[Transitional cell carcinoma of the renal pelvis with cystic formation: a case report].

A 75-year-old man consulted our hospital complaining of gross hematuria. Retrograde pyelography revealed a filling defect and deformity of the upper calix of the left kidney. Abdominal echography and computed tomography revealed a left renal cystic tumor with irregular wall thickness measuring 7 by 5 cm. As left renal pelvic tumor or left renal cell carcinoma was suspected, left total nephroureterectomy was performed. Macroscopically, the cystic tumor contained a papillary tumor connected to the renal pelvis and histopathological diagnosis was grade 1 transitional cell carcinoma. Cystic formation caused by obstruction of the upper calix was suspected. After adjuvant chemotherapy, he has been well without recurrence or metastasis for 19 months after the operation. This is the 15th case of renal pelvic tumors with cystic formation including tumors in the pyelocaliceal diverticulum reported in Japan.

[A case of soft renal calculi with xanthogranulomatous change].

A case of soft renal calculi with xanthogranulomatous change is reported. A 37-year-old female visited our hospital on February 4, 1992 complaining of frequency of urination and right lower abdominal pain. Under the clinical diagnosis of right renal calculi, extracorporeal shock wave lithotripsy was attempted, but no sign of destruction was observed. Right pyelolithotomy was performed on June 8, 1992. Several soft calculi were removed from the right renal pelvis. Microscopic examination showed that the calculi were surrounded by a cell layer including foam cells and giant cells. In addition, the calculi revealed positive reaction by several stainings (alcian-blue, PAS and muticarmin), which showed that the calculi were mainly composed of mucopolysaccharides. We discussed this disease in terms of symptoms, diagnosis, treatment and mechanism in comparison with previous reports.

Causative role of lysosomal enzymes in the pathogenesis of cerebral lesions due to brain edema under chronic hypertension.

In order to clarify the role of lysosomal enzymes in the developmental mechanisms of cerebral lesions under chronic hypertensive conditions, we histochemically and biochemically investigated acid phosphatase, N-acetyl-beta-glucosaminidase, and cathepsin B in the cerebral cortex and subcortical white matter in stroke-prone spontaneously hypertensive rats (SHRSP). Histochemical investigation showed that SHRSP had an increased number of cells with positive reaction to these enzymes in the edematous cortex and degenerated subcortical white matter. The cells with positive reaction were made up of reactive astrocytes and microglias. The activities of all enzymes in the aged SHRSP were higher than those in normotensive rats, the differences being significant at 24 weeks of age. The present study suggests that chronic hypertension or chronic edema causes increased activities of lysosomal enzymes in the cerebral cortex and subcortical white matter, and that the activated lysosomal enzymes take part in the developmental mechanisms of cystic formation as well as the diffuse degeneration of the white matter.

The possible role of lysosomal enzymes in the pathogenesis of hypertensive cerebral lesions in spontaneously hypertensive rats.

In an attempt to clarify the role of lysosomal enzymes in the developmental mechanisms of cerebral lesions under chronic hypertensive conditions, we biochemically investigated the activities of acid phosphatase (AcPase), N-acetyl beta-glucosaminidase (NAGase) and cathepsin B (CathB) in the cerebral cortex and subcortical white matter in stroke-prone spontaneously hypertensive rats (SHRSPs). We also investigated enzyme-histochemically the activities of AcPase and NAGase, and immunohistochemically the distribution of CathB. The activities of all enzymes tended to increase with advancing age. The enzyme activities in the aged SHRSPs were in general higher than those in normotensive rats, the differences being significant at 24 weeks of age. Histochemical investigation showed that SHRSPs had an increased number of cells with positive reaction to these enzymes in the edematous cortex with and without vascular changes, and degenerated subcortical white matter. These cells with positive reaction were made up of reactively increased astrocytes and microglia. Neurons in the edematous area also showed slightly intensified enzyme activities. The present studies suggest that chronic hypertension or chronic edema due to hypertension causes increased activities of lysosomal enzymes in the cerebral cortex and subcortical white matter and, thus, that activated lysosomal enzymes may take part in the developmental mechanisms of cystic formation as well as the diffuse degeneration of the white matter.

Lysosomal enzyme activities in the cerebral microvessels in spontaneously and renal hypertensive rats.

In an attempt to clarify the role of lysosomal enzymes in the developmental mechanisms of the changes of cerebral microvessels under hypertensive conditions, the activities of acid phosphatase, N-acetyl-beta-glucosaminidase, and beta-glucuronidase in the isolated microvessels from the cerebral cortex of spontaneously and renal hypertensive rats were biochemically studied. The activities of all the enzymes were higher than those in normotensive control animals, although there was a variation in intensity according to the age and kind of enzymes. The enzyme activities in spontaneously hypertensive rats showed a tendency to increase with advancing age. Hypertension seems to increase activities of lysosomal enzymes in cerebral microvessels, and this activation may in turn play a role in the development of further hypertensive cerebrovascular and cerebral changes.

Effect of hypertension on lysosomal enzyme activities in aortic endothelial cells.

In order to obtain information about the changes in lysosomal enzyme activities in arterial endothelial cells under hypertensive conditions, a biochemical study was performed on 5 lysosomal enzymes, acid phosphatase, N-acetyl-beta-glucosaminidase (NAGase), cathepsin B, cathepsin D and beta-glucuronidase, in endothelial cells isolated by an enzymatic technique from the aorta of spontaneously and renal hypertensive rats, and normotensive control rats. The aortic endothelial cells in the old spontaneously and the renal hypertensive rats showed increased activities of enzymes examined in comparison with those in the age-matched control rats. Endothelial cells in young spontaneously hypertensive rats did not show any elevated enzyme activities compared with those in the controls, and the enzyme activities tended to increase with aging. From this, it is deduced that hypertension activates lysosomal enzyme activities in aortic endothelial cells. The differences in the activities of NAGase, cathepsin B and cathepsin D between hypertensive and control animals increased markedly with advancing age. These activated lysosomal enzymes seem to be involved in the developmental mechanism of arterial endothelial cell injury in hypertension and in further development of hypertensive vascular changes.

Evaluation of (1-sarcosine, 8-isoleucine) angiotensin II as a therapeutic agent for oleic acid-induced pulmonary edema.

(1-Sarcosine, 8-isoleucine) angiotensin II was assessed as a therapeutic agent for acute respiratory distress syndrome with oleic acid pulmonary edema in sheep used as an experimental model. Under general anesthesia with controlled mechanical ventilation with 100% oxygen, 32 sheep received oleic acid (0.075 ml/kg) intravenously. After oleic acid infusion, 20 animals were treated with continuous intravenous infusion of the angiotensin II analogue; nine received 300 ng/kg/min, six received 600 ng/kg/min, and five received 2000 ng/kg/min. Cardiopulmonary measurements were repeated every 30 minutes for 270 minutes. According to time-integrated PaO2, six of 15 animals of the groups given 300 and 600 ng/kg/min (43%) did not respond to the treatment. All animals responded in the group given 2000 ng/kg/min. Animals in the latter group had lower Qs/Qt, PaCO2, and airway resistance than had the control animals. Elevation of pulmonary vascular resistance was limited and mean arterial blood pressure was well maintained. These results reveal that (1-Sar, 8-Ile) angiotensin II is effective in the treatment of oleic acid-induced pulmonary edema.