Rejection diagnosis and management US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Rejection diagnosis and management. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Rejection diagnosis and management US Medical PG Question 1: 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
Rejection diagnosis and management 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.
Rejection diagnosis and management US Medical PG Question 2: A 10-year-old boy is presented to the hospital for a kidney transplant. In the operating room, the surgeon connects an allograft kidney renal artery to the aorta, and after a few moments, the kidney becomes cyanotic, edematous, and dusky with mottling. Which of the following in the recipient’s serum is responsible for this rejection?
- A. Macrophages
- B. CD4+ T cells
- C. IgA
- D. CD8+ T cells
- E. IgG (Correct Answer)
Rejection diagnosis and management Explanation: ***IgG***
- The rapid onset of tissue necrosis and the immediate signs of rejection (cyanotic, edematous, dusky with mottling) upon vascular anastomosis are characteristic of **hyperacute rejection**.
- **Hyperacute rejection** is mediated by pre-formed recipient antibodies, primarily **IgG**, targeting donor ABO or HLA antigens. These antibodies activate complement, leading to rapid thrombosis and graft destruction.
*Macrophages*
- While macrophages play a role in chronic allograft rejection and delayed type hypersensitivity, they are not the primary mediators of **hyperacute rejection**.
- Their involvement typically presents with a more delayed and less immediate profound tissue damage than seen in this scenario.
*CD4+ T cells*
- **CD4+ T cells** are central to acute cellular rejection, which typically manifests days to weeks after transplantation.
- They are not responsible for the immediate, pre-formed antibody-mediated response seen in **hyperacute rejection**.
*IgA*
- **IgA antibodies** are primarily involved in mucosal immunity and are generally not implicated in solid organ transplant rejection, especially hyperacute rejection.
- While IgA can contribute to immune complex formation, it's not the main antibody type driving hyperacute allograft destruction.
*CD8+ T cells*
- **CD8+ T cells** (cytotoxic T lymphocytes) are key players in acute cellular rejection, mediating direct lysis of donor cells.
- Their action is part of a cellular immune response that takes days to weeks to develop and is not responsible for the immediate, antibody-mediated hyperacute rejection.
Rejection diagnosis and management US Medical PG Question 3: 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
Rejection diagnosis and management 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.
Rejection diagnosis and management US Medical PG Question 4: A 61-year-old-male underwent deceased donor liver transplantation 3 weeks ago. During his follow up visit he complains of nausea and abdominal pain. He has been taking all of his medications as prescribed. He has a history of alcohol abuse and his last drink was one year ago. He does not smoke cigarettes and lives at home with his wife. On physical examination temperature is 98.6°F (37°C), blood pressure is 115/80 mmHg, pulse is 90/min, respirations are 18/min, and pulse oximetry is 99% on room air. He has scleral icterus and a positive fluid wave. Liver function tests are as follows:
Alkaline phosphatase: 110 U/L
Aspartate aminotransferase (AST, GOT): 100 U/L
Alanine aminotransferase (ALT, GPT): 120 U/L
Bilirubin total: 2.2 mg/dL
Liver biopsy shows mixed dense interstitial lymphocytic infiltrates in the portal triad. What is the mechanism of this reaction?
- A. Grafted T lymphocytes reacting against host
- B. CD4+ T lymphocytes reacting against recipient APCs
- C. CD8+ T lymphocytes reacting against donor MHCs (Correct Answer)
- D. Acute viral infection
- E. Pre-existing recipient antibodies
Rejection diagnosis and management Explanation: ***CD8+ T lymphocytes reacting against donor MHCs***
- This scenario describes **acute cellular rejection** following liver transplantation, mediated primarily by **recipient CD8+ T lymphocytes** recognizing donor major histocompatibility complex (MHC) class I molecules on donor hepatocytes.
- The **lymphocytic infiltrates** in the portal triad are characteristic of acute rejection, where activated cytotoxic T cells attack the transplanted organ.
*Grafted T lymphocytes reacting against host*
- This mechanism describes **graft-versus-host disease (GVHD)**, which is much more common after hematopoietic stem cell transplantation.
- While liver allografts contain donor lymphocytes, **GVHD from liver transplant is rare** and typically only seen in highly immunosuppressed patients or specific transplant settings.
*CD4+ T lymphocytes reacting against recipient APCs*
- This describes a reaction of donor CD4+ T cells against recipient antigen-presenting cells (APCs), which is part of the mechanism for **graft-versus-host disease (GVHD)**.
- The primary pathology in this patient, with liver damage and lymphocytic infiltration of the portal triad, points to a rejection of the transplanted liver, not GVHD.
