Pale yellow granules start to adhere in the dialysis circuit immediately after hemodialysis initiation, and coagulate the circuit in some cases. This frequently occurs in winter, and is avoided by warming the dialysis circuit to 37 °C at the time of priming. We investigated the granules and cause of their formation. On electron microscopy, the granules were platelet thrombi formed by activated platelets. There were no common findings in the past medical history of dialysis or primary disease and no common symptom other than coagulation of the circuit among 5 cases. No cryoglobulinemia nor cold agglutinin disease related to cold stimulation was noted, and all antibodies related to heparin-induced thrombocytopenia were negative. Compared to non-granule-forming dialysis patients, no difference was noted on blood testing, and the platelet count was within the normal range, but the rate of heparin-induced reduction of the mean platelet volume (MPV) was greater (p=0.016). An increase in the non-fractionated heparin dose did not influence granule formation, but warming of the dialysis circuit at the time of priming and switch of the anticoagulant to low-molecular-weight heparin or nafamostat inhibited granule formation and avoided coagulation of the circuit. This pathology is similar to thrombocytopenia in patients under systemic heparinization in hypothermic surgery, suggesting that cold stimulation in the dialysis circuit and the macromolecular heparin fraction are involved in pale yellow granule formation.

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A retrospective observational study was conducted to determine the relationship between the treatment time (TT)/blood flow rate (Qb)/dialysis dose (Kt urea) and patient mortality using data from the Japanese Society for Dialysis Therapy Renal Data Registry (JRDR). The 1-year mortality (up to the end of 2003) and 5-year mortality (up to the end of 2007) risks of thrice-weekly HD patients as of the end of 2002 were assessed by performing a logistic regression analysis of HD prescription and dose data, using a cause of death other than accident or suicide as the endpoint. The patients were stratified by sex, post-dialysis body weight (PDBW), predialysis serum albumin (Alb), creatinine generation rate corrected by sex and age (%CGR), and normalized protein catabolic rate (nPCR). The results for patients on HD for 5 or more years were as follows: When a TT of ≥240min and <270min was regarded as the reference, the mortality risk was higher in the group of patients with a shorter TT and lower in patients with a longer TT regardless of subgroups. When a Qb of ≥200mL/min and <220mL/min was regarded as the reference, the mortality risk was higher in the patients with a lower Qb, and lower in the group of patients with a higher Qb, except female patients and patients aged ≥75, PDBW <40kg, Alb <3.0g/dL, %CGR <80%, and nPCR <0.7g/kg/day. When a Kt urea of ≥38.8L and <42.7L was used as the reference, the group of patients with a Kt urea smaller than this had an increased mortality risk, and patients with a larger Kt urea had a decreased mortality risk, except those with Alb <3.0g/dL, %CGR <80%, and nPCR<0.7g/kg/day. The results for patients on HD for less than 5 years were similar. These results suggest that the life prognosis of thrice-weekly HD patients may be improved by increasing the dialysis dose through a longer TT and increased Qb, except for malnourished patients.

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Clinically, the ankle-brachial blood pressure index (ABI) has been widely used to screen for subclinical peripheral artery disease (PAD). PAD is a common complication in hemodialysis patients. In the present study, we investigated the association between the ABI and long-term (maximum of 6 years) mortality among hemodialysis patients and the causes of death. A total of 117 patients receiving maintenance hemodialysis who underwent an ABI examination in 2005 were enrolled. Patients with an ABI of less than 0.9 were considered as the ABI<0.9 group, while those with an ABI of more than 0.9 in both legs were considered as the ABI>0.9 group. Nineteen patients (16.2%) were included in the ABI<0.9 group. The serum albumin and creatinine levels were lower, the serum c-reactive protein level was higher, and the hemoglobin level was lower in the ABI<0.9 group than in the ABI>0.9 group (3.6±0.3g/dL vs. 3.8±0.3g/dL [p=0.002], 9.7±1.8mg/dL vs. 11.8±2.5mg/dL [p<0.001], 0.8±1.3mg/dL vs. 0.2±0.7mg/dL [p=0.003], and 9.6±1.1g/dL vs. 10.2±1.0g/dL [p=0.021], respectively). Multivariate Cox analysis identified an ABI<0.9, a male gender, a low level of serum creatinine, a low level of hemoglobin, and the presence of diabetes mellitus as independent predictors of mortality (p<0.001, p=0.006, p=0.002, p=0.041, and p=0.005, respectively). Infection was the most frequently observed cause of death in the ABI<0.9 group, and was more prevalent in the ABI<0.9 group (6/19) than in the ABI>0.9 group (4/98, p<0.001). An ABI<0.9 was an independent risk factor for mortality among hemodialysis patients. Infection was significantly more prevalent in the ABI<0.9 than in the ABI>0.9 group.

