Urinary stone develops through the process of growth and aggregation of urinary crystalline substances. Therefore, it is considered important to quantify urinary crystals. I recently devised a system composed of a coulter counter model ZBI, a coulter channelyzer C-100 and microcomputer for measuring calcium oxalate (CaOx) crystals accurately and easily. In a preliminary study this system showed a very good reproducibility. By this new system I investigated the amount and size of CaOx crystals in healthy subjects and urinary stone formers on various diets (standard, high protein, high calcium, high oxalate, high protein-high oxalate, high calcium-high oxalate), in an attempt to elucidate the mechanism of CaOx crystal formation.
The results obtained are as follows:
1) Urinary CaOx crystals were detected more frequently in the stone formers than in the normals, except on a high protein diet. The detection ratio was most increased by the intake of oxalate. The diet supplemented with calcium or portein alone had no influence upon the detection ratio.
2) The amount of crystals formed was greater in the subjects on oxalate loading diets than in those on non-oxalate diets and also in the stone formers than in the normals.
3) The number of crystals formed was not different between the stone fomers and the normals. Therefore, the relative affluence of urinary crystals in stone formers indicated that each of the crystals found in their urine was larger than that in the urine of the normal subjects.
4) The formation of urinary CaOx crystals depended strongly upon urinary oxalate levels in both the patient group and the normal group. Urinary calcium levels also had some bearing on crystal formation in the stone formers but not at all in the normals.
5) Citrate and magnesium are known as crystallization inhibitors. There may be some other substances that fall under this category.
6) Urinary CaOx crystals were increased quantitatively in association with elevated urinary oxalate levels. In addition, the increase was dependent upon calcium levels to some extent in the stone formers.

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Human prostate has been known to contain a large amount of acid phosphatase (ACPase). However, little is known about the ultrastructural localization on the human prostatic epithelium. The object of the present investigation is to demonstrate a definite ACPase localization in the human prostatic epithelium by the Gomori method. The activity of ACPase was found not only in the secondary lysosomes at the basal and supuranuclear region, but also in the Golgi apparatus around the nucleus. The localization of ACPase was also documented in the multivesicular bodies. electron microscopic and cytochemical studies also showed that these organelles were extruded and pinched off as a merocrine secretion from the apical cytoplasmic membrane. Therefore, the present ultracytochemical investigation demonstrated that ACPase in the prostatic epithelium plays dual roles as lysosomes enzyme and secretory enzyme.

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DNA histograms were measured by flow cytometry (FCM) for 100 bladder tumors (transitional cell carcinoma) of 94 patients using the rapid detergent method with propidium iodide. The patients were followed clinically for 3 months to 5 years. The mean follow-up time was 23.3±16.0 months. The tumors were classified as diploid or DNA aneuploid. The degree of ploidy was determined by DNA index (DI), the ratio of peak channel number of the G₁ compartment of the tumor cells to that of the diploid standard, and the existence of more than one aneuploid cell clone (clonal heterogeneity) was considered.
1) During the follow-up period, seventeen patients died; 8 of them died of bladder cancer, and 9 of other causes. Five patients were alive with cancer at the advanced stage of bladder cancer, and other 72 patients were alive in a tumor free state. FCM DNA analysis showed that 24 tumors were diploid and 76 tumors were DNA aneuploid. Thirteen patients showed the existence of clonal heterogeneity. Values of DI were distributed from 1.00 to 4.08.
2) All tumors of the patients who died of bladder cancer and patients who were alive with cancer at the advanced stage showed DNA aneuploidy. Namely, all tumors of the poor prognosis patients showed DNA aneuploidy. Patients with more than one aneuploid cell clone showed a poorer prognosis rate (38.5%) than those with only one aneuploid cell clone (13.1%). From these results, it is clear that DNA aneuploidy and the existence of clonal heterogeneity were markers of poor prognosis.
3) To estimate the value of FCM DNA analysis as a marker of intravesical recurrence, thirty-one cases of newly detected superficial bladder tumors were studied. No correlations were observed between tumor recurrence and grade, nor between recurrence and ploidy.
4) It is suggested that, to estimate the malignant potential of bladder tumor, FCM DNA analysis is valuable and ought to have an influence on the treatment of patients with bladder cancer. Considering its rapidity, especially as the preoperative examination of T1, T2 bladder tumors, FCM DNA analysis is a good method to determine whether only the bladder preserving operation is enough or not. We think that tumors with DNA aneuploidy or more than one aneuploid cell clone need more aggressive thearpy than diploid ones.

