, serum creatinine 4.80 mg/dL). Histology findings are demonstrated in Figure 1. A 70-year-old nonsensitized man of identical blood group (A to A) was selected as recipient for both kidneys; a decision was made to not transplant the right kidney secondary to complex vascular anatomy, and thus only the left kidney was successfully transplanted. Induction therapy consisted of rabbit ATG and maintenance therapy of MMF, tacrolimus and prednisone. The recipient had delayed graft function with severe oliguria (urine output <10 cc/h) requiring hemodialysis prompting another allograft biopsy on day 10 posttransplantation (Figure 2). After more than 3 weeks of hemodialysis, allograft function improved gradually, and at 3 months posttransplantation, the creatinine stabilized at 1.22 mg/dL. 1What is the most likely causative factor of acute kidney failure in this donor?aAcute tubular injury secondary to ischemiabAcute tubular injury secondary to nephrotoxinscAcute tubular injury secondary to myoglobin and hemoglobin castsdAcute tubulo-interstitial nephritiseAcute thrombotic microangiopathy2What is the most likely cause of a persistently increased creatinine in the recipient?aCyclosporine toxicitybHyper-acute antibody-mediated rejectioncAcute T cell–mediated rejectiondDelayed graft function due to severe acute tubular injury in the donoreReactivation of cytomegalovirus in the kidney transplant3The following morphologic feature is NOT associated with acute tubular injury:aThickening of the tubular basement membranebThinning and/or detachment of tubular epithelium from underlying tubular basement membranecLoss of PAS-positive brush border of proximal tubular epithelial cellsdDilatation of the tubular luminaeMinimal tubulitis, i.e. single inflammatory cells infiltrating the tubular epithelium4Based on the history of this deceased donor, which of the following is NOT a common cause of rhabdomyolysis?aDrugsbExcessive muscular injurycCrush injurydViral infectioneElectrical current5Which of the following metabolic disorders is observed in patients with rhabdomyolysis?aHyperkalemiabHypophosphatemiacMetabolic alkalosisdHypouricemiaeHypernatremia

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