Adiponectin (ADPN) is a secretory protein from adipose tissue. A plasma ADPN level has been reported to be reduced in patients with atherosclerotic complications. We investigated plasma ADPN levels in patients on peritoneal dialysis to test its predictive power for cardiovascular events.
We measured plasma levels of ADPN, leptin, tumor necrosis factor (TNF)-α, plasminogen activator inhibitor type 1 (PAI-1) in 29 patients on peritoneal dialysis. Plasma ADPN levels were higher in patients on peritoneal dialysis (27.7±17.8, μg/mL) than in healthy subjects.
The plasma ADPN level was inversely related to the plasma leptin level (r=-0.58), %body fat (r=-0.43), homeostasis model assessment (HOMA-R) (r=-0.54), visceral fat area (VFA) (r=-0.50) and aortic calcification index (ACI) (r=-0.40). However, the level of ADPN was not correlated to that of TNF-α or PAI-1 in plasma.
These results indicate that the plasma ADPN level is inversely related to metabolic risk factors, and can be a predictor of cardiovascular outcomes in patients on peritoneal dialysis.

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To identify the clinical usefulness of non-invasive parameters in patients on long-term hemodialysis, we retrospectively analyzed echocardiographic data, and hemodynamic parameters in 50 dialysis patients. Ejection fraction (EF), left aterial dimension (LAD), left ventricular end-diastolic dimension (LVDd), left ventricular end-systolic dimension (LVDs), interventricular septal thickness (IVS) and left ventricular mass (LVmass) were measured on M-mode echocardiograms. Blood pressure and heart rate obtained 2-years, 1-year, 6-months, and within 3-months before death were compared with echocardiographic parameters.
We divided the subjects into 3 groups: 1) normal EF group; 24 patients whose EF remained≥50% throughout the 2 years, 2) decreased EF group; 13 patients whose EF remained<50%, and 3) deteriorating EF group; 13 patients whose EF had been≥50% 2 years previously but decreased to <50% due to a cardiovascular event. The last available data and data 2 years before death were compared. In the normal EF group, LAD and IVS increased significantly. In the decreased EF group, IVS, LAD and LV mass were unchanged. In the deteriorating EF group, LVDd, LVDs, LVmass and heart rate increased, while the systolic blood pressure decreased after EF fell.
Sequential IVS and LAD measurements were useful, especially for normal EF patients. A sudden decrease in systolic blood pressure and rise in the LVDd, LVDs and LVmass suggest that a cardiovascular event due to ischemic myocardial injury will occur.

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Four kinds of neutralized peritoneal dialysis solutions (N-PD) with a low level of glucose degradation products (GDPs) are currently marketed. The GDP concentrations of each N-PD have been confirmed in some reports, but the methods with which the levels have been measured are not uniform. We measured the concentration of GDPs and checked the pH of both the glucose chamber and after mixture of the N-PDs under the same methods and conditions, and compared these with an acid peritoneal dialysis solution (A-PD). The N-PDs studied were Midpeliq L® (Terumo), PD-solita·A® (Shimizu Medical), Perisate NL® (JMS) and Stay·safe balance® (Fresenius Medical Care). The concentrations of GDPs were measured 4 and 12 months after manufacture using high performance liquid chromatography (HPLC). The GDPs assayed were 3-deoxyglucosone (3-DG), glyoxal (Glx), methyiglyoxal (M-Glx), formaldehyde (FoA), acetaldehyde (AcA), 5-hydroxymethylfurfural (5-HMF), furfural (2-FA), formic acid and levulinic acid.
The pH values of the N-PDs ranged from 2.90 to 6.04 in the glucose chamber, and from 6.67 to 7.47 after mixture, and in A-PD ranged from 5.17 to 5.25. The total amount of GDPs (μmol/L) in the N-PDs ranged from 30.4 to 95.1 at 1.5%, from 51.4 to 136.5 at 2.5% and from 78.4 to 192.2 at 4.0%. The concentrations of 3-DG and 5-HMF made up an average of 95% in the total GDPs. The total amount of GDPs in the A-PD at 1.5%, 2.5% and 4.0% was 324.9, 481.8 and 594.2, respectively and they were 3 to 10 times higher than N-PD. As for the change in the concentration of GDPs at a shelf life of 12 months in N-PD, only AcA increased from 1.2 to 2.8 at 1.5%, and from 1.4 to 2.7 at 2.5%, and other GDPs did not change significantly. In A-PD, only AcA decreased, and Glx, FoA and 5-HMF increased. The N-PD was more stable than A-PD during long-term storage.
The N-PD achieved the goal of neutralizing the pH and reducing the concentration of GDPs. However, even in the same N-PD, some differences in the concentrations of GDPs could be recognized. It remains necessary to clarify the cytotoxicity of GDPs and the biocompatibility of each NP-D.

