Renal allograft pathology: The Banff classification

Abstract

The Banff classification[1.Racusen L.C. Solez K. Colvin R.B. Bonsib S.M. Castro M.C. Cavallo T. Croker B.P. Demetris A.J. Drachenberg C.B. Fogo A.B. Furness P. Gaber L.W. Gibson I.W. Glotz D. Goldberg J.C. Grande J. Halloran P.F. Hansen H.E. Hartley B. Hayry P.J. Hill C.M. Hoffman E.O. Hunsicker L.G. Lindblad A.S. Marcussen N. Mihatsch M.J. Nadasdy T. Nickerson P. Olsen T.S. Papadimitriou J.C. Randhawa P.S. Rayner D.C. Roberts I. Rose S. Rush D. Salinas-Madrigal L. Salomon D.R. Sund S. Taskinen E. Trpkov K. Yamaguchi Y. The Banff 97 working classification of renal allograft pathology.Kidney Int. 1999; 55: 713-723Abstract Full Text Full Text PDF PubMed Scopus (2665) Google Scholar] characterizes five categories of renal allograft pathology: (1) antibody-mediated rejection; (2) suspicious of acute rejection; (3) acute rejection; (4) chronic sclerosing allograft nephropathy; and (5) other—changes not considered due to rejection. Taking “other” at face value makes it implicit to the classification that there are basically two types of allograft pathology: (1) that consequent on rejection; and (2) that consequent on other factors. Such a view also implicitly defines chronic allograft nephropathy as a form of rejection and indeed the Banff classification recognizes it as such: “the grading of the severity of chronic rejection continues … (italics ours). This of course does not mean that every histological picture of chronic allograft nephropathy denotes chronic rejection; chronic allograft nephropathy, pathologically, is chronic interstitial nephritis and any of the causes of the latter may produce the histology of chronic allograft nephropathy. Furthermore, considering the vascular lesions of cardiac allograft chronic failure and the known ability of other types of renal lesions to produce chronic interstitial nephritis, it is likely that when chronic allograft nephropathy is due to chronic rejection, the initiating mechanism is arterial injury. In the discussion of the paper on the Banff classification[1.Racusen L.C. Solez K. Colvin R.B. Bonsib S.M. Castro M.C. Cavallo T. Croker B.P. Demetris A.J. Drachenberg C.B. Fogo A.B. Furness P. Gaber L.W. Gibson I.W. Glotz D. Goldberg J.C. Grande J. Halloran P.F. Hansen H.E. Hartley B. Hayry P.J. Hill C.M. Hoffman E.O. Hunsicker L.G. Lindblad A.S. Marcussen N. Mihatsch M.J. Nadasdy T. Nickerson P. Olsen T.S. Papadimitriou J.C. Randhawa P.S. Rayner D.C. Roberts I. Rose S. Rush D. Salinas-Madrigal L. Salomon D.R. Sund S. Taskinen E. Trpkov K. Yamaguchi Y. The Banff 97 working classification of renal allograft pathology.Kidney Int. 1999; 55: 713-723Abstract Full Text Full Text PDF PubMed Scopus (2665) Google Scholar], it is also noted that Type I acute rejection is a manifestation of cell-mediated immunity, while type III is strongly suggestive of an antibody-mediated process. Furthermore, there is also the implication that type II is a mixture of both cell- and antibody-mediated immunity. Given these considerations, rejection allograft pathology may then be reclassified into two major categories based on the anatomical target of the immune reaction: (1) tubular/interstitial rejection; and (2) vascular rejection. Interstitial rejection usually comes in one category, acute, although we have reported an instance of multiple acute interstitial rejection episodes in association with non-compliance that eventually led to chronic interstitial nephritis without vascular lesions on biopsy and arteriography[2.Chen Y. Baltzan M.A. Geoege D. Fate of recurrent acute interstitial cellular rejection in a HLA identical renal transplant: Impact of donor microchimerism.Clinical Nephrology. 1997; 48: 300-306PubMed Google Scholar]. Etiologically, this acute interstitial nephritis is a manifestation of cell-mediated immunity. Pathophysiologically it causes no disturbance or acute renal failure of various grades of severity. Therapeutically, it is almost always reversible. In contrast, vascular rejection comes in three categories based upon both time of onset and histology: hyperacute, acute, and chronic. Etiologically, the first is antibody-mediated, as is the second in most cases. Anatomically, in all categories the immune target is vascular, probably endothelium. Pathophysiologically, the first two are manifest as acute renal failure and the third as chronic renal failure. Therapeutically, all three are most often refractory to therapeutic intervention. It should also be recognized that two forms of rejection may co-exist—for example, acute interstitial and acute vascular, or acute interstitial and chronic vascular. Additionally, one more form of allograft rejection pathology should be included even though it has not been seen since the introduction of cyclosporin: spontaneous graft rupture, usually seen in the latter half of the first week post-grafting. It is associated with hyperplasia of the usually inconspicuous lymph nodes at the medullary cortical junction, which compress the intra-renal veins at that level, causing intrarenal venous hypertension and rupture.