Kidney transplantation US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Kidney transplantation. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Kidney transplantation US Medical PG Question 1: A 31-year-old female receives a kidney transplant for autosomal dominant polycystic kidney disease (ADPKD). Three weeks later, the patient experiences acute, T-cell mediated rejection of the allograft and is given sirolimus. Which of the following are side effects of this medication?
- A. Nephrotoxicity, hypertension
- B. Hyperlipidemia, thrombocytopenia (Correct Answer)
- C. Nephrotoxicity, gingival hyperplasia
- D. Pancreatitis
- E. Cytokine release syndrome, hypersensitivity reaction
Kidney transplantation Explanation: ***Hyperlipidemia, thrombocytopenia***
- **Sirolimus** (rapamycin) is an **mTOR inhibitor** commonly used in transplant immunology, which frequently causes **hyperlipidemia** (elevated cholesterol and triglycerides) and **thrombocytopenia** (low platelet count).
- Other common side effects include **myelosuppression** (leukopenia, anemia), **mouth ulcers**, and **impaired wound healing**.
*Nephrotoxicity, hypertension*
- **Nephrotoxicity** and **hypertension** are more characteristic side effects of **calcineurin inhibitors** like **tacrolimus** and **cyclosporine**, which are also used in transplant immunosuppression but have a different mechanism of action than sirolimus.
- While sirolimus can indirectly affect kidney function, it is generally considered less nephrotoxic than calcineurin inhibitors.
*Nephrotoxicity, gingival hyperplasia*
- **Gingival hyperplasia** is a hallmark side effect of **cyclosporine**, a calcineurin inhibitor, along with **hirsutism** and **nephrotoxicity**.
- Sirolimus does not typically cause gingival hyperplasia.
*Pancreatitis*
- While some immunosuppressants can rarely cause pancreatitis, it is not a common or characteristic side effect of **sirolimus**.
- **Azathioprine** is more frequently associated with pancreatitis among immunosuppressive agents.
*Cytokine release syndrome, hypersensitivity reaction*
- **Cytokine release syndrome** and acute **hypersensitivity reactions** are more often associated with **monoclonal antibodies** (e.g., **basiliximab**, **daclizumab**) used for induction therapy or treatment of acute rejection, particularly within hours or days of administration.
- Sirolimus is less likely to cause these immediate severe reactions.
Kidney transplantation US Medical PG Question 2: A 62-year-old female with a history of uncontrolled hypertension undergoes kidney transplantation. One month following surgery she has elevated serum blood urea nitrogen and creatinine and the patient complains of fever and arthralgia. Her medications include tacrolimus and prednisone. If the patient were experiencing acute, cell-mediated rejection, which of the following would you most expect to see upon biopsy of the transplanted kidney?
- A. Granular immunofluorescence around the glomerular basement membrane
- B. Lymphocytic infiltrate of the tubules and interstitium (Correct Answer)
- C. Crescent formation in Bowman’s space
- D. Drug precipitation in the renal tubules
- E. Sloughing of proximal tubular epithelial cells
Kidney transplantation Explanation: ***Lymphocytic infiltrate of the tubules and interstitium***
- **Acute cell-mediated rejection** is primarily characterized by the infiltration of **T lymphocytes** and macrophages into the allograft, leading to inflammation and damage.
- This cellular infiltrate is typically observed in the **interstitium and tubules** of the transplanted kidney.
*Granular immunofluorescence around the glomerular basement membrane*
- This finding is characteristic of **immune complex-mediated glomerulonephritis**, such as post-streptococcal glomerulonephritis, and signifies deposition of immune complexes.
- It is not typical of acute cell-mediated rejection, which is driven by T-cells rather than circulating immune complexes.
*Crescent formation in Bowman’s space*
- **Crescents** in Bowman's space are indicative of rapidly progressive glomerulonephritis (RPGN), a severe form of glomerular inflammation usually associated with conditions like Goodpasture syndrome or ANCA-associated vasculitis.
- While crescentic glomerulonephritis can cause acute kidney injury, it is not the primary histological hallmark of acute cell-mediated transplant rejection.
*Drug precipitation in the renal tubules*
- **Drug precipitation** can occur with certain medications, leading to acute kidney injury (e.g., sulfonamides, methotrexate), but it is a chemical injury, not an immune-mediated rejection process.
- The patient's symptoms of fever and arthralgia, along with elevated creatinine, point towards an inflammatory immune response rather than drug toxicity alone.
