Thank you frankbj for posting this interesting case.

The first two pictures demonstrate dilated capillaries containing inflammatory cells in lumen. This change is not specific. It may be seen, but not limited to,  in acute tubular necrosis, or acute humoral rejection.

In addition, there are tubular epithelial cells which appear to have intranuclear viral inclusions (picture #6). But I am not sure. I cannot appreciate the nuclear detail.

The picture #3 shows isometric vacuolation of the tubular epithelium which is often present in acute CNI drug toxicity.

Does the picture #4 show a glomerulus with extravasated red cells in Bowman's space?

The picture #9 seems to have occasional mononuclear cells in in arterial intima. By definition, even a single mononuclear cell/lymphocyte in intima is enough for the diagnosis of arteritis. But I am never that kind of aggressive or liberal for arteritis. I often need a few lymphocytes in intima, not single lymphocyte.Alternatively,this may be classified as chronic allograft arteriopathy (chronic active T-cell-mediated rejection). Chronic allograft arteriopathy is characterized by arterial intimal fibrosis with mononuclear cell infiltration in fibrosis.

If the cells in arterial intima are not mononuclear cells or lymphocytes,the photo #5, 7 and 9 demonstrate at least intimal thickening.Given the focal positive C4d, chronic active antibody-mediated rejection would be differential diagnosis.One of criteria for chronic active antibody-mediated rejection is fibrosis/tubular atrophy and/or fibrous intimal thickening, plus positive C4d. The other possibility is the donor disease. You may check donor's history or donor kidney biopsy results or implantation biopsy results.