Ten grams of glucose were intravenously administered at the end of each hemodialysis session, 3 times a week, for a month in 13 non-diabetic hemodialysis patients with secondary hyperparathyroidism (2°HPT), serum intact-PTH being above 500pg/ml. Serum intact-PTH decreased significantly to 83% of the baseline level (p=0.001), but no significant change was observed in serum Ca, Pi, ALP or osteocalcin level. The inhibitory effect of glucose on serum PTH levels was considered to be related either to the low incidence or to a slow progression of 2°HPT in diabetic dialysis patients. Administration of glucose was easy to perform and may be useful for prevention of 2°HPT in non-diabetic hemodialysis patients.

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Two hundred twenty chronic hemodialysis patients (male 131, female 89) underwent urine cytology to screen for urinary tract tumors. The underlying diseases in these patients were chronic glomerulonephritis in 152, diabetic nephropathy in 38, polycystic kidney disease in 8, and other diseases in 22. Their mean age was 58.3 years, and the mean duration of hemodialysis was 1, 238 days. The mean 24-hour urine volume was 466ml. All patients repeated 3 times of examinations.
The results of 660 urine cytology examinations were divided into five classes according to Papanicolaou's criteria, Class I, class II, class III, class IV, and class V were composed of 490, 157, 11, 1, 1, respectively. A 79-year-old diabetic patient with hemodialysis duration of 2 years, who was diagnosed as class V, was revealed a non-papillary bladder tumor by cystoscopy, although transitional cell carcinoma (grade 3) was found by the biopsy. However, in a patient of class IV (53y/o male) had not been found any abnormal lesion by the ureteroscopy and by the cystoscopy.
The incidence of urothelial tumors in hemodialysis patients seems to be increasing, being screening for urinary tract tumors very important. Urine cytology was noninvasive and was considered to be a good screening test for detect urinary tract tumor in hemodialysis patients, who have an adequate urine output.

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To modify the intestinal bacterial flora of hemodialysis patients, a dietary fiber preparation was administered and its effects on immune function were studied.
Thirty patients on maintenance hemodialysis without signs of infection (15 men and 15 women) received a water soluble polydextrose dietary fiber preparation (7g/day: 4 pieces of Touriame) for 8 weeks, and blood concentrations of the products derived from intestinal bacteria as well as hematological parameters before administration were compared to those obtained after administration.
After dietary fiber administration, serum concentrations of bacterial products derived from intestinal bacterial flora (phenol (p<0.05), p-cresol (p<0.01), and indoxyl sulfate (p<0.05)) were significantly decreased as compared with the respective pretreatment values. In addition, lymphocyte blastogenesis, whether induced by PHA (p<0.05), ConA (p<0.01) or PWM (p<0.05), was increased significantly.
It is concluded that dietary fiber is useful for improving the immunocompromised state of hemodialysis patients, as well as for relieving symptoms such as constipation.

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A 38-year-old woman suffering from end-stage renal disease was placed on CAPD therapy in 1989. Her fluid intake was so large that overhydration and marked cardiomegaly (cardiothoratic ratio: 60%) was noted. In 1993, extracorponeal ultrafiltration was added to CAPD therapy because of overhydration. She developed tunnel infection in 1993, the CAPD catheter was removed, and hemodialysis therapy was commenced three times per week. The overhydration and cardiomegaly improved (cardiothoracic ratio: 50%) after receiving hemodialysis therapy. In general, CAPD is considered adequate dialysis therapy for patients with cardiovascular complications such as chronic heart failure. However, hemodialysis therapy may also benefit CAPD patients with normal cardiac function who experience chronic heart failure secondary to excess fluid intake.

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A 32-year-old woman had a fever of approximately 39°C and left flank pain. Abdominal CT revealed marked hydronephrosis of the left kidney, and left percutaneous nephrostomy was performed.
Approximately 1, 000ml of pus was drained, low blood pressure, oliguria, and lung edema were later noted, and the patient was transferred to our hospital for general management and hemodialysis. A chest X-ray on admission showed severe congestion. We made a diagnosis of bacteremia associated with acute renal failure caused by puncture drainage for pyonephrosis following detection of Escherichia coli from both drainage urine cultures and blood cultures.
Disseminated intravascular coagulation (DIC) also developed. Hemodialysis was performed ten times starting on the day of admission. Conservative therapy (for example, platelet transfusion and antibiotics), however, was successful in allowing recovery from this deterioration.

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We encountered a hemodialysis (HD) patient with rhabdomyolysis followed by severe hypoglycemia induced by disopyramide (DP).
The patient, a 66-year-old woman, was treated with DP 300mg/day. Five days later, DP was discontinued because of the development of appetite loss. Seven days later, the patient developed hypoglycemic coma following general fatigue and thirst.
Her consciousness became clear immediately after infusing 40ml of 50% glucose, but thereafter she kept complaining of severe generalized muscular pain. At first we thought that the cause of the muscular pain was the cramps that frequently occur in HD patients. The next day, we made a diagnosis of rhabdomyolysis based on the laboratory findings, which showed AST, ALT, LDH and CPK elevations.
Rhabdium is fed by fatty acids when hypoglycemia occurs, so rhabdomyolysis due to hypoglycemia is rarely reported. We considered the mechanism of rhabdomyolysis in this case to be a disturbance of fatty acid utilization superimposed on hypoglycemia.
As far as we know, this is the first case of rhabdomyolysis following hypoglycemia as a side effect of DP ever reported.

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We report hypothyroidism induced by a closed cap containing povidone-iodine in a 32-year-old female undergoing nightly peritoneal dialysis (NPD). The patient's thyroid became enlarged after switching from continuous ambulatory peritoneal dialysis to NPD in June 1994. In July 1995, the patient's serum thyroid stimulating hormone (TSH) level was found to be markedly elevated to 121μU/ml, and her serum free triiodothyronine (FT₃) and free thyroxine (FT₄) levels were 2.6 pg/ml and 0.4ng/dl, respectively. Thyroid 3-hour radioactive iodine uptake was high. Serum inorganic iodine (II) was elevated to 15.0μg/dl. Antithyroid antibodies including antibodies to thyroglobulin, thyroid peroxidase and TSH receptor were all negative. Histologically, neither lymphocytic infiltration nor fibrosis in the interfollicular space suggestive of chronic thyroiditis was detected. Based on these findings a diagnosis of reversible hypothyroidism induced by iodine excess was made, but strict dietary iodine restriction did not decrease the patient's serum II or TSH levels. During the first infusion of dialysate in NPD, the povidone-iodine that leaks out from a closed cap flows into the peritoneal cavity because of the absence of peritoneal effluents. Preventing the flow of povidone-iodine decreased serum II and TSH levels to 4.6μg/dl and 28.0μU/ml, respectively. Thus, attention should be directed to the complication of hypothyroidism induced by povidone-iodine-containing closed caps in patients undergoing NPD.

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