*Acute viral infection*
- While possible in transplant recipients, an acute viral infection would typically present with different patterns of liver injury and biopsy findings, such as **viral cytopathic effects** or more widespread inflammation distinct from the dense portal triad infiltrates typical of rejection.
- The clinical presentation and biopsy findings are classic for organ rejection rather than a viral infection.
*Pre-existing recipient antibodies*
- **Pre-existing recipient antibodies** are primarily responsible for **hyperacute rejection**, which occurs minutes to hours after transplant and leads to rapid graft failure.
- This patient is presenting 3 weeks post-transplant, which is too late for hyperacute rejection; this mechanism generally leads to thrombosis and necrosis, not the interstitial lymphocytic infiltrates seen here.
Rejection diagnosis and management US Medical PG Question 5: A 57-year-old woman comes to the clinic complaining of decreased urine output. She reports that over the past 2 weeks she has been urinating less and less every day. She denies changes in her diet or fluid intake. The patient has a history of lupus nephritis, which has resulted in end stage renal disease. She underwent a renal transplant 2 months ago. Since then she has been on mycophenolate and cyclosporine, which she takes as prescribed. The patient’s temperature is 99°F (37.2°C), blood pressure is 172/102 mmHg, pulse is 88/min, and respirations are 17/min with an oxygen saturation of 97% on room air. Labs show an elevation in serum creatinine and blood urea nitrogen. On physical examination, she has 2+ pitting edema of the bilateral lower extremities. Lungs are clear to auscultation. Urinalysis shows elevated protein. A post-void bladder scan is normal. A renal biopsy is obtained, which shows lymphocyte infiltration and intimal swelling. Which of the following is the next best step in management?
- A. Add diltiazem
- B. Nephrectomy
- C. Start intravenous steroids (Correct Answer)
- D. Add ceftriaxone
- E. Discontinue cyclosporine
Rejection diagnosis and management Explanation: ***Start intravenous steroids***
- The patient presents with **decreased urine output**, elevated creatinine, and a recent kidney transplant with biopsy showing **lymphocyte infiltration** and **intimal swelling**, all highly suggestive of **acute cellular rejection**.
- **High-dose intravenous steroids** (e.g., methylprednisolone) are the first-line treatment for acute cellular rejection to suppress the immune response and preserve graft function.
*Add diltiazem*
- **Diltiazem** is a calcium channel blocker used to treat hypertension and arrhythmias, and it can also interfere with cyclosporine metabolism, potentially increasing its levels.
- While the patient has elevated blood pressure, adding diltiazem would not address the underlying **immune rejection** and would not be the primary intervention.
*Nephrectomy*
- **Nephrectomy** involves surgical removal of the transplanted kidney. This radical intervention is reserved for **irreversible graft failure** or severe complications like overwhelming infection or malignancy.
- Given the acute presentation and possibility of reversing rejection with immunosuppression, nephrectomy is **premature** and not the next best step.
*Add ceftriaxone*
- **Ceftriaxone** is an antibiotic used to treat bacterial infections.
- There is no clinical evidence in the stem (e.g., fever, signs of infection) to suggest a **bacterial infection** as the cause of her symptoms, making antibiotics inappropriate.
*Discontinue cyclosporine*
- **Cyclosporine** is an immunosuppressant essential for preventing transplant rejection. Discontinuing it would immediately increase the risk of more severe and potentially **irreversible rejection**.
- While cyclosporine can cause nephrotoxicity, the biopsy findings of **cellular infiltration** point more towards rejection rather than primary drug toxicity, and the primary treatment for rejection involves increasing immunosuppression, not withdrawing it.
Rejection diagnosis and management US Medical PG Question 6: An investigator studying immune-mediated pulmonary damage performs an autopsy on a bilateral lung transplant recipient who died of hypercapnic respiratory failure. The patient underwent lung transplantation for idiopathic pulmonary fibrosis. Microscopic examination of the lung shows diffuse eosinophilic scarring of the terminal and respiratory bronchioles and near-complete luminal obliteration by polypoidal plugs of granulation tissue. Examination of the skin shows no abnormalities. The findings in this patient are most consistent with which of the following conditions?
- A. Acute graft rejection
- B. Recurrence of primary disease
- C. Transfusion-related acute lung injury
- D. Chronic graft rejection (Correct Answer)
- E. Acute graft-versus-host disease
Rejection diagnosis and management Explanation: ***Chronic graft rejection***
- Chronic rejection in lung transplant recipients classically manifests as **bronchiolitis obliterans**, characterized by diffuse **eosinophilic scarring** and **luminal obliteration** of small airways by polypoidal granulation tissue.