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Serum level of Le^x and sialosyl Le^x antigen in healthy group, patients with benigne diseases and with urological malignant diseases were quantitatively investigated. Though Le^x elevated little in both benigne and malignant diseases, positive rate of sialosyl Le^x was as follows: Renal adenocarcinoma 33.3%, Prostatic carcinoma 30%, Bladder carcinoma 18.1%, and testicular and penile tumor 0%. False positive rate in healthy group (0.9%) and benigne disease group (3.0%) was very low. These results indicate that serum sialosyl Le^x detected by FH-6 antibody should be a useful serum marker of urologic adenocarcinoma such as renal cell carcinoma and prostatic carcinoma.

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The pathogenicity of Enterococcus faecalis in the urinary tract was investigated clinically and experimentally.
A clinical study was performed on E. faecalis infection in the urinary tract which had been detected at the Department of Urology, Tokyo University Hospital from July 1980 to June 1984. The annual incidence of E. faecalis isolated from the urinary tract had been increased from 8.5% to 15.4% in this period. Totally, 279 strains of E. faecalis were isolated from 271 patients in the four years. Among these 271 patients, 242 (89.3%) were cases of complicated urinary tract infection, and 88 patients (32.5%) were catheter indwelt patients. The percentage of the patients with a single infection of E. faecalis was 58.7%, and the other patients showed polymicrobial infections. Antimicrobial activity tests showed that most strains of E. faecalis were highly sensitive to penicillin G and ampicillin, but were resistant to new cephems and aminoglycosides. In clinical observations, most patients had no significant symptoms but 20 patients developed fever, pain on micturition and urinary frequency. In these symptomatic cases, E. faecalis was thought to be causative in ten patients.
Experimental pyelonephritis was produced by the transurethral inoculation of the organisms into the rat urinary bladder. Two experimental designs were employed. In the first study, infection was induced by E. faecalis alone. Three to seven days after inoculation, pyelonephritis was found in 5 of 20 kidneys. These five kidneys demonstrated mild inflammatory changes localized along the renal pelvis. However, fourteen days after inoculation, no histological change was found in the kidneys and the number of organisms had decreased in the renal tissues. Then, in order to suppress the host defence mechanism, cyclophosphamide was administrered transperitoneally before the inoculation of E. faecalis. These rats showed a high incidence of pyelonephritis, and more severe lesions, some of which extended into the medulla and cortex, were seen in several kidneys. The renal enterococcal populations persisted at high levels in these kidneys. In the second study, rats were infected with both E. faecalis and Proteus mirabilis. The incidence of pyelonephritis was 79.2%, and large numbers of both strains were still present on the fourteenth day after inoculation. The infected rats were treated with latamoxef beginning three days after the inoculation with the two strains. Histological observations proved that the inflammation continued in the kidneys in which P. mirabilis had disappeared. No remarkable change was seen in the numbers of E. faecalis in the renal tissues after the administration of latamoxef.
The results of the clinical and experimental studies indicate that the pathogenicity of E. faecalis seems to be relatively low in the urinary tract. However, when the host defence mechanism is suppressed or when a polymicrobial infection with virulent strains has occurred, the pathogenicity of E. faecalis may increase.

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The total LDH activities and LDH isozymes were measured in 6 normal testicular tissues and 11 seminoma tissues. The total LDH activities of seminoma tissues were 3778.4±3674.7W.U./mg protein (mean±S. D.), significanlty higher than those of mormal testicular tissues (787.2±502.4W.U./mg protein) (p<0.05). In normal testicular tissues, 5 isozymes (from LDH1 to 5) and LDHX were detected, but in semimona tissues only 5 isozymes were detected and LDHX was not detected. In semmoma tissues, compared with normal tissues, LDH1 and LDH2 were elevated. Since it is widely accepted that LDHX appears in primary spermatocytes, these data suggest that the cells of semimoma are composed of less differentiated cells than spermatogonia.