*Sloughing of proximal tubular epithelial cells*
- **Sloughing of proximal tubular epithelial cells** is a hallmark of **acute tubular necrosis (ATN)**, often caused by ischemia or nephrotoxic agents.
- While ATN can also lead to elevated creatinine, the presence of fever and arthralgia, plus the context of transplantation, makes acute cell-mediated rejection a more likely diagnosis.
Kidney transplantation US Medical PG Question 3: A 45-year-old woman comes to the physician because of a 3-month history of worsening fatigue, loss of appetite, itching of the skin, and progressive leg swelling. Although she has been drinking 2–3 L of water daily, she has been passing only small amounts of urine. She has type 1 diabetes mellitus, chronic kidney disease, hypertension, and diabetic polyneuropathy. Her current medications include insulin, torasemide, lisinopril, and synthetic erythropoietin. Her temperature is 36.7°C (98°F), pulse is 87/min, and blood pressure is 138/89 mm Hg. She appears pale. There is 2+ pitting edema in the lower extremities. Sensation to pinprick and light touch is decreased over the feet and legs bilaterally. Laboratory studies show:
Hemoglobin 11.4 g/dL
Leukocyte count 6000/mm3
Platelet count 280,000/mm3
Serum
Na+ 137 mEq/L
K+ 5.3 mEq/L
Cl− 100 mEq/L
HCO3− 20 mEq/L
Urea nitrogen 85 mg/dL
Creatinine 8 mg/dL
pH 7.25
Which of the following long-term treatments would best improve quality of life and maximize survival in this patient?
- A. Peritoneal dialysis
- B. Living donor kidney transplant (Correct Answer)
- C. Cadaveric kidney transplant
- D. Hemofiltration
- E. Fluid restriction
Kidney transplantation Explanation: ***Living donor kidney transplant***
- A **living donor kidney transplant** offers the best outcomes for **quality of life and survival** in eligible patients with end-stage renal disease (ESRD), particularly when compared to dialysis, due to better graft survival rates and reduced complications.
- The patient's symptoms (fatigue, itching, leg swelling, oliguria, high urea nitrogen, creatinine, hyperkalemia, metabolic acidosis) are consistent with **ESRD**, and while she has several comorbidities, she is not explicitly stated to have contraindications for transplantation.
*Peritoneal dialysis*
- While an effective treatment for ESRD, **dialysis generally provides lower quality of life** and survival benefits compared to successful kidney transplantation.
- She already has significant fluid overload symptoms and **oliguria**, making adequate fluid removal through peritoneal dialysis potentially challenging without strict management and impacting her overall well-being.
*Cadaveric kidney transplant*
- A **cadaveric kidney transplant** is a viable option and offers better outcomes than dialysis, but it generally has **poorer graft survival** and a longer wait time compared to a living donor transplant due to delayed graft function and cold ischemia time.
- Given the option, a **living donor transplant is superior** in terms of long-term outcomes and reduces the time spent on dialysis.
*Hemofiltration*
- **Hemofiltration is a form of renal replacement therapy**, similar to hemodialysis, often used in acute settings or for critically ill patients with severe fluid overload or electrolyte imbalances.
- While it can manage her symptoms, it is not a long-term treatment that **improves quality of life or maximizes survival** better than transplantation for ESRD.
*Fluid restriction*
- **Fluid restriction** is a supportive measure to manage fluid overload in patients with ESRD; however, it addresses symptoms rather than the underlying progressive renal failure.
- While necessary as part of supportive care, it does not offer a definitive long-term solution or improve survival for ESRD, which requires **renal replacement therapy or transplantation**.
Kidney transplantation US Medical PG Question 4: Twelve days after undergoing a cadaveric renal transplant for adult polycystic kidney disease, a 23-year-old man has pain in the right lower abdomen and generalized fatigue. During the past 4 days, he has had decreasing urinary output. Creatinine concentration was 2.3 mg/dL on the second postoperative day. Current medications include prednisone, cyclosporine, azathioprine, and enalapril. His temperature is 38°C (100.4°F), pulse is 103/min, and blood pressure is 168/98 mm Hg. Examination reveals tenderness to palpation on the graft site. Creatinine concentration is 4.3 mg/dL. A biopsy of the transplanted kidney shows tubulitis. C4d staining is negative. Which of the following is the most likely cause of this patient's findings?
