To evaluate whether extremely low intact parathyroid hormone (i-PTH) levels in hemodialysis patients is associated with the development of serious bone and joint complications, we assessed parameters of bone metabolism and clinical symptoms. A total of 51 out of 375 (13.6%) patients had i-PTH levels of less than 10pg/ml (hypo-PTH group), all of whom had significantly low serum osteocalcin levels suggesting low turnover bone state. High corrected serum calcium levels (10.2±0.1 mg/dl) as well as a high prescribing dose of 1α(OH)D₃ compared to that of non-hypo-PTH (0.41±0.06 vs 0.32±0.01μg/day) were found in hypo-PTH group. These results suggest that excessive treatment is the cause of hypo-PTH in some patients. The proportion of diabetic patients in the hypo-PTH group was not elevated, therefore original renal diseases are not assumed to be a risk for hypo-PTH. A longitudinal survey of hypo-PTH patients demonstrated that the pattern of PTH changes could be differentiated into 4 patterns: A) Continuously low PTH after the start of hemodialysis (n=28); A-2) persistent low PTH after start of therapy at the pre-dialysis stage (n=2); B) response to 1α(OH)D₃ treatment started after the beginning of hemodialysis (n=18), C) Post parathyroidectomy (PTX) state (n=3). The A-2 group patients had a history of hyperparathyroidism at the pre-dialysis stage and the B group patients had a history of hyperparathyroidism after the start of hemodialysis. Therefore, about 50% of the hypo-PTH patients had a history of hyperparathyroidism and responded well to 1α(OH)D₃ treatment. Special symptoms related to bone and joint complications were found exclusively in post PTX patients by a questionnaire. These results suggest that hypo-PTH state is not necessarily an important factor causing severe bone and joint problems.

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A questionnaire survey was used to investigate the status of hemodialysis clinics and hospitals in Hyogo prefecture one year after the Hanshin-Awaji earthquake. After one year, repairs were still not complete in 18 (35.3%) of the 51 clinics and hospitals where facilities had been destroyed by the earthquake. With regard to hemodialysis equipment, pipes in water-purification systems were destroyed in many clinics and hospitals, along with large equipment such as RO and dialysate-supplying units. It was noteworthy that the pipes had been destroyed with a remarkably high incidence at parts connecting large pieces of equipment. Piping had been earthquake-proofed in only 12 clinics and hospitals (14.6%). Twenty-two clinics and hospitals (30.1%) had not yet returned to their pre-earthquake number of hemodialysis patients. Patients who had moved clinics after the disaster continued to stay because their homes had been largely destroyed. Many other patients had moved to and were staying in hemodialysis clinics close to their homes because of transportation problems. These changes represent a major rearrangement of hemodialysis patients as a result of the earthquake.

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We investigated the death of patients undergoing chronic hemodialysis treatment who died after the Hanshin -Awaji earthquake. The number of hemodialysis patients in Hyogo prefecture who died in the one-year period following the disaster increased 26.0% over the preceding year. More specifically, the number of deaths increased markedly in January 1995, just after the disaster. There were no remarkable differences in the number of deaths between areas damaged by the disaster and those not damaged. An investigation into the cause of death revealed that cardiac diseases including heart failure and acute myocardial infarction accounted for the most of deaths, followed by infectious diseases such as pneumonia, and then cerebro-vascular diseases. The causes of death did not deviate markedly from those mentioned in statistical reports on hemodialysis patients in the country as a whole. The circumstances surrounding the death of 261 hemodialysis patients who died after the disaster were investigated. It was found that out of 79 patients affected by the earthquake, the homes of 52 had been destroyed, and many other patients changed hospitals because their hospitals had been damaged or because of transportation problems. Some changes in health or in laboratory findings were found in 21.8% of the patients and some psychiatric changes were evident in 23.0%. A total of 37.5% of patients were reported to be suffering from some degree of stress. It was estimated that stress to some degree affected the death of 25.2% of the patients. Proven effect of stress as well as changes in health, laboratory findings and mental state were found to a significantly higher degree in patients suffering from the earthquake.

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Angiotensin I converting enzyme inhibitor (ACEI) is known to worsen anemia in hemodialysis (HD) patients. The effect of rHuEPO on ACEI-induced worsening of anemia was evaluated in 19 hypertensive HD patients. Patients were subdivided into two groups according to rHuEPO administration, being rHuEPO (+) group (n=10, 56±4 years old, rHuEPO 1500 units, 3 times a week) and rHuEPO (-) group (n=9, 52±3 years old). Age, HD duration, blood pressure (BP) and hematocrit (Ht) before ACEI (lisinopril) were not significantly different between rHuEPO (+) and rHuEPO (-) group. Lisinopril was started with a dose of 2.5mg once a day in the morning on non-HD day. BP decreased significantly in both groups and adequately maintained throughout the study period. Ht decreased significantly in rHuEPO (-) group from 30±2 to 26±1% (p<0.05), whereas it remained unchanged in rHuEPO (+) group. The dose of lisinopril of 5.0±2.0mg/day in rHuEPO (+) group was significantly higher than that of 3.0±1.0mg/day in rHuEPO (-) group (p<0.05). Serum erythropoietin and plasma angiotensin II concentration decreased but the changes were not significant in both groups. Plasma angiotensin I converting enzyme activity decreased significantly from 51±5 to 30±4U/L only in rHuEPO (-) group (p<0.05). In conclusion, we suggest that the ACEI-induced worsening of anemia could be prevented by a concomitant use of rHuEPO in hypertensive HD patients. However, the higher dose of ACEI was required to control BP in rHuEPO-treated HD patients.

