It has been reported that serum transaminase values, i.e., aspartate aminotransferase (AST) and alanine aminotransferase (ALT), are quite low in patients undergoing chronic dialysis. In this paper we assessed, the serum transaminase values of 200 patients on chronic hemodialysis and found that their mean ±SD AST and ALT values were very low (12.5±6.0 and 10.9±6.0, respectively). To investigate the reason for these low transaminase values, we examined the sera of 10 patients with chronic renal failure who had normal liver function test results and no virus markers. Negative correlations were found between the serum creatinine and transaminase values (both AST and ALT). Comparison of serum transaminase levels in patients on chronic hemodialysis before and after dialysis, and a study of mixing the serum of normal subjects with normal renal function and with chronic renal failure patients after dialysis suggested that unknown uremic substances of an unexchangeable nature inhibit the activity of serum transaminase.

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The mechanism of blood pressure elevation after r-HuEPO administration has not been clearly explained.
We, therefore, investigated left ventricular afterload in relation to the cause. The subjects were hemodialysis patients with renal anemia [hematocrit (Ht) less than 25%, n=16]. Mean age of the patients was 62 years. r-HuEPO was administered intravenously until the Ht increased to 30%. Blood pressure and heart rate were measured before and after r-HuEPO administration, and two-dimensional echocardiography was performed at the same time.
We compared group I with group II. Group I: Mean blood pressure (MBP) increased over 10% after r-HuEPO administration. Group II: MBP either did not change or decreased after r-HuEPO administration.
Results: The Ht increased in most cases after r-HuEPO administration (22.3±1.7%→29.6±5.1%: p<0.001). In group I, MBP, systolic blood pressure (SBP) and diastolic blood pressure (DBP) increased significantly, and cardiac output (CO) decreased. In group II, MBP and SBP decreased slightly, and CO remained unchanged. Total peripheral resistance (TPR) and end systolic wall stress (ESWS) increased significantly in group I, but decreased slightly in group II. ΔTPR and ΔMBP indicate differences in TPR and MBP before and after r-HuEPO administration. The correlation between ΔTPR and ΔMBP was very close (r=0.85).
Conclusion: The rise in blood pressure after r-HuEPO administration is closely correlated with the elevation of TPR. ESWS increased as TPR increased. The increase in ESWS is probably linked to left ventricular hypertrophy when r-HuEPO is administered for long periods.

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Ultrasonically guided percutaneous ethanol injection therapy (PEIT) for enlarged parathyroid glands was performed in nine patients with refractory hyperparathyroidism on maintenance hemodialysis. The serum calcium levels of these patients before PEIT ranged from 10.0 to 10.8mg/dl, and low-dose active metabolites of vitamin D (0 to 2μg/week) had been administered to all of them except one (6μg/week). The 22 enlarged parathyroid glands of nine patients, were injected a total of 98 times with 0.05 to 2.8ml of absolute ethanol, based on estimated gland volume as the upper limit. PEIT was performed three times at intervals of one or two weeks, and after confirming increased echogenicity of the parathyroid glands, an additional procedure was performed if needed. Levels of highly sensitive (HS) PTH ranged from 26, 410 to 156, 100pg/ml (mean: 83, 500pg/ml) before PEIT, and decreased in all patients from 3, 000 to 70, 600pg/ml (mean: 30, 500pg/ml) three to 12 months after treatment. Serum calcium levels also decreased in all patients, allowing a higher dose of 1, 25(OH)₂D₃ to be administered by pulse therapy. Although six of the nine patients were well controlled, HS-PTH levels increased again in three patients. Ultrasonically it was determined that an additional procedure was required because of detection of new parathyroid glands in two patients, and regrowth of a treated gland in another. Levels of intact PTH and alkaline phosphatase showed the same changes as the HS-PTH levels. Side effects were limited to mild local pain in all patients and transient dysphonia in two patients.
In conclusion, PEIT was useful, and it may be possible to control patients with refractory hyperparathyroidism with medical treatment, such as pulse therapy, again.

