Background: Hyperkalemia is a risk factor for cardiac sudden death in dialysis patients, whereas hypokalemia induces fatal arrhythmia in patients with cardiac disease. We investigated the association between cardiovascular death and predialytic serum potassium (SK) in patients with maintenance dialysis. Methods: A four-year (April 2006 to October 2010) cohort of 309 maintenance dialysis patients from Yoshikawa Hospital Dialysis Unit was studied. The eligible patients were divided into four groups stratified by predialytic SK (SK≤4.5，4.5<SK≤5.0, 5.0<SK≤5.5, SK>5.5 mEq/L). The prognostic factors for cardiovascular death were extracted from our cohort by the Cox proportional-hazards method. Stratified SK groups, age, gender, underlying disease, vintage of dialysis, blood pressure before and after dialysis, and biochemical and peripheral blood test values were used as explanatory variables. Results: In total, 33 and 16 patients were excluded due to loss to follow-up and inadequate data, respectively. A total of 260 patients, 149 men and 111 women, entered this study. Their mean age was 68.8 years old and mean duration of dialysis was 5.6 years. Overall, 89 patients had diabetes mellitus and 97 patients had cardiac disease as comorbidities. Their mean predialytic SK was 4.97 mEq/L and observation period was 3.3 years. Forty-three patients died due to cardiovascular disease. Elderly, long-term dialysis, hemofiltration, diabetes, cardiac disease, low SK, and high CRP were the risk factors for cardiovascular death. Two stratified low-SK groups, SK≤4.5 mEq/L and 4.5≤SK≤5.0 mEq/L, were associated with poor prognosis and their hazard ratios were 2.733 and 6.377, respectively. Conclusion: This study suggests that keeping predialytic SK above 5.0 mEq/L is favorable for cardiovascular prognosis in dialysis patients.

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Background and objective：A number of established oral antidiabetic drugs are unsuitable for hemodialysis patients with type 2 diabetes. Some hemodialysis patients use insulin in their glucose management despite having sufficient endogenous insulin secretion. Liraglutide, a human glucagon-like peptide-1 analogue that is administered as a once-daily subcutaneous injection, induces glucose-dependent insulin secretion, which limits the risk of hypoglycemia. Liraglutide may be safe and effective treatment in hemodialysis patients. Switching from insulin to liraglutide in hemodialysis patients with type 2 diabetes may have some advantages, such as reducing hypoglycemia and the number of injections. However, little is known about the switching. We accumulated and analyzed the clinical information of hemodialysis patients with type 2 diabetes who underwent switching from insulin to liraglutide. Design：Descriptive epidemiology study. Participants and setting: Among 48 hemodialysis patients with type 2 diabetes at Heiwadai Hospital from September 2010 to April 2011, 10 patients who had fasting serum C-peptide immunoreactivity (s-CPR) ≥1.0 ng/mL and 2h-postprandial s-CPR≥4.0 ng/mL by meal tolerance test were included in this study. Exposure: Switching from insulin to liraglutide. Main outcome measure: Glycoalbumin (GA) value at three months after switching. Results: 3 out of 10 patients discontinued due to nausea and vomiting, and 2 patients due to hyperglycemia. In 5 patients who were able to continue liraglutide, GA levels were decreased from 21.8±3.3 at baseline to 19.6±1.9 at 3 months after switching, but this was not statistically significant. Conclusion: Switching from insulin to liraglutide is expected to be one of the useful strategies for hemodialysis patients with type 2 diabetes who have sufficient endogenous insulin secretion. When prescribing liraglutide, care should be taken for nausea and vomiting.

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In 2012, we conducted a survey for the facilitation of dialysis therapy for HIV-infected CKD patients, and found that there must be many obstacles for private dialysis facilities to accept HIV-infected dialysis patients without public assistance. From these results, we conducted a survey of the base hospitals for AIDS across the country for activities to support dialysis facilities. Sending a questionnaire to 380 base hospitals, core base hospitals, and block base hospitals, 190 responses (response rate 50.0%) were analyzed. Their average bed number was 542. They had 3.79 urologists and 3.05 nephrologists, with 17.2 dialysis machines. A total of 44 patients needed substitution therapy, 28 were treated with hemodialysis, and 16 with peritoneal dialysis. Initiation and chronic therapy was supplied in 19 cases at their own hospital, initiation at their own hospital but chronic therapy at other dialysis facilities in 11 cases, and initiation and chronic therapy at other dialysis facilities in 7 cases. Although the facilities of 3/4 support medical care for “needle-stick injuries” of dialysis staff, 69.7% of base hospitals do not supply HIV post-exposure prophylaxis medicine to dialysis facilities for accidents at night and during holidays. Educational activities for the neighborhood by base hospitals were not done regularly in 63%. Educational activities for dialysis staff were done in only 6％ of base hospitals. We found that the relationships between the base hospital and satellite dialysis facilities were not close. We must enhance the closeness of cooperation between base hospitals and neighborhood dialysis facilities.