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Encapsulating peritoneal sclerosis (EPS) is a serious complication of long-term peritoneal dialysis, sometimes requiring long-term nasogastric-tube (NG tube) intubation for continuous decompression of gastrointestinal pressure caused by bowel obstruction.
A fifty-eight-year-old man being treated with regular hemodialysis after switching from CAPD because of loss of ultrafiltration developed EPS and was managed with total paraenteral nutrition (TPN). Two months after continuous drainage of a large volume of bile, he suddenly complained of dryness of eyes and xanthopsia. On suspicion of vitamin A deficiency, 50, 000 IU of retinol palmitate (vitamin A) was administered intramuscularly after drawing blood for the measurement of plasma vitamin A concentration. Three consecutive vitamin A injections rapidly restored normal vision. Vitamin A concentration in blood was 10 IU (65-276 IU in healthy males). Although this patient was treated by TPN with fat-soluble vitamins every two weeks, vitamin A deficiency occurred. The reason vitamin A deficiency became symptomatic was explained by interruption of the duodenohepatic circulation of fat-soluble vitamins due to continuous drainage of bile through NG-tube.
This case demonstrates that caution is required to prevent deficiency of fat-soluble vitamins during long-term bile drainage due to bowel obstruction accompanying EPS.

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A 50-year-old man underwent hemodialysis for end-stage chronic renal failure due to diabetic nephropathy for 2 years. He was admitted with right pleural effusion and appetite loss. After he was admitted, pleural effusion and ascites increased rapidly. Bloody fluid was obtained by thoracocentesis and malignant cells were demonstrated in the pleural fluid. Despite various modalities of examination we could not determine the origin of the tumor. His general condition rapidly deteriorated and he finally died on the 30^th hospital day. Autopsy demonstrated widely disseminated tumors on the mesenterium and parietal peritoneum, and invading the right ureter. Nodules existed in the liver, the upper pole of the right kidney, the right adrenal gland, the upper lobe of the left lung and the thyroid. Although we could not diagnose the origin of the tumor macroscopically, we assumed that the cause of death was probably cancerous peritonitis. Pathological diagnosis showed sarcomatoid renal cell carcinoma (RCC) arising from the right kidney mass.
It is well known that RCC occurs in hemodialysis patients more frequently than in healthy people. To diagnose this disease in the early stage, regular examinations are essential, but in sarcomatoid renal cell carcinoma, renal tumors remain difficult to diagnosis correctly, even with computed tomography (CT). Further examinations are necessary to develop a plan for screening or therapy for sarcomatoid renal cell carcinoma.

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The patient was a 60-year-old man who had begun continuous ambulatory peritoneal dialysis (CAPD) in January 1998 due to polycystic kidney disease. In May 2001, he presented with gross hematuria, and petechiae in the limbs and general fatigue 3 days after he first felt signs of common cold.
Abdominal CT showed a high density area in the cyst of the right kidney, and peripheral platelet cell counts was 1.5×10⁴/μL, and PAIgG was 73.9ng/10⁷ cells (9.0-25.0).
Cytologic examination of bone marrow showed increased megakaryocytes. He was diagnosed with idiopathic thrombocytopenic purpura (ITP), and treated with steroids alone. One month later, the peripheral platelet cell count was 0.8×10⁴/μL. He was diagnosed with ITP refractory to steroids therapy, and treated with cyclosporine A (CyA) combined with steroids. Two months later, the peripheral platelet cell count was 10×10⁴/μL and general condition was improved. These drugs were tapered gradually, then discontinued. To date, the platelet cell count has remained over 10×10⁴/mm³.

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A 53-year old woman was referred to our hospital with fever and anuria. On admission, her serum creatinine was 7.7mg/dL and CRP was 28.2mg/dL. The electrocardiogram showed a QS pattern and ST segment elevation in the V1-V3 leads, and echocardiography demonstrated decreased wall motion in the left ventricle. Cardiac enzymes such as creatine kinase, myoglobin, and cardiac troponin I were elevated, suggesting the onset of acute myocardial infarction. However, coronary angiography did not show any pathological lesions, and left ventriculography demonstrated akinesis in the apical segment and hyperkinesis in the basal segment. Based on these findings, we diagnosed Takotsubo cardiomyopathy evoked by acute renal failure and sepsis.
Thereafter, we immediately started endotoxin-absorbing therapy using polymyxin B and continuous hemodiafiltration with antibiotics. Her general condition and laboratory data gradually improved, and left ventricular wall motion returned to normal. On the 7^th hospital day, intermittent hemodialysis (HD) was initiated. On the 13^th hospital day, renal function began to improve with an increase in urine volume. HD was successfully discontinued on the 25^th hospital day.
We report here a rare case of acute renal failure complicated by Takotsubo cardiomyopathy. Severe stress such as acute renal failure and sepsis resulted in Takotsubo cardiomyopathy, leading to the acceleration of renal dysfunction. Takotsubo cardiomyopathy needs to be considered as a potential complication of acute renal failure.

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