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Papillary renal cell carcinoma (RCC) is known by its tendency to avascularity by angiography; however, data concerning its clinicopathologic spectrum and prognosis are not available. In a review of 224 renal cell carcinomas accesioned in our files, 34 were found to be papillary and 190 of other histologic types. A comparative analysis of these two gropus revealed marked differences. The majority of papillary tumors (85.3%) were in pathologic stage I, whereas more than half of the nonpapillary tumors had extended beyond the limits of the kidney. Follow-up data revealed that the survival for papillary RCC was significantly higher than that for nonpapillary tumors. This difference held true even when tumors in the same pathologic stage were compared. Many papillary tumors, particularly those with a favorable course, were massively necrotic, densely infiltrated by macrophages, or both. In view of these findings, the possibility that host mechanisms are involved in destruction and confinement of the tumor is discussed. Examination of kidney tissue distant from the tumor disclosed, in some cases, atypical hyperplastic changes of collecting tubules; this raises the possibility that some papillary tumors arise from distal tubular epithelium. Hypo- or avascularity was present in all papillary RCC's studied by angiography.
Papillary renal cell carcinoma (RCC) is known by its tendency to avascularity by angiography; however, data concerning its clinicopathologic spectrum and prognosis are not available. In a review of 224 renal cell carcinomas accesioned in our files, 34 were found to be papillary and 190 of other histologic types. A comparative analysis of these two gropus revealed marked differences. The majority of papillary tumors (85.3%) were in pathologic stage I, whereas more than half of the nonpapillary tumors had extended beyond the limits of the kidney. Follow-up data revealed that the survival for papillary RCC was significantly higher than that for nonpapillary tumors. This difference held true even when tumors in the same pathologic stage were compared. Many papillary tumors, particularly those with a favorable course, were massively necrotic, densely infiltrated by macrophages, or both. In view of these findings, the possibility that host mechanisms are involved in destruction and confinement of the tumor is discussed. Examination of kidney tissue distant from the tumor disclosed, in some cases, atypical hyperplastic changes of collecting tubules; this raises the possibility that some papillary tumors arise from distal tubular epithelium. Hypo- or avascularity was present in all papillary RCC's studied by angiography.
The increased occurrence of hypernephroma in kidneys with renal cysts has been documentedThe incidence rate of this association ranges from 2.1% to 3.5%.3 Despite these statistics, our literature review reveals only one case of ultrasound demonstrated renal cyst categorized as atypical because of concomitant hypern e p h r~m a .~We recently encountered a case where computed tomography (CT) demonstrated a small mural tumor at the base of a renal cyst. In retrospect, this was present on the renal ultrasound examination. Since ultrasound plays such a pivotal role in the radiographic evaluation of renal masses we believe that review and analysis of this case is instructive. This presentation, coupled with a discussion of the relationship between cyst and hypernephroma, should provide the understanding necessary to better perform and interpret renal sonograms for suspected cyst. CASE REPORTA 47-year-old white male presented with complaints of easy fatigability and occasional shortness of breath. He denied orthopnea, pedal edema, dysuria, and hematuria. A coronary artery bypass had been performed 10 months earlier with relief of Class I11 angina symptoms. Physical examination was unremarkable with no evidence of hepatosplenomegaly , flank tenderness or masses, or peripheral lymphadenopathy. Laboratory studies done during surgical follow up revealed persistent hematocrits between 52% and 56%. On re-admission the hematocrit was 56%, hemoglobin 18.4 g/dl, white blood cell count 7700 m3, and creatinine 1.4 mg/dl. Urinalysis showed occasional white blood cells, but no red cells. A chest radiograph was normal. The electrocardiogram showed an old diaphragmatic myocardial infarction. As part of the evaluation for polycythemia, a red cell mass study and intravenous urography were ordered. Stress polycythemia was documented by a normal red cell mass and slightly decreased plasma volume.Urography (Fig. 1) demonstrated a peripheral 2-cm hypovascular right renal mass with an imperceptible rim. However, the mass was not sharply demarcated from the subjacent renal parenchyma. Ultrasound examination (Fig. 2) revealed findings of a septated renal cyst. Since neither the urogram nor ultrasound examination confirmed a simple renal cyst, CT was recommended.CT (Fig. 3) identified a renal cyst with septation. Despite repeat 5-mm sections, a sharp demarcation between cyst and adjoining renal parenchyma could not be demonstrated and the possibility of mural tumor was suggested. An arteriogram was recommended.Arteriography (Fig. 4) showed a predominately hypovascular mass which corresponded to the renal cyst imaged earlier. However, medially within the cyst, a smaller hypervascular contrast blush confirmed the presence of mural tumor. The right renal vein and inferior vena cava appeared unremarkable.A right radical nephrectomy was then performed. To facilitate imaging correlation the resected kidney was sectioned in a transverse plane (Fig. 5). Clear amber fluid was identified within the septated cyst. Within the wall of the cyst adjacent to t...
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