The natural history of small renal masses.

PURPOSE: Ultrasound, computerized tomography and magnetic resonance imaging are widely available. Incidentally discovered small renal masses are reported more frequently. Most of these masses are low stage renal cell carcinomas. To understand better the natural history of these lesions and offer appropriate management, we followed prospectively a series of patients with this type of lesion. MATERIALS AND METHODS: A total of 13 patients with radiologically detected solitary small renal masses who were unfit for or refused surgery were followed with abdominal imaging for a median of 42 months. Median patient age was 69 years and mean lesion volume at diagnosis was 13.6 cm.3 or 2.95 cm. in diameter. Growth rate was calculated based on tumor volume rather than bi-dimensional diameter. Individual slopes of tumor size in time were calculated. RESULTS: Of the 13 patients 5 underwent surgery following a period of surveillance because of apparent tumor enlargement or new onset of symptoms. Pathological evaluation revealed renal cell carcinoma in all 5. No patient had metastases. Only 2 tumors were fast growing and these were the only 2 cases in which symptoms developed. When these patients were excluded from analysis, average growth rate was 1.32 cm.3 per year (p = 0.5, 95% confidence interval -3.00 to 5.76 cm.3 per year), which was not statistically significantly different from 0 slope or no growth. CONCLUSIONS: These results demonstrate that the growth rate of small renal tumors is variable, tumors that are destined to grow and possibly metastasize do so early and most small tumors grow at a low rate or not at all.

Identification of a unique glomerular factor X activator in murine lupus nephritis.

The role of glomerular procoagulant activity (PCA) was studied in mice (MRL/lpr, NZBxWF,, and BXSB) that are known to develop lupus nephritis. In young mice (6 to 8 wk) without renal disease, there was no increase in spontaneous glomerular PCA. In contrast, older (5 to 8 mo) autoimmune mice had significant augmentation in glomerular PCA, coinciding with the histologic appearance of severe glomerulonephritis and renal fibrin deposition. The PCA was characterized as a serine protease that directly activated factor X. This factor X activator is not tissue factor because (1) expression of PCA was not dependent on factor VII; (2) a monoclonal antibody against the factor X activator inhibited glomerular PCA, but not tissue factor; (3) the molecular weight (66 kD) of the activator was different from that of tissue factor; and (4) concanavalin A inhibited tissue factor but not glomerular PCA. Immunohistochemical studies localized the factor X activator to the glomerular mesangium and capillary wall of 4- to 6-mo-old diseased MRL/lpr mice. Immunogold-labeled antibody bound to the dense deposits, macrophages, and endothelial cells of diseased glomeruli. These studies define the role of a unique glomerular factor X activator in murine lupus nephritis.