The aim of this study was to evaluate the outcome of CAPD as a form of long-term maintenance dialysis. We examined the clinical results of 72 patients (47 males and 25 females; mean age at the beginning of CAPD 46.2 years old; mean duration of CAPD 54.3 months; non diabetics 87%, diabetics 13%; positive selection 82%, negative selection 18%) who were initiated on CAPD as of December, 1982, in our clinic. The duration of CAPD was between 5 and 10 years in 28 patients and was more than 10 years in 3 patients (the longest; 11 years and 7 months.) Among the 72 patients, 47 (65%) have continued CAPD, 6 (8%) were converted to HD, 1 underwent renal transplantation and 18 (25%) died. The overall technical success rates were 71% and 33% and the survival rates 77% and 50% at 5, 10 years, respectively. The technical success rate at 5 years was 50% in diabetics and 25% in negatively selected patients. The females and the patients initiated on CAPD between 1989 and 1994 showed high technical success rates of 77% and 80%, respectively, while the elderly patients (above 60 years) had a low rate. The causes of conversion to HD were peritonitis in 4 patients (57%), mental problems in 2 (29%) and loss of UF in 1 (14%). The causes of death were cerebral vascular disease in 5 patients (28%), infection in 4 (22%) heart disease in 4 (22%) and malignant disease in 2 (11%).
To achieve the long-term continuation of CAPD, measures against peritonitis, loss of UF and mental problems are needed and, moreover, early treatment of peritonitis and exit site infection, improvement of the CAPD system, adequate nutritional management, adoption of a modified CAPD method, mobility enhancement for patients, and patient education, especially regarding independence and acceptance of self-treatment, are important.

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Serum transferrin receptor (TfR) is a new index allowing non-invasive evaluation of bone marrow erythropoiesis. We measured serum TfR levels in maintenance hemodialysis patients, whose body iron stores were sufficient, under conditions of receiving and not receiving recombinant human erythropoietin (rHuEPO). IfR values of those not receiving rHuEPO (A group: n=5, hematocrits (Ht) lower than 25%), those receiving rHuEPO longer than 6 months (B group: n=5, Hts higher than 25%) and controls (n=11) were 346±146ng/ml, 1, 216±356ng/ml and 910±100ng/ml, respectively. TfR values were significantly lower in group A than in group B (p<0.003) and controls (p<0.001). TfR values in group B and controls were not significantly different. Ht and TfR values were elevated after administration of rHuEPO in group A, such that by 12 weeks and 8 weeks, respectively, Ht and TfR had reached levels not significantly different from those of group B. In conclusion, even though body iron stores may be sufficient, if the erythropoietin (EPO) level is insufficient in hemodialysis patents, TfR and Ht values will be low. They will, however, rise after rHuEPO administration. TfR measurements in renal anemia patients are useful for non-invasively evaluating erythropoiesis and as an indication of the effectiveness of rHuEPO administration.

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To clarify the sulfur amino acid metabolism in patients undergoing dialysis, we measured plasma levels of methionine, cystine and homocysteine, as well as serum levels of vitamin B₆, vitamin B₁₂ and folate, after an overnight fast in 36 CAPD patients (age 48.0±12.3 years), 14 HD patients (54.9±16.4) and 20 normal subjects (40.7±14.5). Plasma levels of total homocysteine were measured by fluoro-HPLC after treatment of plasma with dithioerythritol. Plasma levels of total homocysteine (μmol/l) in both CAPD and HD patients were significantly higher than those of normal subjects (38.2±37.2, 27.3±10.2, 19.0±14.9, respectively). In the normal subjects, plasma levels of total homocysteine were inversely related to serum folate levels. However, this relationship was not noted in CAPD nor HD patients. These findings suggest that plasma levels of total homocysteine are regulated by the degree of conversion from homocysteine to methionine in normal subjects, while other regulatory factors determine plasma levels of total homocysteine in patients undergoing dialysis. There was also a significant correlation between atherosclerotic score and plasma levels of total homocysteine in CAPD patients. These results suggest that hyerhomocysteinemia may play a role in atherosclerosis in patients undergoing dialysis.

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The safety and accuracy of an on-line monitoring system, developed for the continuous observation of serum biochemical data during hemodialysis sessions, were clinically verified. This system consists of two parts: The UF cell on the arterial side of the blood circuit where ultrafiltrate is withdrawn and the measuring unit which measures the biochemical data of the ultrafiltrate every minute for electrolytes and every five minutes for ureanitrogen. In seven stable hemodialysis patients, the Na, K, Cl and urea nitrogen concentrations in the ultrafiltrate withdrawn from the UF cell were continuously measured during a dialysis session using this system and were compared to the serum concentrations obtained from the arterial side of the circuit both pre- and postdialysis. In 72 sessions, enough filtrate was drawn during the entire session and no adverse reactions, such as blood coagulation, hemolysis and hypotension just after initiation, were observed. Significant positive linear correlations were observed between filtrate concentrations measured by this system and serum concentrations measured by antomatic analyzer for Na, K, Cl and urea nitrogen (p<0.001). However, differences in Na and Cl concentrations between the filtrate and serum were rather large and further evaluation is therefore necessary. In conclusion, this system, with which blood sampling is not necessary and continuous monitoring of serum biochemistry is possible, was demonstrated to be safe for use during a hemodialysis session and to provide data which reflect the serum data. This device is thus expected to be clinically useful for the observation of patient condition during hemodialysis.

