Hyperacute = minutes to hours, host preformed Ab against graft endothelial cell Ag = compliment activation, endothelial damage, inflammation (within the tissue, NOT interstitium), clotting cascade, ischemic necrosis and thrombosis. https://tpis.upmc.com/tpislibrary/kidney/KHAcuRej.html

Acute = weeks to months = graft Ag activates host CD4 and CD8 T cells leading to parenchymal cell damage, interstitial lymphocytic infiltration, and endotheliaitis. https://tpis.upmc.com/tpislibrary/kidney/KARejMod.html

Chronic = months to years, chronic DTH (type IV hypersensitivity) reaction in vessel wall leading to intimal smooth muscle cell proliferation and vessle occlusion, with biopsy showing narrowed vascular lumen and extensive smooth muscle.

GVHD = graft cells (most typically bone marrow transplants) recognize host cells as self/foreign and lead to destruction of host tissue leading to rash, jaundice, diarrhea, and GI hemorrhage (this occurs because most bone marrow transplant patients have undergone full radiation which attacks the rapidly providing cells most (i.e. skin, GI mucosa, hair, hepatocytes) so graft destruction of host cells in those areas leads to symptoms).

https://tpis.upmc.com/

This is a case of acute transplant rejection. weeks to months after the transplant, recipient cd8 and/or cd4 t cells are activated against the donor (a type 4 HSR) and the donor starts making antibodies against the transplant. This presents as a vasculitis with dense interstitial lymphocytic infiltrates. (FA2018 pg 119)

page 119 FA Patient is presenting months after the transplant, which means it can't be hyperacute unless he stopped taking his immunosuppressants. Acute/chronic/GVH disease are mediated by T cells for the most part (I think), so this would mean lymphocytic infiltrates.

I think the three most reasonable answers can be put into the different boxes of rejection

Glomerular neutrophils and necrosis->hyperacute (? I usually just think neutrophils are the earlier onset things)

Lymphocytes infiltrating tubular epithelium-> Acute [<6 mo]

Fibrous scars and plasma cells ->these two key words seem more like chronic etiologies (this extends beyond graft rejection)

My best guess at the other options are:

Arteriolar C3 deposition- some sort of nephritic syndrome, whether it's SLE, PSGN etc.

Dilation of Bowman's space-post-renal obstruction

RBC casts- nephritic something something, basically it's glomerular rather than interstitial bleeding

Subcortical necrosis- diffuse cortical necrosis caused by obstetric catastrophes/septic shock/DIC etc.