- A. Drug-induced nephrotoxicity
- B. Allorecognition with T cell activation (Correct Answer)
- C. Irreversible fibrosis of the glomerular vessels
- D. Donor T cells from the graft
- E. Preformed cytotoxic antibodies against class I HLA
Kidney transplantation Explanation: ***Allorecognition with T cell activation***
- The patient's symptoms (pain at graft site, fatigue, decreasing urinary output, elevated creatinine) 12 days post-transplant, along with **tubulitis on biopsy** and negative **C4d staining**, are indicative of acute cellular rejection, mediated primarily by **T-cell recognition of donor HLA antigens**.
- **Hypertension** and **fever** also support acute rejection, and the immunosuppressive regimen may not be fully effective in preventing this T-cell mediated response.
*Drug-induced nephrotoxicity*
- While cyclosporine and enalapril can cause kidney injury, the **histological finding of tubulitis** is highly specific for acute cellular rejection, not typically seen with drug-induced nephrotoxicity alone.
- Drug-induced nephrotoxicity usually presents with a more **gradual rise in creatinine** and may lack the systemic signs like fever or the specific pathological features of rejection.
*Irreversible fibrosis of the glomerular vessels*
- This description is more consistent with **chronic allograft nephropathy** or long-term damage, which typically develops months to years after transplantation, not within 12 days.
- The findings described (pain, fever, tubulitis) point to an acute process, not chronic fibrosis.
*Donor T cells from the graft*
- This scenario describes **graft-versus-host disease (GVHD)**, which is rare in solid organ transplantation due to the much smaller lymphocyte load compared to bone marrow transplants.
- GVHD typically affects the skin, liver, and gut, and while it involves T-cell mediated injury, the primary damage in renal transplant rejection is directed at the transplanted kidney by the recipient's immune system.
*Preformed cytotoxic antibodies against class I HLA*
- This describes **hyperacute rejection**, which occurs within minutes to hours of transplantation due to pre-existing antibodies in the recipient against donor antigens.
- The patient's symptoms developing 12 days post-transplant, along with the biopsy showing tubulitis and negative C4d staining (indicating absence of significant antibody-mediated complement activation), rule out hyperacute rejection.
Kidney transplantation US Medical PG Question 5: Several weeks following a kidney transplantation, a 50-year-old Caucasian female presents for evaluation of the transplanted organ. Biopsy shows inflammation involving the endothelial cells of the kidney vasculature and the presence of mononuclear cells in the interstitium. Which cells are most likely responsible for this presentation?
- A. Recipient T-cells (Correct Answer)
- B. Donor antibodies
- C. Preformed recipient antibodies
- D. Deposition of antibody immune complexes
- E. Donor T-cells
Kidney transplantation Explanation: ***Recipient T-cells***
- The presence of **mononuclear cells in the interstitium** and inflammation of the **endothelial cells** several weeks post-transplantation is characteristic of **acute cellular rejection (ACR)**.
- ACR is primarily mediated by the recipient's **cytotoxic T-cells** recognizing donor major histocompatibility complex (MHC) molecules on graft cells.
*Donor antibodies*
- Donor antibodies are not responsible for rejection; rather, recipient antibodies (either preformed or newly formed) are implicated.
- The donor's immune system is suppressed or non-existent in the context of the transplanted organ itself after removal from the donor.
*Preformed recipient antibodies*
- While preformed recipient antibodies cause **hyperacute rejection**, which occurs minutes to hours after transplant, the presentation here is several weeks later.
- Hyperacute rejection involves widespread thrombosis and necrosis due to rapid antibody-mediated complement activation within the graft vasculature.
*Deposition of antibody immune complexes*
- Immune complex deposition typically causes a different pattern of injury (e.g., glomerulonephritis) and is not the primary mechanism of acute cellular rejection.
- This mechanism is more associated with certain autoimmune diseases or chronic transplant rejection, not the acute phase described.
*Donor T-cells*
- Donor T-cells would not be attacking the transplanted organ since it is *their own tissue*.
- Donor T-cells can cause **graft-versus-host disease (GVHD)** in bone marrow transplantation, where immunocompetent donor T-cells attack recipient tissues, but this is not applicable to solid organ transplantation.
Kidney transplantation US Medical PG Question 6: A 42-year-old woman comes to the physician because of right flank pain that started 3 days following a procedure. Her vital signs are within normal limits. Physical examination shows right costovertebral angle tenderness. An intravenous pyelogram shows a dilated renal pelvis and ureter on the right with a lack of contrast proximal to the ureterovesical junction. This patient most likely recently underwent which of the following procedures?