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The clinical evaluation of prostate specific antigen (PA) as a serum marker of prostatic cancer was performed.
Serum PA was determined by Yang Laboratories radioimmunoassay (RIA) kit in 229 male patients (untreated prostatic cancer-13, treated prostatic cancer-75, benign prostatic hypertrophy (BPH)-88, prostatitis-13, bladder neck contracture-3, other malignant diseases-14, other benign diseases-23), and it was evaluated using three ranges, i. e. normal range, BPH range and cancer range (PA positive). The upper limit of the normal range was set at 3.7ng/ml which was the mean+2S.D. from 23 patients without prostatic and malignant diseases. The upper limit of the BBH range was set at 20.4ng/ml, the mean+2S.D. from 88 BPH patients.
Serum prostatic acid phosphatase (PAP) was also determined by GammaDab RIA kit and the upper limit of the normal range was set at 3.3ng/ml in the same way.
PA positive rate (PA>20.4ng/ml) was 92.3% (12/13) in the untreated postatic cancer group (stageA-100% (2/2), stageB-67% (2/3), stageC-100% (2/2), stageD-100% (6/6), 6.8% (6/88) in the BPH group and 4.3% (6/141) in the non-prostatic cancer group.
PAP positive rate (PAP>3.3ng/ml) was 41.7% (5/12) in the untreated prostatic cancer group (stageA-0% (0/2), stageB-0% (0/3), stageC-0% (0/2), stageD-100% (5/5)), 4.5% (4/88) in the BPH group and 5.7% (8/141) in the non-prostatic cancer group.
In other words, the sensitivity of PA in the prostatic cancer group is superior to PAP while the specificity is much alike between them.
Determination of PA alone is not satisfactory. Combination of both PA and PAP is thought to work as a wider spectrum marker of prostatic cancer in various pathologic states.

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The human evoked electrospinogram (EESG) of bulbocavernosus reflex was examined by an epidural recording method. When the recording electrode was located at the level of the sacral spinal cord in the epidural space, the potentials elicited by penile electrostimulation could be recorded from 10 subjects with suprasacral lesions. This electrospinogram is a response in the corresponding spinal segment and termed as a segmental EESG. In addition, the urodynamic study was done in 6 of these 10 subjects with detrusor hyperreflexia with DSD.
The segmental EESG consisted of the initial positive spike (P₁) and a subsequent slow and sharp negative wave (N₁), followed by a slower positive wave (P₂). The P₁-wave had a peripheral latency of 9.8msec and a duration of 1.20msec. The N₁-wave had a peripheral latency of 13.4msec, a central latency of 3.6msec and a duration of 6.1msec. The P₂-wave had a peripheral latency of 25.8msec, a central latency of 15.8msec and a duration of 28.0msec.
The P₁-wave easily noticed at the stimulation strength of 20V and had the lowest threshold among these components. As the stimulation strength was increased, the amplitude of the P₂-wave grew quickly to reach a maximum while the increase in amplitude of the N₁-wave had a wider range.
These characteristics were very similar to those of EESG elicited by stimulation of the peripheral nerve at an extremity. Thus, in the segmental EEGS of bulbocacernosus reflex, the origin of each component (P₁, N₁, and P₂) seems to have the same basis as that established in the evoked spinal somatosensory potentials, showing that the P₁-wave is related to the arrival of afferent volleys at the dorsal root and the subsequent N₁ and P₂-waves reflect the activity of interneurons and primary afferent depolarization, respectively.
In 2 patients with sacral lesions or peripheral neuropathy, the urodynamic evaluation showed that both patients had the detrusor areflexia. Regarding the EESG of these 2 subjects, any potentials could not be recorded from 1 patient with sacral lesion. However, in the remaining one with peripheral neuropathy, only the P₁-wave was recorded.
It seems from these results that the epidural recording of EESG is an important means in neurourology because it provides with much infromation on the spinal cord function.

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Contact-micro-cystoscopy is a new technique to stain the bladder epithelium and examine it with a high magnification in vivo. Storz Micro-endoscope 27015B was used for the method.
0.5% cresyl violet acetate solution was instilled into the bladder. 5 minutes after instillation the bladder was lavaged and examined cystoscopically. We evaluated the degree of staining, the appearance of the surface and the size and the density of nuclei of the bladder epithelium. Normal epithelium was stained lightly, and showed a smooth surface and small, sparse nuclei. Neoplastic lesions were stained moderately, and showed a irregular surface and large, dense nuclei. Erosion was, however, stained remarkably and showed very sparse nuclei.
Since the differentiation between normal epithelium and neoplastic lesions was possible to some degree, this method is thought to be useful to detect neoplastic lesions which can not be proved by usual cystoscopy.

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Continence mechanism was studied by urethral pressure profilometry during bladder empty and filling phases in “internal sphincter dogs”, i. e., female mongrel dogs whose external urethral sphincter had been removed three weeks before examintion. Urethral pressure at 0.5cm distal to the bladder neck showed no significant changes during bladder empty and filling phases. Urethral pressure at 1.5cm distal to the bladder neck during filling phase was significantly lower than that during empty phase. The avove difference of urethral pressure disappeared after propranolol administration. These findings indicate that relaxation of the internal sphincter seems to play some parts of continence mechanism.

