In a 60-year-old male who received a deceased‑donor kidney transplant and within minutes the graft turned mottled, flaccid and blue with arterial flow but no venous outflow, accompanied by severe coagulopathy (aPTT >100 seconds, high D‑dimer, hyperkalemia, metabolic acidosis, diffuse bleeding), what is the most likely diagnosis?

Catastrophic Renal Vein Thrombosis with Secondary DIC

This is renal vein thrombosis (RVT) with secondary disseminated intravascular coagulation (DIC), not primary ABMR or thymoglobulin-induced DIC. The immediate intraoperative urine output followed by sudden cessation, the finding of arterial pulses but absent venous flow on re-exploration, and the flabby blue kidney are pathognomonic for acute RVT 1.

Clinical Reasoning

The Vascular Catastrophe

The sequence of events is classic for RVT:

• Initial good output (400 mL in 30 minutes) indicates the kidney was viable initially
• Sudden cessation of output within 30 minutes is the hallmark warning sign of acute vascular compromise 1
• Re-exploration findings are diagnostic: arterial pulses present but no venous flow, flabby blue kidney with no venous return on flushing 1

This is not hyperacute antibody-mediated rejection (ABMR) because:

• ABMR would show immediate thrombosis from the moment of reperfusion, not delayed 30 minutes
• The kidney had excellent initial function with immediate diuresis
• ABMR typically presents with diffuse cortical necrosis and immediate non-function, not this pattern

The Coagulopathy is Secondary

The DIC developed secondary to the massive tissue necrosis and ischemia from the thrombosed kidney, not as a primary event 2, 3. Your laboratory findings confirm overt DIC by the 2025 ISTH criteria 2:

• D-dimer >10 (>7× upper limit = 3 points)
• aPTT >100 seconds (prolonged PT/aPTT)
• Platelet consumption (though not severe drop yet)
• Fibrinogen consumption requiring cryoprecipitate

The progression was:

1. RVT occurs → venous outflow obstruction
2. Kidney becomes ischemic and necrotic → massive tissue factor release
3. Systemic coagulation activation → consumption of clotting factors
4. Overt hemorrhagic DIC → diffuse oozing, coagulopathy

Why Not Thymoglobulin-Induced DIC?

Only 25 mg of thymoglobulin was infused before hypotension developed. While thymoglobulin can cause cytokine release syndrome and rarely DIC, this would:

• Present earlier during infusion
• Not explain the specific vascular findings (arterial flow present, venous absent)
• Not cause sudden cessation of urine output in a previously functioning kidney

Why Not Sepsis?

• Procalcitonin 0.6 argues strongly against bacterial sepsis
• Timeline too rapid (surgery at 12:30 AM, catastrophic by 2:30 AM)
• No identified source despite "all antibiotics in the world"

Risk Factors Present in This Case

This patient had multiple risk factors for RVT 1, 4:

• Deceased donor with prolonged ischemia time (on ventilator 2 days)
• Recipient hypercoagulable state: diabetes, CAD, PVD, recent pituitary surgery
• Technical factors: The donor had renal artery stenosis noted on CT angio, suggesting vascular disease that may have extended to venous system
• Hemodynamic instability: Baseline BP 130/90 dropped to 100/60 at extubation, compromising venous return

The Catastrophic Progression

Even after nephrectomy at 4 AM, the DIC continued to worsen because:

• Massive tissue factor and cytokine release had already occurred
• Consumption coagulopathy was established
• Metabolic derangements (K+ 7.6, lactate 9) indicate systemic inflammatory response syndrome (SIRS)
• The hemorrhagic phenotype of DIC was fully manifest with diffuse oozing 2

The drop in hemoglobin from 10.5 to 5.5 post-dialysis reflects ongoing consumption and dilution despite transfusions.

Management Considerations (Though Prognosis Dire)

Immediate priorities:

1. Aggressive DIC management 2, 3:

   • Continue FFP, cryoprecipitate, platelets to maintain fibrinogen >100 mg/dL
   • Target INR <1.5, platelets >50,000

2. Hyperkalemia management (K+ 7.6) 5:

   • Calcium for cardiac membrane stabilization
   • Insulin/dextrose for intracellular shift
   • Continue dialysis as needed

3. Hemodynamic support:

   • Vasopressors to maintain perfusion
   • Judicious fluid resuscitation (already causing hemodilution)

4. Source control achieved: Nephrectomy removed the necrotic tissue source

Common Pitfalls

• Mistaking RVT for ABMR: The key is the temporal sequence—initial function followed by sudden cessation
• Delaying re-exploration: The 2-hour window from output cessation (12:30 AM) to exploration (2:30 AM) was appropriate, but RVT has very poor salvage rates even with immediate intervention 1, 4
• Attributing all complications to immunosuppression: Only 25 mg thymoglobulin was given; this is insufficient to cause primary DIC

Outcome Reality

Renal vein thrombosis requiring nephrectomy has dismal outcomes 1, 4. Only 1 of 3 RVT cases in one series was salvaged, and all developed delayed graft function. Your patient's progression to multi-organ dysfunction (coagulopathy, metabolic acidosis, hyperkalemia, shock) within hours indicates the severity of the systemic insult from the necrotic kidney and subsequent DIC.

The mortality from this combination of RVT, emergency nephrectomy, and overt hemorrhagic DIC is extremely high, as you recognize clinically.