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To clarify the role of brain natriuretic peptide (BNP) in patients on chronic hemodialysis, BNP, dry weight, cardiothoracic ratio (CTR) and blood pressure were measured in 30 identical patients on two separate occasions in January and October, 1995. BNP was decreased by hemodialysis (p<0.002), and was correlated with mean blood pressure (MBP) but not with CTR, ΔBW, or the duration of hemodialysis. A change in BNP values between January and October (ΔBNP) was strongly correlated (p<0.001) with a change in MBP over this period (ΔMBP). The mean ejection fraction of the patients was 0.69, the EA ratio was 0.66, and no correlation was found with BNP. A significant correlation was demonstrated between BNP and ANP both before and after hemodialysis in 13 patients. The correlation between ΔBNP and ΔANP was also significant. In conclusion, because BNP was correlated with ANP and blood pressure in patients on chronic hemodialysis, BNP values may reflect blood pressure and body fluid status.

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A 29-year-old man who had been on continuous ambulatory peritoneal dialysis (CAPD) since 1987 because of neurogenic bladder, was treated with 1α(OH)D₃ (0.25→1.0μg/day) to control hyperparathyroidism for 1 year. During the 1 year of CAPD, he suffered from 4 episodes of persistent peritonitis, resulting in abdominal pain, vomiting and bloody dialysate. After additional 3 episodes of peritonitis, he was transfered to regular hemodialysis because of ultrafiltration failure and loss of urine volume. In addition to ectopic calcification of joints and skin, severe metabolic alkalosis was accelerated at this point.
The patient did not show frequent vomiting and/or diarrhea, and severe calcification of the bowel wall was confirmed by CT. Therefore, the metabolic alkalosis was thought to be caused by hyposecretion of bicarbonate ion in the mucosa of intestines.
This case was similar to previous reports of calcifying peritonitis or peritoneal calcification. The calcification in this case was thought to be caused by the use of dialysate with high osmolality or the administration of high dose vitamin D during persistent peritonitis. To prevent this malignant cycling between ectopic calcification and metabolic alkalosis, inhibition of gastric juice secretion may be an appropriate therapeutic strategy.

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We report a case of sclerosing encapsulating peritonitis (SEP) successfully treated by steroid pulse therapy. The patient was a 42-year-old man with end stage renal failure who had been maintained on continuous ambulatory peritoneal dialysis (CAPD) since January 1985. He attended our outpatient clinic with complaints of persistent nausea and frequent vomiting for a week in August 1996. Cloudy dialysate was observed from the day before his visit, and he lost 5kg in weight in 7 days. He was admitted to our hospital immediately because of increasing weakness. Laboratory examination showed an increase of WBC in the dialysate (361cells/μl), elevated CRP (26.3mg/dl) and leukocytosis (14100/μl) in peripheral blood. An abdominal CT disclosed diffuse adhesion of the small intestine. With these findings, the patient was finally diagnosed as having SEP. A nasogastric tube was inserted to correct his bowel pressure because he had symptoms of ileus on admission. We performed pulse therapy 3 times and the patient showed good recovery of both subjective symptoms and laboratory and physical findings. This case suggested that steroid pulse therapy is quite effective for SEP especially when the therapy is started at an early stage of the disease.

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In April 1995 a 71-year-old male patient with a 12-year history of hemodialysis therapy for chronic glomerulonephritis was diagnosed as anemic. Recombinant human erythropoietin (r-HuEPO) was administered, but the anemia did not improve. Gastrofiberscopy in August and colonfiberscopy in September revealed no abnormalities. In January 1996 the man was hospitalised for progressive anemia, but gastrofiberscopy again revealed no abnormalities. In March frequent blood transfusions were necessary due to the presence of blood in the feces, at which time he was admitted into our hospital. Upon admission, RI scintigraphy (^99mTcO₄^-) revealed a hot spot in the left middle section of the abdomen. A CT scan revealed a mass about 3cm in diameter. An angiographic study revealed a mass suspected of being an aneurysm of the mesenteric artery of the ileum. Abdominal MRI and RI scintigraphy (^99mTc-HSA) revealed a large tumorous mass and flow of blood. In addition, a barium enema showed a narrowing lesion of the middle ileum of approximately 15cm in size. Ischemic enteropathy of the small intestine with an aneurysm of the mesenteric artery of ileum was diagnosed. On April 22 1996 ileostomy and resection of the aneurysm were performed. We conclude that careful examination for lesions of the ileum as well as the stomach, duodenum and colon are needed upon diagnosis of progressive anemia in long-term hemodialysis patients.

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It is generally thought that eosinophilic peritonitis in CAPD patients spontaneously resolves and does not impare peritoneal function. We treated a 54-year-old female patient who suffered from recurrent eosinophilic peritonitis and ultrafiltration failure. The peritoneal equilibration test (PET) revealed a D/P value of 0.973, and a D/D₀ value of 0.171, showing characteristics of hyperpermeability of the peritoneal membrane. Peritoneal biopsy showed loss of mesothelial cells, and fibrosis, edema and eosinophilic cell infiltration in the submesothelial tissue. Based on these results, we stopped CAPD and switched to HD.
These results suggested that CAPD patients with recurrent eosinophilic peritonitis should be treated carefully because massive peritoneal membrane damage may occur, resulting in functional failure.

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