Transplant pathology: hyperacute rejection: practice question

A Pathology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Pathology · Transplant pathology: hyperacute rejection

Sample item

During a renal transplant, within minutes of releasing the vascular clamps the kidney turns mottled and cyanotic and stops producing urine. The recipient had received multiple transfusions earlier. What is the mechanism?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Preformed anti-donor antibodies causing endothelial injury, complement activation and thrombosis

Hyperacute rejection is a type II hypersensitivity in which preformed antibodies, such as against ABO or HLA antigens, develop after prior transfusion, pregnancy or transplant. They bind graft endothelium, activate complement and cause fibrinoid necrosis and thrombosis of vessels, so the graft infarcts within minutes to hours. It is prevented by ABO matching and a negative crossmatch.

Option by option

  • A. Recipient CD8 T-cell infiltration with tubulitis

    Tubulitis from CD8 infiltration describes acute cellular rejection, which takes days to weeks.

  • B. Slow intimal fibrosis of graft arteries from chronic injury

    Intimal fibrosis is the vascular lesion of chronic rejection, over months to years.

  • C. Donor T-cell recognition of recipient antigens

    Donor T cells attacking the host are the basis of graft-versus-host disease, not a rejection of the kidney.

  • D. Preformed anti-donor antibodies causing endothelial injury, complement activation and thrombosis (correct)

    Correct. Preformed antibodies produce immediate vascular rejection.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is D, Preformed anti-donor antibodies causing endothelial injury, complement activation and thrombosis. Hyperacute rejection is a type II hypersensitivity in which preformed antibodies, such as against ABO or HLA antigens, develop after prior transfusion, pregnancy or transplant.

Why is "Recipient CD8 T-cell infiltration with tubulitis" not the answer?

Tubulitis from CD8 infiltration describes acute cellular rejection, which takes days to weeks.

Why is "Slow intimal fibrosis of graft arteries from chronic injury" not the answer?

Intimal fibrosis is the vascular lesion of chronic rejection, over months to years.

Why is "Donor T-cell recognition of recipient antigens" not the answer?

Donor T cells attacking the host are the basis of graft-versus-host disease, not a rejection of the kidney.

What concept does this question test?

It tests Transplant pathology: hyperacute rejection in Pathology. They bind graft endothelium, activate complement and cause fibrinoid necrosis and thrombosis of vessels, so the graft infarcts within minutes to hours. It is prevented by ABO matching and a negative crossmatch.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Transplant pathology: hyperacute rejection?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.