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A 54-year-old woman with end-stage renal disease secondary to immunoglobulin A nephropathy presented with purulent discharge from the exit site. She had been undergoing continuous ambulatory peritoneal dialysis for three years. Mountain spring water was used as a cleaning solution for the exit site for one year. Mycobacterium fortuitum grew on culture of the purulent discharge. Acid-fast staining of the water revealed acid-fast bacilli (Gaffky 2). The patient was treated with oral levofloxacin and clarithromycin. After six weeks of therapy, the exit-site infection showed no improvement. Therefore, the peritoneal catheter was removed and renal replacement therapy was switched to hemodialysis. This is the first report in which a definite infection source was determined in M. fortuitum exit-site infection. Source of infection and weakness of the exit-site skin barrier are regarded as important to establish M. fortuitum exit-site infection. Routine evaluation and re-education for exit-site care would have prevented M. fortuitum exit-site infection and the additional catheter surgery.

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A 39-year-old diabetic woman with end-stage renal disease due to congenital renal hypoplasia was started on peritoneal dialysis (PD) using a PD catheter (Medi-tech Co., Ltd., Tokyo, Japan) and 1.35 w/v % glucose peritoneal dialysate (Midpeliq 135 L; Terumo Corporation, Tokyo, Japan). Six months after catheter placement, the PD catheter was removed due to recurrent peritonitis and tuberculous peritonitis. Six months later, she restarted PD using the same devices. However, catheter replacement was repeated due to occlusion of the catheter at seven days after restarting PD. From postoperative day 9, her body weight increased due to ultrafiltration failure (-4.6 dL/day) and peritoneal effluent became cloudy with fibrin clots. The number of cells in the peritoneal effluent was more than 500/μL and more than 80% of the cells were eosinophils; thus, she was diagnosed with eosinophilic peritonitis. Because of the possible adverse effect of steroids on blood sugar, she was treated with antihistamine at 5 mg/day, namely, olopatadine. After starting this treatment, the numbers of total cells and eosinophils in the peritoneal effluent decreased markedly by 94% compared with the baseline. Moreover, the volume of peritoneal effluent increased (+3.3 dL/day), suggesting that the ultrafiltration failure had improved. In general, steroid is a standard therapy for eosinophilic peritonitis in patients on PD, if self-resolution does not occur. Our case is the first report of eosinophilic peritonitis successfully treated with olopatadine alone. Olopatadine could be a substitute for steroid in the treatment of eosinophilic peritonitis associated with PD catheter insertion.

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A 74-year-old man with nephrosclerosis had been treated with CAPD since 2007, until he passed away in 2011. He was admitted to our hospital three times in June, July, and November 2010 due to bacterial peritonitis. In each episode, he responded to antibiotic treatment. In January 2011, he was again admitted to the hospital due to peritonitis. Abdominal CT showed a tumor mass in the upper pole of the spleen and multiple intra-abdominal nodules. Despite highly suspected malignancy, a biopsy was not performed due to his poor state. In March 2011, he was admitted to the hospital again (his fifth hospital admission) due to peritonitis. His clinical condition deteriorated progressively and he passed away on the day of admission. Clostridium perfringens and Streptococcus mitis were identified as the pathogens of the peritonitis by culture of CAPD fluid. The result of the autopsy proved that multiple intra-abdominal nodules were the peritoneal seeding of malignant mesothelioma. Although bacterial peritonitis was ultimately the cause of his death, malignant mesothelioma may be considered as the proximate cause of the peritonitis. Herewith, we present this case as an interesting and rare case in terms of the pathogenesis.

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A middle-aged man with end-stage renal disease associated with chronic glomerulonephritis developed pain and ulcers in his left dorsal foot. Skin biopsy strongly suggested calciphylaxis since there were some mineral deposits in the dermal lesion. Serum calcium and phosphorus levels were beyond their target ranges. Further examination, such as enhanced computed tomography and ^99mTc-MIBI scintigraphy, detected an ectopic enlarged parathyroid gland in the anterior mediastinum. In addition to the classical treatment including administration of antibiotic agents and prostaglandin, a low-calcium-concentration dialysate (2.5 mEq/L), cinacalcet, was administered to control his secondary hyperparathyroidism. After the start of the cinacalcet, not only PTH, but also serum Ca and P, was suppressed and maintained in their target ranges. Furthermore, the ulcer in the dorsal foot showed marked improvement. The suppression of PTH and the correction of serum calcium and phosphorus by cinacalcet might have contributed to the improvement in this case. Although only a few cases have been reported in which cinacalcet had beneficial effects on calciphylaxis, our case suggested that cinacalcet could be a choice of treatment for calciphylaxis in patients with secondary hyperparathyroidism, particularly when there are coexisting hypercalcemia and hyperphosphatemia.

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