Retrograde venous invasion in renal cell carcinoma: a complication of sinus vein and main renal vein invasion.

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.

Renal veins and venous extension in clear cell renal cell carcinoma.

The 2002 TNM formulation defines a pT3b tumor as one that 'extends into the renal vein or its segmental (muscle containing) branches.' This definition elicits uncertainty when veins with little muscle are involved or the relationship to the main renal vein is unknown. The diameter and medial thickness of 10 normal renal venous systems were studied and compared to sinus veins involved in 54 pT3b clear cell renal cell carcinomas (CC). All tumors were grossly examined and sampled for histology by the author. An immunoperoxidase cocktail containing CD 31 and actin, Masson trichrome and elastic stains were employed to aid identification of intravenous tumor. The venous dissections showed variable numbers of primary and secondary divisions with substantial overlap in diameter and medial thickness. The medial thickness decreased with each proximal division and ranged from being nonexistent to being thick. Study of the 54 pT3b CC revealed that the initial phase of extrarenal extension involved large caliber veins draining the primary tumor. With extensive venous involvement, tumor invaded through the vein wall into sinus fat or demonstrated retrograde venous extension into adjacent cortex. Correlation between gross and histology revealed that most nodules of tumor within the sinus fat contained evidence of pre-existing veins. The following observations were made: (1) the diameter of a sinus vein or the quantity of muscle is a poor indicator of vein segment or relationship to the main renal vein; therefore, the wording used to define pT3b should be clarified; (2) extrarenal spread in CC begins with intravenous extension whereas sinus fat invasion is usually secondary; (3) retrograde venous extension occurs in cases with massive renal vein involvement; and (4) nodules within the sinus fat usually represent venous involvement.

Intravenous Tamm-Horsfall protein polyps: report of a case in association with a hematoma that mimicked a renal neoplasm.

Tamm-Horsfall protein (THP) is a glycoprotein produced only in the thick ascending limb of the loop of Henle. Its primary physiological function is unknown, but it may have a role in host defense against infectious organisms. THP is the primary scaffolding protein in all varieties of tubular casts. Under certain conditions, THP may be extruded from tubular lumens into the interstitium and lymphatic channels. It even may be found within lymph nodes sampled for staging of neoplastic conditions. THP deposits were described in lumens of large veins. The pathogenetic basis of this finding is not known, but obstruction of renal outflow was suggested, and several cases were associated with macroscopic hematuria. We report a case of intravenous THP polyposis in which, in addition to abundant hemorrhage, there was formation of a hematoma. This measured 12 cm in diameter and caused clinical concern for the possibility of renal cell carcinoma. Although the cause of the hematoma was not apparent, the association with striking intravenous polyps of THP is noteworthy because this represents the first association of intravenous THP polyps with a large intraparenchymal hematoma.

Bilateral renal artery stenosis and renovascular hypertension.

Experience with the diagnostic evaluation and operative management of 38 hypertensive patients having bilateral renal revascularization is presented. Twenty-four patients had atherosclerotic occlusions and 14 had fibromuscular dysplasia. Renal vein renin assays (RVRA) and/or split renal function studies (SRFS) were performed in 37 of the 38 patients before operation. Although RVRA was negative in 29 percent and SRFS negative in 31 percent, 24 of 26 patients (92 percent) having both tests done had at least one positive study. Twenty-one patients had simultaneous bilateral repairs and 12 had staged bilateral reconstructions. The incidence of technical failures in these two groups was 21 and 9 percent, respectively. Excluding three uncorrected technical failures and two patients with recurrent branch renal artery lesions, 90 percent of patients with atherosclerosis and all patients with fibromuscular dysplasia had a favorable blood pressure response to operation. This study supports the use of both RVRA and SRFS in the diagnostic evaluation of hypertensive patients with renal artery stenosis. If these functional tests lateralize to one side, repair of that side only is recommended. If the functional studies do not lateralize, operation is suggested only when hypertension is severe and is not controlled readily with medications. In this circumstance reconstruction of the side that appears to be diseased most severely is recommended. Contralateral repair is undertaken only when hypertension persists and when repeat functional studies lateralize to the unoperated side.