Extracorporeal ascitic fluid dialysis (EAD) and extracorporeal ultrafiltration of ascitic fluid (EUA) were performed in eight patients with intractable ascites and chronic renal failure. The chronic renal failure was due to chronic glomerulonephritis in five patients and diabetic nephropathy in three patients. In six of the patients, the ascites occurred prior to dialysis, while in the other 2 it developed during hemodialysis. The ascites was secondary to liver cirrhosis in six patients, and the etiology was unknown in the other two cases. The ascites presented an exudate in one patient and a transudate in the others. A total of 55 EAD procedures were performed in the five patients, over a 1.0 to 6.8 month period. The duration of the procedures averaged 2.8±0.4h. Ascitic fluid (2.7±0.6l), body weight (2.7±0.7kg) and abdominal girth (5.3±2.5cm) were reduced effectively. Ascitic fluid total protein, albumin and calcium were significantly higher after the procedures (p<0.005). Serum creatinine (p<0.05) and ascitic urea nitrogen, creatinine, potassium and phosphorus (p<0.005) were significantly lower after EAD. A total of 61 EUA procedures were performed in the five patients, over a 0.3 to 10 month period. The duration of the procedures averaged 3.0±0.2h. Ascitic fluid (3.0±0.2l), body weight (3.0±0.4kg) and abdominal girth (6.7±3.0cm) were reduced effectively. Ascitic fluid total protein and albumin were significantly higher after EUA (p<0.005). Three of the five patients were ascites-free for 0.7 to 5 months after EAD and/or EUA. EAD was effective in one of two patients with improved ascites, and the other patient was switched to CAPD, which proved useful. Hemodialysis (1 to 3 times per week) combined with EAD (1 to 2 times per week) was required to manage chronic renal failure in five patients. Serious hypotension and arrythmias did not occur in any of the patients during EAD or EUA. Peritonitis occurred in six patients at 0.5 to 4 months after these procedures. Five of the six patients were successfully treated with antibiotics after catheter removal. EAD and EUA thus offer safe and effective means of treatment in patients with ascites and chronic renal failure.

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Elevated blood pressure without correction of anemia has been described in a few patients with renal anemia treated with recombinant human erythropoietin (rHuEPO). The effects of rHuEPO on plasma endothelin (ET), renin activity (PRA), angiotensin-I (AI), and angiotensin-II (AII) levels were studied in 20 hemodialysis patients with anemia. The patients were treated with rHuEPO, 1, 500 or 3, 000 units three times a week, intravenously, for three months. None of the patients had been treated with angiotensin converting enzyme (ACE) inhibitors. Early morning blood samples were collected from all patients before, and after three months of rHuEPO therapy. PRA, AI, AII and ET concentrations were measured by radioimmunoassay (RIA). Treatment with rHuEPO significantly raised the patients' ET levels and depressed their AII levels, but no differences were found in between PRA or AI levels before and after therapy. In conclusion, rHuEPO treatment of renal anemia induces elevation of ET levels and may a effects the renin-angiotensin system in hemodialysis patients. Futhermore, ET may play a role in the development of hypertension during long-term rHuEPO therapy. However, since there were no significant differences in the levels of these factors in the group whose blood pressure increased (10 patients) and the group whose blood pressure did not increase (10 patients), it may be necessary to investigate the relationship between increases in ET and vital body sensitivity, or to investigate etiologies other than ET.

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Plasma levels of phenol, p-cresol and indican are markedly elevated in uremic patients, but it is impossible to efficiently reduce them by hemodialysis (HD). Such uremic toxins are produced in the intestine as bacterial putrefactive metabolites.
Analysis of fecal microflora revealed an imbalance in its composition characterized by the overgrowth of aerobic bacteria during HD. Balance was restored by oral administration of the lactic acid bacteria preparation Lolon^® S. Oral feeding of this lactic acid bacteria compound also reduced levels of putrefactive substances in the stools.
These findings demonstrated that oral feeding of lactic acid bacteria to uremic patients is effective in reducing the accumulation of uremic toxins by reducing bacterial production through the correction of imbalances in intestinal microflora.
Based on the results of this study, we propose the introduction of “probiotics”, such as the lactic acid bacteria employed in this study, as a means of reducing uremic toxins.

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Methicillin-resistant Staphylococcus aureus (MRSA) has become one of the most important pathogens in nosocomial infections. In this study, we attempted to clarify the epidemiology of MRSA in our kidney center with implications for management. MRSA was cultured from the anterior nares in 10 out of 109 (9.2%) dialysis patients on two separate occasions. Because these patients had no infections caused by MRSA, they were considered to be nasal carriers. There were no differences in sex, age, duration of dialysis or underlying diseases between carriers and noncarriers. However, in the carrier group there were significantly more patients with a history of admission or long-term antibiotic use within one year before this study, or in need of daily living assistance. MRSA was not detected in the nares of 20 staff members, but was cultured from some inanimate objects in the kidney center including linens used for MRSA carriers, floors, nurses' shoes and white coats. Therefore, we attempted to eliminate the carriage of MRSA and sterilize the environment according to our own infection control guidelines. In 6 (60%) of 10 carriers, MRSA disappeared with the use of povidone iodine. Moreover, MRSA contamination of inanimate objects was completely eradicated and new carrier development was prevented. Clearly, in order to prevent MRSA nosocomial infections it is important to manage the cleanliness of outpatients, especially dialysis patients with a high risk for colonization, in addition to that of inpatients.

