In Reply
Makaleler > Kısa Makale · 2011
Yazarlar: Sait ŞEN, Banu SARSIK KUMBARACI
Archives of Pathology & Laboratory Medicine, Uluslararası, Wos, 2011, cilt 135, ss 168-169
DOI: 10.5858/135.2.168.b
Özet
In Reply.—First, we thank the authors for their comments because they provide further opportunity to discuss the classification, scoring, and grading system for renal amyloidosis. Most of our cases were defined as amyloid-associated (AA) amyloidosis based on anti-AA immunohistochemistry.1 Our experience is very different from that found in the current literature and the last 2 studies from Europe and the United States.2,3 Ethnicity (regions where familial Mediterranean fever is prevalent), chronic inflammations, infections (such as tuberculosis), rheumatic diseases, and obstructive lung disease were important etiologic factors in our study.Most of our AA amyloidosis cases were classified as classes II, III, and IV, in which glomerular amyloid deposits were more commonly associated with the arteriolar walls. Watanabe and Saniter4 found amyloid in vessels in nearly 80% of renal biopsies. Our findings also were much higher than those of Verine et al5 and similar to those of Watanabe and Saniter.4 Class IV cases were also associated with interstitial amyloid deposits. Nearly half of the patients with class I AA amyloidosis were recipients of renal transplants with recurrent AA amyloidosis. Nontransplant class I AA amyloidosis cases were generally associated with hilar and arteriolar amyloid deposits. These deposits were also considered and classified as the glomerular form. In the recurrent renal transplant AA amyloidosis cases, distinct histopathologic and clinical courses were identified. In these patients, minute amyloid deposits were found in the small vessels, and glomerular deposits were nearly absent on light microscopy. Additionally, in this pattern, renal function was not significantly influenced. This situation might be related to colchicine administration, especially in those patients with familial Mediterranean fever.6The vascular form of renal amyloidosis was considered when amyloid deposits were found predominantly on those vessels bigger than the afferent arteriole or interlobular arteries. We observed only one vascular form of renal non-AA amyloidosis. Our case had minimal glomerular amyloid deposition associated with medium-sized vessel deposits.7 This situation is very different from an early stage of glomerular form also classified as class I.Glomerular involvement scores are doubled because of the importance of glomerular involvement. Renal survival and proteinuria are very relevant to glomerular amyloid deposits but not to vascular or interstitial amyloid deposits.In our study, class V cases were all non-AA amyloidosis. Our non-AA amyloidosis experience is very limited, but survival for these patients seems more ominous than for patients in class IV.7 In our experience, the class V cases have no more than 3 scores for percentage of glomerular amyloid deposition, but class IV cases have more than 3 and are associated with more prominent vascular and interstitial deposits. Because of this observation, renal amyloid prognostic score was developed. Renal amyloid prognostic scores give more detailed information, and cutoff points can be changed based on further studies.The authors have a point that using the scores (0–4, 0–5, and 0–6) make the scoring system more complicated and may limit its intraobserver and interobserver reproducibility. We also aimed to score nil and unimportant findings and to differentiate minimal changes. Using the score 0 to 3 was argued by some of the authors because of the frequent use of the score 2. Detailed scores provide more satisfactory and additional scientific knowledge.We would like to mention once again that the biochemical classification is mandatory after diagnosing, scoring, and staging amyloidosis. The most common method for classifying amyloidosis in renal pathology is immunohistochemistry, applied to either formalin-fixed or fresh-frozen tissues. Immunohistochemical typing can be confusing sometimes because of the strong, even, and homogenous staining of the amyloid deposits with more than one antibody. Because of these pathologic findings, we should correlate them with the patients' clinical and laboratory data.Finally, we believe that using, sharing, and discussing the standardized evaluation system of renal (and also other organs, such as liver and bone marrow) amyloidosis will promote international clinicopathologic collaborative studies on amyloidosis. Future investigators and authors can debate the different properties of their findings in the non-AA cases, which we see infrequently and add them to the system. Like the other renal classification systems, the classification system for renal amyloidosis will be modified and improved following the addition of further data from carefully conducted international studies, including those about different biochemical types of amyloid deposits.We find all these contributions valuable as we develop a classification proposal that can be used as a baseline by different institutions and can be modified in due course according to different experiences and study results.