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To determine why patients with diabetic end-stage renal failure tend to develop congestive heart failure, we investigated transmitral flow patterns using pulsed Doppler echocardiography before and during the passive leg raising maneuver (LRM).
The subjects consisted of 10 diabetic (DM) and 15 non-diabetic (nonDM) patients with chronic renal failure. Fifteen normal subjects served as controls (C). Peak early mitral flow velocity (E), peak atrial filling velocity (A), A/E and the deceleration half-time of E (DHT) were analyzed before and during LRM. A/E and DHT were significantly higher in DM and nonDM than in C. Transmitral flow patterns in DM were similar to those in nonDM before LRM. E was increased and DHT was decreased by LRM in all three groups. A was significantly increased by LRM in C and nonDM, but A was unchanged in DM.
Thus, in addition to the left ventricular diastolic dysfunction generally observed in both DM and nonDM patients left atrial dysfunction may become overt in DM as a result of LRM. This latent left atrial dysfunction may be one of the reasons patients with diabetic end-stage renal failure tend to develop congestive heart failure.

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Cardiovascular disease is one of the leading causes of death among hemodialysis patients. In 30% of hemodialysis patients who experience sudden death, arrhythmia is the final event, and QTc prolongation is considered a risk factor for sudden death due to arrhythmia. We therefore studied the effect of hemodialysis on the QTc interval. We examined the QTc interval, serum electrolytes, ionized Ca, plasma HANP, and blood gases of 32 hemodialysis patients (24 males, 8 females, age 55.5±11.2 years) before and after hemodialysis. The QTc interval was also measured in age- and sex- matched normal controls. The QTc interval in hemodialysis patients (0.439±0.025sec) was significantly longer than in the normal controls (0.396±0.021sec) (p<0.01), and the upper limit of QTc was defined as 0.438sec. ΔQTc was defined as QTc (after hemodialysis) minus QTc (before hemodialysis), and Δ serum electrolytes as serum electrolytes (after hemodialysis) minus serum electrolytes (before hemodialysis). ΔQTc was correlated with Δserum Ca, Δionized Ca, and ΔHCO₃^-. Hemodialysis patients were divided into group A (QTc>=0.438sec) and group B (QTc<0.438sec). There were 15 patients in group A and 17 patients in group B. There were no significant differences between the two groups in levels of serum electrolytes, ionized Ca, plasma HANP, or blood gas levels, only in serum Ca. Serum Ca levels in group A (8.8±1.0mg/dl) were higher than (9.8±1.2mg/dl) in group B (p<0.05). In group A, the level of serum Ca increased to 9.6mg/dl after hemodialysis, but QTc remained prolonged (0.450sec). These data suggest that in addition to serum Ca, autonomic nerve dysfunction and myocardial damage may be involved in the etiology of the QTc prolongation in hemodialysis patients.

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Whether the use of dialyzers with HPMs has a beneficial effect on renal anemia in hemodialyzed patients is still a matter of controversy. We therefore addressed this issue by comparing two HPM dialyzers, BK-F and FB-U, in dialyzed patients undergoing short-time maintenance hemodialysis.
Following a change in dialyzer from BK-F to FB-U, the patient's hematocrit (Ht) and hemoglobin levels rose significantly. Consequently, the dose of human recombinant erythropoietin required during the BK-F-treatment period was lower than during the FB-U-treatment period. In contrast, serum albumin concentrations (Alb) were lower in the BK-F-treatment period than during the FB-U-treatment period. This amelioration of renal anemia by BK-F was greatly diminished when BK-F was switched back to FB-U.
The results of the present study indicate that BK-F alleviates renal anemia, presumably by removing erythropoiesis-suppressing factors from the serum of uremic patients. However, one must be alert to BK-F's Alb reducing effect, especially in patients with low Alb.

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We assessed the timing of withdrawal of continuous intravenous infusion of glyceol to prevent dialysis-induced hypotension (DIH). Three patients on hemodialysis (HD) undergoing continuous intravenous infusion of glyceol during HD at a rate of 100ml/hr (continuous period) were selected. After all patients had been dialyzed thirty times by the above method, they were dialyzed thirty times with continuous infusion of glyceol, stopping 30 minutes (30-minute period) and 60 minutes (60-minute period) before the end of HD. In the continuous period, thirst developed as a result of increased plasma osmolality due to elevation of the serum glycerol concentration. Thirst did not develop during the 30-minute period because of significant decreases in plasma osmolality and serum glycerol concentration, in comparison with the continuous period. In addition, there was no significant difference between blood pressure levels in the continuous period and the 30-minute period. In 60-minute period, plasma osmolality and serum glycerol levels were significantly lower than in the 30-minute period, however, blood pressure in one of three patients was significantly decreased. This suggests that continuous intravenous infusion of glyceol to prevent DIH should be stopped 30 minutes before the end of HD.