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The pattern of recovery from unilateral ischemic acute renal failure (ARF) and the effects of post-ischemic infusion of mannitol, methylprednisolone and adenosine triphosphate magnesium chloride (ATP-MgCl₂) on the process of the recovery were investigated in 29 dogs. The variables used for separate renal function study were inulin clearance (Cin), creatinine clearance (Ccr), para-aminohippuric acid clearance (C_PAH), osmolar clearance (Cosm), fraction of filtered sodium excreted (FE_Na) and fraction of filtered pottasium excreted (FE_K). Individual renal urine was obtained from the left cutaneous ureterostomy made on the abdomen and from the bladder in which the right kidney alone drained. Unilateral ischemic ARF was produced by complete occlusion of the left renal artery and vein for 90 minutes.
In the first 9 dogs, renal clearance study was repeated at consecutive 1, 3, 5 and 7 weeks following the occlusion. Histological observation of the kidney was finally done.
The results were as follows:
1) Cin, Ccr and C_PAH dropped to their nadirs 1 week after ischemia, then were followed by a gradual recovery.
2) The decrease of Ccr, Cin and C_PAH in the ischemic kidney was significant for 5, 3 and 3 weeks, respectively.
3) Significant increase of FE_Na in the damaged kidney was observed at only 1 week after ischemia.
4) No significant change of FE_K and Cosm was observed through the period of the experiment.
5) At 7 weeks after occlusion, no more functional or histological differences could be observed between the ischemic and the control kidneys.
The results indicated that this type of ischemic ARF was reversible within 7 weeks, and might be useful as a model for a short-term comparative study of therapeutic agents for ARF.
Immediately after release of the left renal artery occlusion, 10ml/kg of 20% mannitol solution, 30mg/kg of methylprednisolone, and 200μmol/kg of ATP-MgCl₂ were intravenosuly administered in 5 dogs. Another 5 dogs were untreated after ischemia for the control study. In these second experiments, renal clearance study was repeated at 1, 4 and 7 days after occlusion.
The results were as follows:
1) The post-ischemic decrease of Cin, Ccr and C_PAH was significantly prevented by intravenous administration of mannitol.
2) Significant increase of Cosm was observed in the contralateral kidney at 1 day after ischemia by use of methylprednisolone. Protective effects against the ischemic injury, however, could not be observed by the use of methylprednisolone and ATP-MgCl₂.
These experiments endorse the clinical effect of mannitol infusion for unexpected renal ischemia.

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It has been reported that there is the highest γ-GTP activity of human organs in renal proximal tubular cells. In this article γ-GTP activities in various renal tumors, containing 13 renal cell carcinoma, 1 Wilms tumor, 1 renal haemangioma and 1 renal pelvic tumor, were evaluated by biochemical and histochemical methods. Biochemical study showed that γ-GTP activity of normal renal cortex was highest of all renal tissues examined, and γ-GTP activity of clear cell carcinoma was a quarter of normal renal cortex, but much higher than other tumors. By histochemical examination specific localization of γ-GTP was proved only in normal renal cortex and clear cell carcinoma.
Correlationship between renal tissue and γ-GTP activity was discussed, and it was suggested that granular cell carcinoma might not be originated from proximal tubules but from other tissues.

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Inulin clearance (Cin), water and sodium excretion were determined in experimental hypertensive rats utilizing isolated renal perfusion. To determine the effect of perfusates on water and sodium excretion, various solutions such as lactated Ringer (L), 5% glucose in water, 0.9% saline with 4% bovine serum albumin (BSA), L plus 4% BSA and 0.9% saline were used. The results obtained with 0.9% saline were almost equal or superior to those with other solutions, 0.9% saline was therefore used for the following experiments.
In spontaneously hypertensive rats (SHR), Cin, water and sodium excretion were decreased markedly at and after 5 weeks of age.
Cin in post-DOCA hypertensive rats was identical to that in Wistar rats, but Cin per kidney weight, water and sodium excretion determined by perfusion study, were significantly decreased. When renal perfusion was performed extracorporeally, the excretion was significantly larger than that from in situ kidney, indicating that denervation increased the renal excretion of water and sodium in 13-week-old SHR.
In conclusion, hypertension in SHR and post-DOCA hypertension are considered at least partly due to the impairment or renal excretion of water and sodium, and the renal nerve participates in their excretion.