- A. Hysterectomy (Correct Answer)
- B. Foley catheter insertion
- C. Cesarean delivery
- D. Appendectomy
- E. Inguinal hernia repair
Kidney transplantation Explanation: ***Hysterectomy***
- **Ureteral injury** is a known complication of hysterectomy due to the ureter's close proximity to the uterine arteries and adnexa, especially near the **ureterovesical junction**.
- The presented symptoms of flank pain, CVA tenderness, and hydronephrosis (dilated renal pelvis and ureter with lack of contrast flow) occurring post-procedure strongly indicate **ureteral obstruction** or injury during the surgery.
*Foley catheter insertion*
- While catheterization can cause trauma, it would typically lead to **urethral or bladder injury**, not a ureteral obstruction at the ureterovesical junction causing hydronephrosis.
- The symptoms are more consistent with an injury higher up in the urinary tract that is not usually associated with a Foley catheter.
*Cesarean delivery*
- A C-section involves opening the abdomen to deliver a baby, but it generally does not involve dissection near the ureters to the extent that a hysterectomy does, making ureteral injury less common.
- The primary surgical field during a C-section is the uterus, while ureteral injury is more characteristic of procedures involving extensive pelvic dissection, such as hysterectomy.
*Appendectomy*
- An appendectomy is a procedure to remove the appendix and typically involves the right lower quadrant of the abdomen, away from the course of the ureter and ureterovesical junction.
- Injury to the ureter is a very rare complication of appendectomy and would not typically manifest as this type of obstruction.
*Inguinal hernia repair*
- Inguinal hernia repair involves structures in the groin region, anterior to the peritoneal cavity, and is far removed from the ureters and bladder.
- Ureteral injury is not a recognized complication of inguinal hernia repair.
Kidney transplantation US Medical PG Question 7: A 55-year-old woman recently underwent kidney transplantation for end-stage renal disease. Her early postoperative period was uneventful, and her serum creatinine is lowered from 4.3 mg/dL (preoperative) to 2.5 mg/dL. She is immediately started on immunosuppressive therapy. On postoperative day 7, she presents to the emergency department (ED) because of nausea, fever, abdominal pain at the transplant site, malaise, and pedal edema. The vital signs include: pulse 106/min, blood pressure 167/96 mm Hg, respirations 26/min, and temperature 40.0°C (104.0°F). The surgical site shows no signs of infection. Her urine output is 250 mL over the past 24 hours. Laboratory studies show:
Hematocrit 33%
White blood cell (WBC) count 6700/mm3
Blood urea 44 mg/dL
Serum creatinine 3.3 mg/dL
Serum sodium 136 mEq/L
Serum potassium 5.6 mEq/L
An ultrasound of the abdomen shows collection of fluid around the transplanted kidney with moderate hydronephrosis. Which of the following initial actions is the most appropriate?
- A. Re-operate and remove the failed kidney transplant
- B. Continue with an ultrasound-guided biopsy of the transplanted kidney (Correct Answer)
- C. Start on pulse steroid treatment or OKT3
- D. Supportive treatment with IV fluids, antibiotics, and antipyretics
- E. Consider hemodialysis
Kidney transplantation Explanation: ***Continue with an ultrasound-guided biopsy of the transplanted kidney***
- The patient's symptoms (fever, malaise, abdominal pain, rising creatinine) and ultrasound findings (fluid collection, hydronephrosis) are highly suggestive of **acute renal allograft rejection** or an **obstructive uropathy**, necessitating a definitive diagnosis through biopsy.
- A biopsy will differentiate between rejection, drug toxicity, or other causes of allograft dysfunction, guiding appropriate and specific treatment.
*Re-operate and remove the failed kidney transplant*
- Removing the transplanted kidney is a drastic measure and premature at this stage, as the cause of dysfunction is not yet confirmed.
- The elevated creatinine and hydronephrosis could be reversible with proper treatment once the underlying cause is identified.
*Start on pulse steroid treatment or OKT3*
- While pulse steroids or OKT3 (muromonab-CD3) are used to treat acute rejection, administering them without a definitive diagnosis from a biopsy could be inappropriate and potentially harmful.
- The symptoms could also be due to infection or obstruction, which would not respond to these immunosuppressive therapies and could worsen with increased immunosuppression.
*Supportive treatment with IV fluids, antibiotics, and antipyretics*
- Supportive care alone is insufficient given the potential for acute allograft rejection or severe obstruction, which requires specific intervention.
