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| Renal cell adenocarcinoma |
| Etiology •Unknown. •Evidence for genetic factors with association with von Hippel Lindau disease, an abnormality on chromosome 3. •Evidence for environmental factors. |
| Pathogenesis •Unknown. •Proliferation of renal tubular cells., |
| Epidemiology •Renal adenocarcinomas represent 1 to 3 precent of visceral cancers. •Male to female ratio is about 2:1. •Wide age range with peak incidence in the 6th decade of life. •Seen in 20 to 50 percent of patients with von Hippel-Lindau disease. |
| General Gross Description •Tumor may affect any region of the kidney. There is a predilection for the upper pole. •On cut surface, the tumor may be bright yellow and this feature correlates with high lipid content. •A geographic pattern to the cut surface is frequently seen due to ischemia, necrosis, and hemorrhage. •Tumor-parenchymal interface is usually sharp. •Large tumors may distort the calyces and pelvis •Tumor can invade and exit the kidney as renal vein tumor thrombi. |
| General Microscopic Description •Tumor cells may have abundant clear cytoplasm due to lipids and glycogen. •Histologic patterns may be tubular, trabecular or solid. •Tumor is graded on a scale from I to IV depending on cytologic nuclear features. •A sarcomatoid variant is recognized which has a worse prognosis. |
| Clinical Correlation •Patients may present with costovertebral angle pain, palpable mass and hematuria. •Paraneoplastic clinical conditions include polycythemia, Cushings syndrome, feminization, masculinization, hypertension, and hypercalcemia. ization or masculinization. |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 986-987. •Weiss LM et al: Adult renal epithelial neoplasmx, AJCP, 1995 (103) pp.624-635. |
| Renal cell adenocarcinoma |
| Synopsis by: Harold Yamase M.D. (T71000M83123)[196] |
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