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During the past 5 year period, oral morphine hydrochloride was administered to 31 cases with end-stage urologic cancer to eliminate their intractable pain. Initial dose, usually 20-30mg/day, was augmented every 2 days and given in divided dosis 6 times a day.
Twenty-two cases (71%) were relived of their pain. The average dosis and administered period were 53mg/day and 74 days, respectively. Excluding 4 cases who were administered for more than 200 days, 51 days was the mean period when opium was nesessary.
Although mild, constipation, vomiting, somnolency and illusion were noted as the side effects of opium.
After achieving analgesia by this therapy, discontinuation or reduction of morphine hydrochloride was possible without any withdrawal symptom.
There is no optimum dose of opium for cancer pain. Therefore, use of enough opium should not be hesitated. It is advisable to use sufficient opium to eradicate intractable pain due to end-stage urological cancer during the final 50 days of their life and let the patient die in peace.

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Sodium malate, malic acid, sodium succinate, succinic acid, and sodium bicarbonate were added to a calcium-oxalate lithogenic diet (a glycolic-acid diet) in order to determine their effects in preventing lithogenicity. Male Wistar-strain rats who had been fed the glycolic-acid diet developed marked urinary calculi within 4 weeks. Rats in the sodium malate and succinate groups had, however, almost no stones in the urinary system. Rats in the bicarbonate, malic-acid and succinic-acid groups showed less effect than those in the malate and succinate groups. Urinary oxalate excretion was high in all the groups during the experiment. Urinary citrate excretion was high in the malate, succinate and bicarbonate groups, but low in the malic-acid, succinic-acid, and glycolic-acid groups; the urinary citrate concentration was relatively higher in the malate and succinate groups than in the bicarbonate group, especially towards the end of the experiment. The urinary calcium and magnesium concentrations were unrelated to the diets administered.
Therefore, it can be concluded that sodium malate and succinate inhibit urinary calculi formation by increasing the urinary citrate concentration; bicarbonate works in the same manner, but a little less effectively; malic acid and succinic acid have no such effect.

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In order to clarify the role of phagocytes in urinary tract infection and to study the enhancement of phagocytic capacities by immunomodulators, a model for ascending urinary tract infection with Escherichia coli was developed in C57BL/6 mice and its beige mutant mice. Beige mouse is an animal model that exhibits most of the phenotypic characteristics of human Chediak-Higashi syndrome. In the mouse, the recessive beige gene is on the proximal end of chromosome 13. Homozygous beige mice are susceptible to infection, and in defect of chemotaxis and bactericidal activity of granulocytes and natural killer cell activity.
Adhesiveness of E. coli strain TN 648 to bladder epithelial cells was examined by in vitro adherence assay. In vivo infection of E. coli was performed via urethra or intraperitoneally. The viable number of the infected microorganisms in the bladder, kidney and peritoneal cavity was determined by quantitative cultivation 24hr after the infection. In some experiments, nonviable Corynebacterium parvum was injected intraperitoneally 7 days before the infection as an immunomodulator.
The results obtained were as follows:
1) No significant difference was observed between C57BL/6 and beige mice, when the bacterial adherence to the bladder epithelial cells of these strains was examined in vitro.
2) Bactericidal activity in beige mice was impaired, since the recovery of infecting microorganisms in their peritoneal cavities was significantly greater than that in C57BL/6 mice.
3) Treatment of mice (either C57BL/6 or beige mice) with C. parvum increased their resistance to infection, since the recovery of microorganisms in the peritoneal cavities of the treated mice was less than that of non-treated mice.
4) Provided that beige and C57BL/6 mice were given tap water ad lib., there was no significant difference in the recovery of microorganisms from the bladders of both strains. However, when these mice were given no water for 48hr or 5% glucose solution for 5 days, a significant persistence of microorganisms was seen in the bladders of beige mice in comparision with C57BL/6 mice.
5) Previous treatment of mice (either C57BL/6 or beige mice) with C. parvum increased the rate of bacterial clearance from the bladders in comparision with that of non-treated mice.