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ESA responsiveness in hemodialysis patients is influenced by various factors such as inflammation, secondary hyperparathyroidism and nutrition. Recently, hepcidin-25, a key regulator of iron homeostasis, was shown to be involved in the pathogenesis of low ESA responsiveness. However, the precise mechanisms of ESA responsiveness remain to be fully elucidated. We examined the relationship between ESA responsiveness and the various clinical parameters of hemodialysis patients with sufficient iron stores (ferritin over 100ng/mL). Twenty-nine hemodialysis patients under epoetin beta (EPO) treatment were divided into two groups, Hb-Low (Hb less than 10g/dL) and Hb-High (Hb more than 10g/dL) groups, and their hematological parameters, the status of iron metabolism and inflammatory markers were compared. Hepcidin-25 and ferritin of the Hb-Low group were significantly higher than those of the Hb-High group (Hb-Low vs. Hb-High, hepcidin-25: 74.7±48.8 vs. 40.1±24.5ng/mL, p=0.018; ferritin: 257±148 vs. 140±61ng/mL, p=0.007). CRP tended to be higher in the Hb-Low group compared to Hb-High group (0.41±0.55 vs. 0.14±0.23mg/dL, respectively, p=0.074), and there was a negative correlation between CRP and Hb in the Hb-Low group. Although the reticulocyte count tended to be higher in the Hb-Low group compared to Hb-High group, this led to no improvement in Hb (Hb: 9.4±0.6 vs. 10.5±0.5g/dL, p<0.001; RET‰: 12.9±4.5 vs. 9.9±4.2‰, p=0.083, respectively). Our data suggest that, in hemodialysis patients presenting with low hemoglobin and sufficient iron stores, high ferritin and a high hepcidin-25 concentration might induce defective iron utilization. In addition, from the tendencies of high CRP and high reticulocytes, a shortened erythrocyte lifespan and micro-inflammation might exist in these patients. The combined impact of these factors may contribute to the low ESA responsiveness.

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We report two patients on hemodialysis in whom a single dose of γ-aminobutyrate (GABA) analogues caused muscle weakness of the lower extremities. Both patients had a history of long-term hemodialysis for 23 and 31 years, respectively. They used benzodiazepine receptor stimulants for insomnia and complained of neuralgia caused by spinal canal stenosis. A single administration of either pregabalin (25mg) or gabapentin (200mg) provoked muscle weakness of the lower extremities and gait disturbance, and no pain relief was obtained. The adverse effect of these agents had completely resolved the next day without receiving hemodialysis. GABA analogues should be cautiously administered to anuric patients on long-term hemodialysis who receive drugs that augment the effects of GABA analogues.

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We present the case of a 57-year-old Type2 diabetic man with chronic renal failure under hemodialysis, who injected himself with 1,200 units of regular insulin subcutaneously in a suicide attempt. He had been diagnosed with chronic hepatitis C and treated for depression. He was admitted to our hospital two hours after the overdose injection, because of severe hypoglycemia and unconsciousness. Despite continuous glucose injection, hypoglycemia persisted for twenty-four hours. He recovered completely without any complications.

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We report 2 cases of successful plasma exchange in patients with acute kidney injury in minimal change nephrotic syndrome. Case1 was a 39-year-old man and case2 was a 33-year-old woman. Both patients developed acute kidney injury in spite of methylprednisolone pulse therapy, and required hemodiafiltration. The serum albumin level in case1 was 1.8mg/dL and that in case2 was 1.6mg/dL. Albumin infusion was ineffective against acute kidney injury in both cases. Although hemodiafiltration was performed 3 times, it did not improve acute kidney injury in either case. Therefore, plasma exchange was performed using 5% albumin solution. At the end of plasma exchange, the urinary volume markedly increased, the renal function of the patients rapidly returned to the normal level, and further hemodiafiltration was not required. The pathological findings on renal biopsy showed typical minimal change disease with severe foot process effacement and without acute tubular necrosis in either case. Proteinuria began to improve 3 days after plasma exchange in case1 and after 1 day in case2. The renoprotective effects of plasma exchange cannot be ascribed to the correction of severe hypoalbuminemia. In addition, plasma exchange may involve the removal of unknown circulating pathogenic factors. The results suggested that plasma exchange might have a multiplier effect on the treatment of acute kidney injury in minimal change nephrotic syndrome when we attempted it after steroid therapy.

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Catheter malfunction is one of the most common complications of peritoneal dialysis, and it can result from catheter migration, fibrin deposition, omental wrapping, or occlusion due to other different intraperitoneal organs. The obstruction of a peritoneal dialysis catheter by the fimbria of the fallopian tube is an unusual complication. We report a successful case of laparoscopic salvage of peritoneal dialysis catheter obstruction caused by the fimbria of the fallopian tube. In July 2011, a 76-year-old woman with chronic renal failure due to nephrosclerosis had a peritoneal dialysis catheter placed through a right paramedian transrectal incision. On July 25, continuous ambulatory peritoneal dialysis (CAPD) was started without difficulty. She began automated peritoneal dialysis (APD) on the fourth day without difficulty, but, on the fifth day, in-flow disability triggered an alarm. After that, she developed in- and out-flow problems. The injection of a water-soluble contrast agent into the peritoneal dialysis catheter radiographically demonstrated filling defects (called an “octopus sign”) which are occlusion of the side holes and partial lumen obstruction. On August 29, diagnostic laparoscopy was performed. The peritoneal dialysis catheter was found to be enveloped by the right fimbria of the fallopian tube. The fimbria of the fallopian tube appeared to have entered the side holes and lodged in the lumen of the catheter. The fimbria of the fallopian tube were carefully removed, and the fallopian tube was sutured to the parietal peritoneum in the hope of preventing recurrence. Two hundred milliliters of heparinized saline were instilled in the abdominal cavity through the catheter. Eight days later, CAPD was restarted without difficulty.

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