- This process leads to irreversible airflow obstruction and progressive respiratory failure, which aligns with the patient's death from **hypercapnic respiratory failure**.
*Acute graft rejection*
- Acute graft rejection typically presents with perivascular and interstitial mononuclear infiltrates, not necessarily diffuse eosinophilic scarring or luminal obliteration of bronchioles.
- While it can cause respiratory decline, the described microscopic features are more characteristic of a chronic process.
*Recurrence of primary disease*
- **Idiopathic pulmonary fibrosis** is characterized by usual interstitial pneumonia (UIP) pattern with patchy interstitial fibrosis, honeycombing, and fibroblast foci, which is distinct from the described bronchiolar scarring and obliteration.
- While IPF can recur, the histological findings described are not typical for recurrent IPF but rather for chronic rejection.
*Transfusion-related acute lung injury*
- **TRALI** is an acute lung injury reaction to blood products, usually occurring within 6 hours of transfusion, and is characterized by non-cardiogenic pulmonary edema.
- The described pathology of chronic scarring and obliteration is not consistent with the acute inflammatory and edematous changes seen in TRALI.
*Acute graft-versus-host disease*
- **Acute GVHD** primarily affects the skin, liver, and gastrointestinal tract; lung involvement is rare and typically presents as a diffuse interstitial pneumonitis.
- The absence of skin abnormalities and the specific bronchiolar pathology described do not fit the typical presentation of acute GVHD.
Rejection diagnosis and management US Medical PG Question 7: 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
Rejection diagnosis and management 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.
Rejection diagnosis and management US Medical PG Question 8: A 14-year-old boy has undergone kidney transplantation due to stage V chronic kidney disease. A pre-transplantation serologic assessment showed that he is negative for past or present HIV infection, viral hepatitis, EBV, and CMV infection. He has a known allergy for macrolides. The patient has no complaints 1 day after transplantation. His vital signs include: blood pressure 120/70 mm Hg, heart rate 89/min, respiratory rate 17/min, and temperature 37.0°C (98.6°F). On physical examination, the patient appears to be pale, his lungs are clear on auscultation, heart sounds are normal, and his abdomen is non-tender on palpation. His creatinine is 0.65 mg/dL (57.5 µmol/L), GFR is 71.3 mL/min/1.73 m2, and urine output is 0.9 mL/kg/h. Which of the following drugs should be used in the immunosuppressive regimen in this patient?
- A. Belatacept
- B. Sirolimus
- C. Omalizumab
- D. Daclizumab
- E. Basiliximab (Correct Answer)
Rejection diagnosis and management Explanation: **Basiliximab**
- **Basiliximab** is a **monoclonal antibody** that targets the **IL-2 receptor (CD25)** on activated T cells, preventing their proliferation and inducing immunosuppression.
- It is commonly used as **induction therapy** in kidney transplant recipients due to its good safety profile, especially in pediatric patients, without the nephrotoxicity associated with calcineurin inhibitors, minimizing acute rejection risks immediately post-transplant.
*Belatacept*
- **Belatacept** works by co-stimulation blockade, binding to **CD80 and CD86** on antigen-presenting cells to prevent T-cell activation.
- It is typically reserved for patients who cannot tolerate calcineurin inhibitors due to **nephrotoxicity** or require a steroid-sparing regimen, which is not indicated as an immediate need in this patient.
*Sirolimus*
- **Sirolimus** is an **mTOR inhibitor** that works by blocking T-cell proliferation and B-cell differentiation.
- It is associated with several side effects, including **delayed wound healing**, **thrombocytopenia**, and **hyperlipidemia**, which are undesirable in the immediate post-transplant period, especially in a growing adolescent.
*Omalizumab*
- **Omalizumab** is an **anti-IgE monoclonal antibody** primarily used for allergic asthma and chronic spontaneous urticaria.
- It has no role in **immunosuppression for organ transplantation** as its mechanism of action is unrelated to preventing graft rejection.
*Daclizumab*
- **Daclizumab** is another **monoclonal antibody** that also targets the **IL-2 receptor (CD25)**, similar to basiliximab.
- However, daclizumab has been **withdrawn from the market** due to serious adverse effects including severe liver injury and autoimmune encephalitis, making it unavailable for clinical use in transplantation.
Rejection diagnosis and management US Medical PG Question 9: 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
Rejection diagnosis and management 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.
Rejection diagnosis and management US Medical PG Question 10: 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
Rejection diagnosis and management 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.
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