Objectives: While progress has been made over the past 2 decades in our understanding of the development of abdominal aortic aneurysms (AAA), far less is understood about the development and pathobiology of aneurysms of the renal arteries. A valuable collection of renal artery tissue collected over the course of many years was used to directly compare histology, as well as some known mediators of AAA development in end-stage tissue from renal arteries aneurysm (RAA) and AAA. Methods: Tissues were collected and stored (frozen fresh and FFPE) at the time of aneurysm repair or renal transplant for normal aortic specimens. Histologic morphometry was performed to quantify elastin staining and immunohistochemistry for CD68, alpha-actin, MMP9 and Osteopontin (OPN). Gelatin zymography was performed on protein extracts from the tissues. Results: All aneurysms (AAA, n=9, RAA, n=9) tissues demonstrated a significantly (P<0.05) reduced percentage of mural elastin than that seen in normal aorta (16.3±3.4%, n=5). Loss of medial elastin was nearly complete in AAA (.11±.04%). Elastin in all RAA was substantially greater (3.6±1.4%) than AAA but this did not reach statistical significance (P=0.1). Elastin content is significantly greater in RAA due to fibromuscular dysplasia (RAA-FMD, n=5, 6.6±1.8%) than AAA (P<. 02) and idiopathic RAA (iRAA, 0.72±0.48%, P<.03). RAA had greater preservation of smooth muscle cell (SMC) mass in the aortic wall, and unlike AAA, the cells were in typical laminar formation in the media. Few macrophages were seen in any RAA tissue. By immunohistology, qualitatively there is substantially greater OPN in all RAA. There was also very little immunreactive MMP-9 in the RAA specimens, whereas AAA specimens had substantial MMP-9 present in inflammatory cells and SMC. MMP9 activity on zymography was found to be significantly lower in RAA (n=3) than in AAA (n=3; p=0.03). Conclusions: These important and unique studies demonstrate that the histology and general pathobiology of RAA is distinct from AAA. Elastin degradation is significantly lower in RAA, particularly in RAA-FMD. Infiltrating macrophages and elastolytic enzyme MMP-9 appear to play a relatively small role in the development of RAA.