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We experienced a case of chronic renal failure with drug-induced liver injury, and recombinant human erythropoietin (rHuEPO) was considered to be the pathogenic agent.
The patient was a 72-year-old female who had a 15 year history of diabetes mellitus. On December 1994, this patient was admitted to our hospital because uremia due to diabetic nephropathy had developed. Normal liverfunction was found by clinical test on admission, and allergic diathesis or a history of the blood transfusion were not detected. On February 1, 1995, hemodialysis was initiated due to a gradual deterioration of renal function and a reduction in urinary output in spite of hospitalization. When 1, 500 units of epoetin alfa (Espo^®) per hemodialysis was administered to this patient for the correction of renal anemia, she complained of fever and general fatigue, and developed leukocytosis and liver dysfunction (T-Bil; 2.0mg/dl, GOT; 560U, GPT; 637U, ALP; 11.8U, LDH; 1, 550U) on February 6. After the cessation of all medication abnormal liver function returned to normal.
After the re-administration of epoetin alfa abnormal liver function was found again, and treatment with epoetin alfa was stopped immediately. Subsequently, liver function was normalized, and symptoms disappeared. Both the lymphocyte stimulation test and an assay for anti-erythropoietin antibodies were negative. Since the maintenance of hematocrit level without rHuEPO was difficult in this patient irrespective of blood transfusion, epoetin beta (Epogin^®) was administered to this patient. The effect of epoetin beta was sufficient without any adverse effects.
These results indicate that epoetin alfa was the etiological drug. Though the incidence of adverse effect of rHuEPO is low, we should pay attention to the possibility of drug-induced liver injury.

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A 43-year-old man who had been diagnosed with chronic renal failure had no symptoms over previous years, had had less lunch than usual, and ingested nothing orally other than 75ml of ethanol on the evening of May 1, 1994. He was admitted to hospital early the next morning, in a coma of unknown cause with mydriasis. His blood glucose level was 7mg/dl and he responded dramatically to intravenous administration of glucose. However renal function deteriorated and he was reffered to NTT Kyusyu Hospital. Renal function was not restored, and he began to undergo regular hemodialysis. Hypoglycemia caused by ethanol is considered to also require long periods of fasting in this case, the period of fasting was short and there was no excessive consumption of ethanol. Attention should be given to hyperglycemia and to hypoglycemia in the treatment of chronic renal failure.

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A 54-year-old woman under maintenance hemodialysis for 6 years had suffered pain in her right lower extremity since December 1992. In September 1994, she was admitted because of difficulty walking due to increasing pain which was refractory to analgesics. Neurological examination showed no abnormal findings in muscle strength, deep tendon reflexes or sensation. Plain X-ray failed to demonstrate any remarkable changes in the vertebral column, but a spinal cord tumor was found at the L1 to L2 level by myelography, CT scan and MRI. Postopoperative pathological examination of the resected tumor revealed a benign neurinoma. It is relatively common for patients on long-term maintenance hemodialysis to complain of pain caused by metabolic bone disease or localized amyloid deposition. However, a benign spinal cord tumor should be taken into consideration among the origins of unexplainable pain in these patients.

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A 70-year old woman was hospitalized for treatment of leukopenia and a 3-day history of fever and sore throat. Three years before admission the patient had been diagnosed as having interstitial pneumonia and had been treated with steroids. Because of impairment of renal function, regular hemodialysis had been initiated 3 months previously. Two months before admission treatment with steroids was necessitated by exacerbation of the pneumonia. Since 1 month before admission she had been treated with ranitidine, 150mg once a day, for gastritis. Her leukocyte count was 1, 100/mm³ with 0% neutrophils. Bone marrow examination showed granulopoietic hypoplasia. Ranitidine therapy was immediately discontinued and administration of G-CSF was started. One month later, her leukocyte counts had recovered.
Since myelosupression due to ranitidine may occur because of impaired excretion, physicians should be alert to this complication.

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A 79-year-old man with chronic renal failure secondary to nephrosclerosis, who had been on maintenance hemodialysis for 54 months, was evaluated because of a prostatic nodule palpated on a screening digital rectal examination. Histopathological examination of the biopsy specimens taken from the right lobe of the prostate disclosed moderately to poorly differentiated adenocarcinoma of the prostate.
Antiandrogen therapy was begun with 3.75mg of LH-RH agonist (leuprorelin acetate) subcutaneously every four weeks and 100mg of chlormadinone acetate (CMA) orally per day, under a diagnosis of stage B1 carcinoma of the prostate.
The serum prostate specific antigen (PSA) level before treatment was elevated to 13.8ng/ml (normal<3), but normalized within two months of initiating therapy. After 8 months of treatment with LH-RH agonists and CMA, the serum PSA remained at this level.
Prostatic cancer has an increased incidence in aged men. Because of the increasing aged population, prostatic cancer in elderly patients on hemodialysis should be carefully considered.

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We experienced three cases of crush syndrome in the immediate aftermath of the Hanshin-Awaji earthquake. Three patients, all males from 36 to 46 years old, were admitted with azotemia, rhabomyolysis, and oliguria.
On admission, consciousness was alert and respiration and blood pressure were normal. Systemic X-ray revealed no fractures. First, we conducted hemofiltration (HF) for three days. The dialyzer was a PNF-17DX PAN membrane and the replacement fluid was Sublood A. However, we discontinued HF and started hemodialysis (HD) because two patients complained of nausea and malaise during HF probably due to acetate intolerance. The dialyzer was a BK-1.6U PMMA membrane and the HD fluid was Kindary AF-2. The anticoagulant was nafamostat mesilate. HF was done 4 times and HD 7 times in one case, while HF done 5 times and HD 12 times in the other two cases.
We found immunoglobulin-binding (IgG, IgA, κ, λ) creatine kinase (CK), that is macrocreatinekinasemia type I, in all three cases. It gradually disappeared with recovery. This is the first report, to our knowledge, of macrocreatinekinasemia type I in crush syndrome.

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