title: Retrograde venous invasion in renal cell carcinoma: a complication of sinus vein and main renal vein invasion.
abstract: Renal cell carcinoma, especially clear cell, gains access to the venous system as the initial route of extrarenal spread. Intravenous growth can involve extrarenal veins or renal veins in other portions of the kidney, referred to herein as retrograde venous invasion. This study investigates the incidence and defines the pathological features of retrograde venous invasion. Retrograde venous invasion is defined as rounded nodules of tumor separated from the primary tumor and in a location that conforms to the venous outflow. Nine cases of retrograde venous invasion were identified in a series of 115 renal cell carcinomas (8%). Two blocks from each case were stained with elastic van Gieson, Masson trichrome, CD31 and desmin to evaluate intravenous involvement. All cases were staged using the 2010 TNM staging schema. The tumors ranged in size from 4.2 to 17 cm. All cases showed sinus vein and main renal vein invasion (pT3a); three cases involved the vena cava (pT3b). Direct continuity between the primary tumor and tumor in the main renal vein was grossly evident in every case. Involved sinus veins could be followed retrograde to the cortex between renal pyramids with tumor nodules arrayed along the pyramid-cortex interface. Histologically, the involved parenchymal veins lacked a smooth muscle media and elastica. CD31 demonstrated an endothelial cell lining around many nodules. As intravenous nodules enlarged endothelium was lost, extra-venous invasion occurred and nodules coalesced and merged with the primary tumor. In conclusion, retrograde venous invasion occurred only with main renal vein involvement. Gross evaluation allowed detection in every case. Histological confirmation of intravenous nature is challenging due to the absence of smooth muscle in parenchymal veins. As retrograde growth becomes extensive nodules coalesce and merge with the primary tumor and may be included in measurement of primary tumor size if this process is unrecognized.
authors.affiliation: Department of Pathology, Louisiana State University Health Sciences Center, Shreveport, LA, USA. sbonsi@lsuhsc.edu
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Bonsib
authors.forename: Ami
authors.initials: A
authors.lastname: Bhalodia
mesh_terms: D014408:Biomarkers, Tumor / Q000032:analysis; D002292:Carcinoma, Renal Cell / Q000737:chemistry / Q000473:pathology*; D003893:Desmin / Q000032:analysis; D006801:Humans; D007150:Immunohistochemistry; D007680:Kidney Neoplasms / Q000737:chemistry / Q000473:pathology*; D009361:Neoplasm Invasiveness; D009367:Neoplasm Staging; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D012082:Renal Veins / Q000737:chemistry / Q000473:pathology*; D013194:Staining and Labeling; D047368:Tumor Burden
chemical_list: D014408:Biomarkers, Tumor; D003893:Desmin; D019408:Platelet Endothelial Cell Adhesion Molecule-1