- Although the patient has fever, there are no clear signs of infection, and empirical antibiotics may delay necessary diagnostic steps.
*Consider hemodialysis*
- While the patient's creatinine is elevated and potassium is high, these parameters alone do not immediately warrant hemodialysis without exploring the underlying cause of allograft dysfunction.
- Dialysis is typically considered when there are severe indications like refractory hyperkalemia, fluid overload, acidosis, or uremic symptoms that cannot be otherwise managed, and the primary goal should be to treat the cause of decreasing kidney function.
Kidney transplantation US Medical PG Question 8: A 38-year-old kidney transplant recipient maintained on tacrolimus presents with a 2-week history of progressive confusion, ataxia, and visual disturbances. MRI shows multifocal white matter lesions without mass effect or enhancement. CSF analysis reveals mild pleocytosis with elevated protein. JC virus DNA is detected in CSF by PCR. Serum tacrolimus level is therapeutic at 8 ng/mL. Apply knowledge of this condition to determine the appropriate management strategy.
- A. Significantly reduce or discontinue immunosuppression and provide supportive care (Correct Answer)
- B. Switch from tacrolimus to sirolimus to preserve graft while treating infection
- C. Continue current immunosuppression and administer IVIG therapy
- D. Maintain immunosuppression and start cidofovir antiviral therapy
- E. Reduce tacrolimus by 50% and start high-dose corticosteroids
Kidney transplantation Explanation: ***Significantly reduce or discontinue immunosuppression and provide supportive care***
- The patient presents with **Progressive Multifocal Leukoencephalopathy (PML)** caused by **JC virus** reactivation; the primary treatment is **immune reconstitution** to allow the body to fight the virus.
- Reducing or stopping agents like **tacrolimus** is critical for survival, even though it carries a high risk of **allograft rejection**.
*Switch from tacrolimus to sirolimus to preserve graft while treating infection*
- While **sirolimus** has some antiproliferative effects, it is still an **immunosuppressant** and will not allow for the aggressive immune recovery needed to halt **JC virus** replication.
- Managing the life-threatening neurological condition takes precedence over **graft preservation** in the acute phase of PML.
*Continue current immunosuppression and administer IVIG therapy*
- Maintaining current levels of **tacrolimus** prevents the T-cell mediated response necessary to clear the **JC virus** from the CNS.
- **IVIG therapy** has not been proven effective in clinical trials for the treatment of PML and does not address the underlying **immunosuppressed state**.
*Maintain immunosuppression and start cidofovir antiviral therapy*
- **Cidofovir** was previously studied for PML, but it has failed to show significant clinical benefit and is associated with severe **nephrotoxicity**.
- Antiviral therapy without addressing the **cellular immune deficiency** is insufficient to treat this opportunistic infection.
*Reduce tacrolimus by 50% and start high-dose corticosteroids*
- Adding **high-dose corticosteroids** is contraindicated as it further suppresses the immune system, potentially accelerating the progression of **PML**.
- Steroids are typically reserved only for patients who develop **Immune Reconstitution Inflammatory Syndrome (IRIS)** after immunosuppression is withdrawn.
Kidney transplantation US Medical PG Question 9: A 41-year-old heart transplant recipient (5 years post-transplant) on cyclosporine, azathioprine, and prednisone develops progressive dyspnea on exertion. Echocardiogram shows preserved ejection fraction but abnormal diastolic dysfunction. Right heart catheterization reveals elevated filling pressures. Endomyocardial biopsy shows interstitial fibrosis without significant cellular infiltration. Coronary angiography shows diffuse, concentric narrowing of distal vessels. Synthesize these findings to determine the underlying pathophysiology and evaluate management options.
- A. Cardiac allograft vasculopathy requiring consideration for retransplantation evaluation (Correct Answer)
- B. Restrictive cardiomyopathy from previous rejection episodes requiring diuretic therapy
- C. Drug-induced cardiomyopathy from calcineurin inhibitor toxicity requiring switch to mTOR inhibitor
- D. Acute cellular rejection requiring pulse steroids and optimization of immunosuppression
- E. Antibody-mediated rejection requiring plasmapheresis and rituximab therapy
Kidney transplantation Explanation: ***Cardiac allograft vasculopathy requiring consideration for retransplantation evaluation***
- **Cardiac allograft vasculopathy (CAV)** is the leading cause of late graft failure, characterized by **diffuse, concentric intimal hyperplasia** and narrowing of the distal coronary vessels.