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A 37-year-old man was admitted to Kinki University Hospital for renal transplantation. He had a history of nephrotic syndrome for 32 years. Hemodialysis had been instituted two years prior to admission because of gradually deteriorating renal function. On admission, a diagnosis of active systemic lupus erythematosus (SLE) was made on the basis of the results of various blood studies and the physical findings, and the patient was placed on corticosteroid pulse therapy. His serum complement activity and anti-DNA antibody titers subsequently decreased, but his condition suddenly deteriorated and he died of pneumonia and hemorrhagic cerebral infarction. Autopsy revealed extensive hemorrhagic cerebral infarction due to aspergillus enbolization. Cerebrovascular disorders are rarely detected in SLE. When found they are obliterative in approximately 50 percent of the cases. Aspergillosis of the central nervous system in SLE, as occurred in this patient, is rarely reported.

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A 74-year-old male hemodialysis patient with a history of pulmonary tuberculosis developed severe edema of his left upper extremity and many vericosities of his chest wall after the creation of an A-V fistula in his left antecubital space. Venous angiography via the A-V fistula failed to reveal any constrictions nor thromboses in the left subclavian vein, but the vein was found to have an abnormal course, reaching the left subclavian vein under the aortic arch. Enhanced computed tomography of the chest showed compression of the vein between the chest wall and the ascending aorta.
The patient had no history of catheter ization of his left subclavian vein, so we suspect that the venous hypertension in this case may have resulted from the abnormal course of the left brachiocephalic vein.

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We report a case of end-stage renal disease due to diabetic nephropathy with intractable ascites. A 63-year-old male was admitted to our hospital with a 1-month history of appetite loss, malaise, edema and abdominal fullness. Laboratory findings on admission showed a BUN of 113mg/dl and a serum creatinine of 9.4mg/dl. The ratio of total protein in the ascitic fluid to serum total protein was 0.42, i.e., the ascitic fluid had the characteristics of a transudate. Cytological examination of the patient's ascitic fluid was negative, and cultures of the ascitic fluid for bacteria, fungi and M. tuberculosis were all negative. Hemodialysis and extracorporeal ultrafiltration failed to reduce the ascites because of hypotension during dialysis. It was also difficult to reduce his ascites by intravascularly infusing ascitic fluid which had been remored and subjected to ultrafiltration. A peritoneal catheter was surgically placed, and tidal peritoneal dialysis (TPD) with an automated peritoneal dialysis device (Baxter, PAC-XII cycler^®) was begun. This was followed by gradual reduction of the ascites over several days. The patient was then transferred to continuous ambulatory peritoneal dialysis (CAPD) and became capable of being treated as an outpatient. We think that TPD with an automated peritoneal dialysis device should be the new treatment of choice for patients with intractable ascites.

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We encountered three cases of fecal peritonitis due to perforated diverticulitis in patients on continuous ambulatory peritoneal dialysis (CAPD). Case 1 is a 32-year-old man admitted because of peritonitis. The duration of CAPD was 16 months. The peritonitis and the patient's complaints failed to resolve, and on his fourth hospital day he developed severe defance, and crude fibers were found in the dialysate.
Acute abdominal surgery was performed and perforated diverticulitis was found in the sigmoid colon. E. coli was cultured from the dialysate. The patient is still alive and on maintenance hemodialysis.
Case 2 was 73-year-old man admitted because of general malaise. On the 61st hospital day he developed peritonitis, and E. coli and K. pneumoniae were cultured from the dialysate, but in accordance with the wishes of the patient and his family surgery was not performed. The patient died 7 days after the onset of peritonitis, and autopsy revealed perforated diverticulitis in the sigmoid colon.
Case 3 was a 67-year-old man admitted with persistant peritonitis, and E. coli was cultured from the dialysate. Surgery was performed on the 7th hospital day, and perforated diverticulitis was found in the descending colon. The patient developed a subphrenic abscess and died two months postoperatively.
Fecal peritonitis is a very rare complication of CAPD, but since diagnosis is very difficult and mortality is very high, the possibility of its occurrence must be borne in mind.

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We report a rare case of end-stage renal disease complicated by malignant lymphoma and successfully treated with chemotherapy and radiation therapy. The patient was a 67-year-old man who had been treated for hypertension since 1971. He developed chronic renal failure in 1990. In March 1994, he was admitted to our hospital because of upper abdominal pain. A hard mass was detected in the epigastric region. Abdominal computed tomography revealed many swollen lymph nodes in the same region, and a diagnosis of malignant lymphoma (diffuse large, immunoblastic B cell type) was made based on the results of a para-aortic lymph node biopsy. Regular hemodialysis was instituted after the first course of chemotherapy, and the lymph node swelling gradually decreased. After six courses of chemotherapy, the patient was treated with radiation therapy, and remission of the malignant lymphoma was achieved in September 1994. The patient's course has been uneventful for one year with no evidence of recurrence.

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A 36-year-old diabetic woman with a 3-year history of CAPD (1989-1992) and a 3-year history of chronic hemodialysis (1992-), began to experience intermittent loss of consciousness in 1990. No history of alcohol or drug abuse could be elicited, and no members of the patient's family suffered from a similar disorder. Subsequent evaluation included cranial and abdominal computed tomography and abdominal sonography, the results of which were all normal. The venous phase of a celiac arteriogram revealed abnormal opacification of the splenic vein and demonstrated the inferior vena cava. It was suspected that the episodes of consciousness loss this patient experienced were attributable to this abnormal communication and it was decided to ligate the shunt surgically. The patient did very well postoperatively.

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