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From June, 1983 to April, 1984, 11 patients with advanced and/or recurrent urothelial carcinoma were treated by ACE chemotherapy (adriamycin, 30mg/body, i.v., day 1, 2; cyclophosphamide, 500mg/body, i.v., day 1; cisplatin, 30mg/body, i.v., day 1-5) and following NEO chemotherapy (cyclophosphamide, 500mg/body, i.v.; neocarzinostatin, 1000units/body, i.v.; vincristine, 0.5mg/body, i.v.; once/1-2 weeks), combined with operation.
Effect of preoperative ACE chemotherapy was evaluated in 7 patients, and considerable tumor regression was observed in 3 cases who had not received prior chemotherapy and irradiation. Mean overall survival in these 3 cases was 14.7 months.
In 4 patients, ACE chemotherapy, followed by NEO chemotherapy, was added as post-operative adjuvant therapy. Only 1 is still alive with no evidence of disease 36 months after operation. But other three died of cancer 3, 6, 8 months after operation, respectively.
Nausea, vomiting, alopecia and bone marrow supression were the most common side effects of ACE chemotherapy, but all patients tolerated well.
ACE chemotherapy is considerably effective against advanced urothelial carcinoma, but the result is far from satisfaction in terms of prolonged survival and response rate. Clearly new protocol is necessary.

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Two channel-balloon occluded arterial infusion of Cis-diaminedichloroplatinum (CDDP) using angiotensin II (two-channel-BOAIA) was attempted in 17 patients with bladder cancer. The anticancer agent infused was mostly CDDP. Thirteen patients were objectively evaluated and the response rate was 77%. All effective cases seemed to respond to only one shot treatment of 90 to 165mg/body (mean 137mg/body) CDDP. Curative transurethral resection (TUR-Bt) for advanced bladder cancer in 5 cases was perfectly carried out because of tumor size reduction and downstaging by the treatment.
The technique was safe and time saving. No major side effect was noticed. Excellent antitumor effect was obtained by lower total doses of CDDP in this series than used in the conventional method. This therapy is thought to be useful for inoperable cases with advanced bladder cancer.

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A case of Wilms' tumor associated with congenital malformations of the eye and abnormal chromosomes 46XX, t(11; 13) (p13; p11) was presented.
Only 13 cases of aniridia-Wilms' tumor syndrome have been reported in Japan and this is the 14th.
The patient was a 1-year-old girl weighting 2480g at birth, and recognized 3 months after birth to have congenital sporadic aniridia, nystagmus, glaucoma and macular aplasia. There was no family history of aniridia or other malformations.
When she was 1 year old, an abdominal mass was proved to be a Wilms' tumor, and aniridia-Wilms' tumor syndrome was diagnosed. After left nephrectomy for Wilms' tumor she received Linac irradiation to the tumor bed, and Actinomycin-D and Vincristin were given at several intervals.
One year after the operation, she died of staphylococcal scalded skin syndrome and pneumonia during chemotherapy.
The present case clearly emphasizes that, along with a check for aberrations of chromosome 11 children with congenital sporadic aniridia should be carefully followed by ultrasound or intravenous urography as the early detection of the tumor, so often association with it, is of vital importance in the prognosis of the disease.

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A case of androgen producing adrenocortical adenoma is reported. Patient was 31-year-old woman, who was admitted to our hospital with the complaints of hypertrichosis, amenorrhea, hypertension and general fatigue. Diurnal rhythm of cortisol secretion disappeared. Plasma ACTH was not detected and no responce was observed in dexamethasone suppression test and rapid ACTH test. Moreover, plasma testosterone, DHEA, DHEA-S and urinary 17-KS were high. CT-scan and scintigram revealed the presence of left adrenal tumor and left adrenalectomy was performed. Microscopic examination revealed no malignant findings and tumor was regarded as adrenocortical adenoma. Electronmicroscopic findings did not indicate definitely the presence or absence of the malignancy.
Tissue concentration of testosterone was high but not so high as that of adrenal cancer.
Differentiation between adrenocortical adenoma and cancer was difficult by endocrinological analysis.

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A 46-year-old female has abused phenacetin-containg analgesics because she had severe headache since 1957. In 1978 she was admitted to the Department of Internal Medicine in our hospital because of severe headache. The diagnosis of psychogenic headache, phenacetin nephropathy and granulocytopenia due to analgesic abuse was made. DIP showed left contracted kidney but normal right pyelogram. On April 25, 1983 she visited the Department of Urology in our hospital because of gross hematuria since November 1982. Her total intake of phenacetin was about 4.7kg during the 25 year period. Retrograde pyerography revealed a right renal pelvic tumor. Urine cytology showed class IV. Right ureteronephrectomy was performed on July 5, 1983. Histological diagnosis was transitional cell carcinoma, grade 2, stage T_1a. At present, 32 months after the operation, she has no sign of recurrence and metastasis.

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