- The presentation of **progressive dyspnea**, diastolic dysfunction, and **interstitial fibrosis** on biopsy—without acute cellular or antibody-mediated rejection—is pathognomonic for advanced CAV, where **retransplantation** remains the definitive surgical option.
*Restrictive cardiomyopathy from previous rejection episodes requiring diuretic therapy*
- While **interstitial fibrosis** can mimic a restrictive phenotype, this option overlooks the specific **angiographic finding** of distal concentric narrowing which points directly to CAV.
- **Diuretic therapy** may provide symptomatic relief for heart failure but does not address the underlying **progressive vasculopathy** and graft failure.
*Drug-induced cardiomyopathy from calcineurin inhibitor toxicity requiring switch to mTOR inhibitor*
- **Cyclosporine** (a calcineurin inhibitor) primarily causes **nephrotoxicity** and hypertension rather than direct cardiomyopathy with concentric vascular narrowing.
- While **mTOR inhibitors** (like Sirolimus) are used to slow the progression of CAV, they do not resolve established diffuse vascular disease with hemodynamic compromise.
*Acute cellular rejection requiring pulse steroids and optimization of immunosuppression*
- **Acute cellular rejection** is excluded by the endomyocardial biopsy, which specifically showed **no significant cellular infiltration**.
- This condition typically occurs earlier in the post-transplant period and would show **lymphocytic infiltration** and myocyte necrosis rather than concentric vessel narrowing.
*Antibody-mediated rejection requiring plasmapheresis and rituximab therapy*
- **Antibody-mediated rejection (AMR)** is characterized by **capillary endothelial injury** and C4d deposition on biopsy, which were not described in this patient.
- AMR typically presents with more acute graft dysfunction rather than the **slowly progressive** course and distal vessel pruning seen in this case.
Kidney transplantation US Medical PG Question 10: A 52-year-old man with hepatocellular carcinoma (single 4.5 cm lesion) within Milan criteria is listed for liver transplantation with MELD exception points. While waiting, alpha-fetoprotein increases from 125 to 850 ng/mL over 3 months despite locoregional therapy. Repeat imaging shows the tumor has grown to 6 cm with possible vascular invasion. He has no extrahepatic disease. His wife offers to be a living donor. Synthesize the clinical data and evaluate the most appropriate management decision.
- A. Remove from transplant list and pursue systemic therapy with sorafenib (Correct Answer)
- B. Perform surgical resection then relist if recurrence occurs within criteria
- C. Downstage with aggressive locoregional therapy then reassess for transplantation
- D. Proceed with living donor transplantation given no extrahepatic disease
- E. Continue locoregional therapy and maintain listing with exception points
Kidney transplantation Explanation: ***Remove from transplant list and pursue systemic therapy with sorafenib***
- This patient no longer meets the **Milan criteria** due to the lesion size exceeding 5 cm and the presence of suspected **vascular invasion**, which significantly increases the risk of recurrence.
- A rapid rise in **alpha-fetoprotein (AFP)** to >400 ng/mL is a strong predictor of poor post-transplant survival and biological aggressiveness, necessitating **delisting** and alternative systemic management.
*Perform surgical resection then relist if recurrence occurs within criteria*
- **Surgical resection** is generally contraindicated in cases of suspected **vascular invasion** as it is associated with extremely high rates of early systemic metastasis.
- This approach does not address the underlying biological aggressiveness evidenced by the soaring **AFP** and likely poor outcome.
*Downstage with aggressive locoregional therapy then reassess for transplantation*
- While **downstaging** is an option for tumors just outside criteria, the combination of **vascular invasion** and a rapidly rising **AFP** suggests the disease is no longer localized or controllable by these methods.
- Failure of previous **locoregional therapy** to control the AFP and tumor growth indicates a resistant phenotype that is unlikely to respond to further local intervention.
*Proceed with living donor transplantation given no extrahepatic disease*
- Even with a **living donor**, transplanting a patient with suspected **vascular invasion** and high **AFP** is ethically controversial due to the very high risk of rapid disease recurrence.
- **Living donor liver transplantation (LDLT)** does not bypass the need for favorable tumor biology to ensure a successful long-term oncologic outcome.
*Continue locoregional therapy and maintain listing with exception points*
- National matching rules generally require patients to stay within **Milan criteria** to maintain **MELD exception points**; exceeding 5 cm and vascular invasion disqualifies the patient.
- Maintaining the current status ignores the clear radiographic and biochemical evidence of **tumor progression**, which would result in a waste of a donor organ.
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