Review of systems showed pertinent negatives for any cyanosis, rashes, or ulcerations of the extremities. The patient had no history of vertigo except during occasional use of left arm especially when raised above the head but not consistently. He also denies any transient paralysis, syncope , diplopia, vision loss or slurred speech, No history of hematuria or hematochezia.

Physical exam revealed a marked discrepancy of 75 mmHg in the systolic pressures of his left and right arms (left being lower) and a soft left subclavian artery bruit. The patient maintained left radial pulse when the arm was raised above the head. Patient also had no palpable pulses or edema of the feet. No splinter hemorrhages were noted to the nail beds. The patient had no ulcers to the mouth or skin. No purpuric or petechial lesions were noted. The patient had normal brachioradialis and patellar tendon reflexes bilaterally. Patient had good sensation to the fingers, hands, and arms to light touch. Patient had a negative Tinel and Phalens sign. No tremors were noted.

There are approximately 13.6 cases of renal cell carcinoma per 100,000 persons, and the average age at disease onset is 64. There are approximately 30,000 new cases per year and 12,000 deaths per year from the disease. Males are twice as likely to be affected. Renal cell carcinoma has a 5 year survival rate of 68.4%; however if the tumor is caught before it spreads the rates are much better. Localized disease has a 5 year survival rate of 90.4%, regional disease has a 5 year survival rate of 62.3%, and metastatic disease has a 5 year survival rate of 10.4%. The most significant risk factor for renal cell carcinoma is tobacco use.

Histologically, there are 4 different kinds of renal cell carcinoma: Clear Cell, Papillary, Chromophobe, and Collecting Duct. Clear cell accounts for 70-80% of all renal cell carcinomas and is the type that will be discussed here. The tumor is composed of cells with only a clear or granular cytoplasm, hence its name. There are both sporadic and familial cases of the malignancy, with the majority of cases being sporadic. Though the majority of cases arise spontaneously, 98% of both sporadic and familial cases have a mutation or deletion in the VHL gene on the short arm of chromosome 3. The VHL gene is a tumor suppressor gene that codes for a protein that is part of an ubiquitin ligase complex in the kidney; its function is to “tag” unwanted and unneeded proteins for degradation. One of its targets, hypoxia-inducible factor 1 (HIF-1) is a protein that enables the cancer to gain multiple functions. HIF-1 is always active, and it increases the transcription and translation of multiple growth factors such as vascular endothelial growth factor, platelet derived growth factor, tumor growth factor alpha and tumor growth factor beta. It also upregulates the transcription of insulin-like growth factor 1, and by the addition of these various growth factors the tumor is able to both increase its size and blood supply.

Morphologically, most renal cell carcinomas grow in the upper or lower poles of the kidney and arise as unilateral, solitary, spherical masses. They tend to be yellowish, grayish, white masses that can distort the normal shape of the kidney. The yellowish coloration can be owed to the lipid rich contents of the cells and the grayish-white areas are usually areas of ischemic or necrotic tissue where the tumor has outgrown its vascular supply.

One of the interesting features of renal cell carcinoma is its tendency to invade the renal vein as a solid tumor mass. This mass can then proceed to invade the inferior vena cava, and has been known to grow into the right atrium of the heart, remaining a solid tumor mass directly growing out of the primary tumor in the kidney. When the tumor invades the renal vein and inferior vena cava it is termed a “tumor thrombi”, and a classification system has been built for these thrombi to help guide clinical and surgical management of the tumors. The classification system is typically divided into four classes, and is as follows: I) At the level of the renal vein or <2 cm above renal vein II) >2cm above renal vein but at or below the hepatic veins III) above hepatic vein but below diaphragm IV) above diaphragm. Tumor thrombi in classes I or II can usually be performed without cardiopulmonary bypass in a relatively healthy, hemodynamically stable patient but levels III & IV require cardiopulmonary bypass due to the involvement of the portal venous system and also due to atrial involvement in some instances of level IV tumor thrombi.