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Synovial amyloidosis occurs as one form of amyloid osteoarthropathy. Not only synovia but bursae with the same synovia histologically are subject to amyloid deposition. Joint swelling is one of the symptoms of bursitis due to amyloid deposition, and while there have been reports of femoral nerve paralysis due to the iliopectineal bursitis, there seem not to have been any reports of median nerve palsy due to subscapularis bursitis. In this report, we made a diagnosis of subscapularis bursitis with median nerve palsy by bursography. Crystal bursitis was suspected as one of the causes on the basis of a calcificated bursa on X-ray. Treatment by puncture and drainage of the synovial fluid, steroid injection into the bursa and low-dose steroids per os was effective.

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A 68-year-old female on chronic hemodialysis therapy for 20 years was admitted with an intravascular foreign body, a migrating broken plastic catheter for dialysis-access, in December 1990. The dialysis-access, a brachiocephalic fistula, is usually inserted by puncture with an ordinary plastic catheter in the left antecubital fossa. Migration of the broken tip was recognized because of hemorrhage from the puncture site. The proximal portion of the access was compressed to avoid central migration. The migrated radiolucent catheter was not localized by palpation or a portable X-ray film, but by high-resolution ultrasonography with a 7.5MHz probe. The catheter was easily removed under local anesthesia. The broken tip of the catheter had pulled away from the underlying structure, but had not been cut by the needle within the catheter during the procedure. The cause of the breakdown seemed to be a manufacturing defect in the catheter. Ultrasound was very effective in localizing the intravascular radiolucent foreign body. No other case reports of a migrating broken plastic catheter for dialysis-access could be found in the literature.

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We report a hemodialysis patient who developed wrist and elbow tuberculosis.
A 63-year-old male on hemodialysis for 2 years complained of swelling and pain in the left forearm on the shunt side. A subcutaneous abscess was detected in the left wrist. Since intermittent fever persisted and a bone X-ray examination 4 months after the onset showed bone destruction in the elbow and wrist, the lesion was curetted. Mycobacterium tuberculosis was identified in this lesion. A simultaneous bone biopsy showed on deposition of amyloid or aluminum. After two weeks of treatment with isoniazid, rifampicin and streptomycin, the fever resolved, and the swelling and pain in the left forearm improved. Tuberculosis must be considered and included in the differential diagnosis in dialysis patients who exhibiting destructive articular lesions.

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Bucillamine (Bu) is a new anti-rheumatic agent synthesized in Japan. Use of this agent has been prohibited in patients with impaired renal funtion, because it is eliminated via the kidneys. This paper reports the favorable effect of Bu in a hemodialysis patient with amyloidosis secondary to rheumatoid arthritis (RA), and an investigation of the pharmacokinetics of this agent.
A 56-year-old woman with RA since 1967 developed renal failure in 1984. A diagnosis of secondary amyloidosis was made on the basis of a lip biopsy. Hemodialysis therapy was begun in 1985. At the start of hemodialysis therapy, the patient's RA was classified as stage IV, class III. In 1992, when her arthralgia became uncontrollable with steroid hormones and analgesic agents, and her quality of life deteriorated, she was treated with Bu.
First, we investigated the pharmacokinetics of this agent. On non-dialysis days, the serum half-life of Bu was almost the same as in a subject with normal renal function, but the serum half-life of its two active metabolites, SA-981 and SA-679, was considerably prolonged (9.3 hours and 24.4 hours, respectively). On dialysis days, Bu and its active metabolites could be removed by hemodialysis. Based on the results of the phrmacokinetic study, the dosage was set at 100mg after each hemodialysis session.
Four weeks after the start of Bu, the patient's arthralgia, objective findings and Lansbury index had markedly improved. Improvement of her arthralgia enabled the patient to climb stairs, and her quality of life also improved. There were no signs of accumulation of Bu or its metabolites in the blood.
Although this is only a single case report, the results suggest that Bu is useful in patients with RA accompanied by renal dysfunction by decreasing the dosage of Bu according to the results of the pharmacokinetic investigation.

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