Renal cell carcinoma (RCC) may metastasize to any site of the body, but clinically evident metastatic intestinal involvement by RCC is extremely rare^1–7). To our knowledge, simultaneous duodenal and colonic metastases have not been reported in the English literature. We report a case of pathologically proven simultaneous duodenal and ascending colonic metastases about four years after a left nephrectomy for RCC.

A 76-year-old female patient who had undergone a left radical nephrectomy 4 years previously for RCC (mixed clear and granular cell type, TNM stage III) presented with a 1-month history of dyspepsia, lethargy and pain in the right upper abdomen. Her blood pressure was 110/70 mmHg, pulse rate 80/min, respiration rate 22/min and body temperature 36.8°C. Her conjunctiva were slightly pale and chest was normal to auscultation. Abdominal examination revealed slight tenderness but normal peristalsis; however, a movable mass was palpated in the right upper abdomen.

The hematocrit was 28.1% and the white cell count was 9700/mm³ with 77% polymorphonuclear cells and 14% lymphocytes. Serum sodium was 134 mEq/L, potassium 3.5 mEq/L, chloride 101 mEq/L and calcium 9.5 mg/L. The result of liver function tests were as follows: total protein 6.5 g/dL, albumin 3.5 g/dL, cholesterol 165 mg/L, bilirubin 0.6 mg/dL, alkaline phosphatase 105 IU/L, AST 28 IU/L and ALT 21 IU/L. The result of a stool examination revealed positive occult blood. A chest X-ray showed no evidence of lymphadenopathy. Tumor marker levels, such as carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9) and α-fetoprotein (AFP), were within normal limits.

An abdominopelvic CT scan showed circumferential wall thickening with high enhancement at the second portion of the duodenum and additional enhancement of an irregular protruding mass into the lumen of the ascending colon with multiple lymphadenopathy in the aortocaval area (Figure 1). A gastroscopy showed a large, irregular multi-lobed, partially necrotic and ulcerative protruding mass nearly obstructing the second portion of the duodenum. A colonoscopy revealed a polypoid, nodular mass in the ascending colon, which was purplish in color, had sharp margins and was pliable (Figure 2). Microscopic findings of biopsy specimens showed features identical to those of the renal cell carcinoma which was resected 4 years earlier in this patient and immunohistochemical stainings for vimentin was positive (Figure 3).

Interferon was given at a dose of 2 million IU per square meter three times a week. However, interferon therapy was discontinued after three months due to anemia, anorexia and general weakness. She is still alive 1 year later.

The biological behavior of RCC is characteristically variable and the prognosis is unpredictable⁸⁾. The clinical course of the disease ranges from months to several decades and even spontaneous regression has been documented⁹⁾. Renal cell carcinoma can disseminate locally by contiguity and metastatize to distant sites. Approximately 25% of patients with RCC have metastatic disease at the time of diagnosis²⁾. The delayed occurrence (as late as 31 years after a nephrectomy) of metastatic RCC is well known³⁾. Solitary metachronous metastases from RCC are rare; however, they can occur very late in the course of the disease¹⁾. Renal cell carcinoma may metastasize to almost every organ of the body, but 95% of the metastatic lesions involve the lung, lymph nodes, liver, bone, adrenal glands and the opposite kidney³⁾. However, there are scattered reports in the literature of clinically evident intestinal metastasis from RCC^1–7). To the best of our knowledge, simultaneous duodenal and colonic metastases have not been reported in the English literatures.

A secondary tumor involving the intestinal tract may be caused by direct extension, lymphatic spread, peritoneal or hematogenous dissemination⁴⁾. In the present case, duodenal and colonic metastases are not generalized carcinomatosis because any other metastasis is not occurred in common metastatic sites and duodenal and ascending colonic involvement are remote from a primary cancer of the left kidney.

Metastatic RCC, like the primary tumor, is frequently hypervascular^{1, 5)}. Hypervascularity of the present tumor, as suggested by a CT scan, gastroscopy and colonoscopy, was compatible with the characteristics of metastatic renal cell carcinoma. Also, positive immuno-histochemical stain for vimentin elucidated that the duodenal and colonic masses are compatible with carcinoma rather than adenocarcinoma.

Surgical excision of the local recurrence is the best procedure for therapy, but this can be radical only when the recurrence can be completely excised³⁾. Chemotherapies, including hormonal and interferon therapies, are effective in some patients with metastatic renal cell carcinoma⁸⁾. In our case, only interferon treatment was done without surgical excision. Although Interferon treatment was used to treat metastatic RCC, it is not easy to evaluate Its effectiveness because of premature discontinuance of the treatment.

In our opinion, endoscopists should consider the possibility of intestinal metastasis of RCC when endoscopic and CT studies show a hypervascular mass in a patient with a previous history of RCC.