We developed a method of calculating the dialysis fluid flow rate at which targeted Kt/V will be attained. The total body fluid volume is calculated by regional blood flow urea kinetic modeling based on serum urea concentrations actually measured before and after a hemodialysis session performed on the day of regular blood sampling once a month, along with other parameters. Then, for one month beginning on the blood sampling day, the dialysis fluid flow rate at which targeted Kt/V is attained is also calculated by urea kinetic modeling based on the previously determined total body fluid volume and other parameters. In 60 hemodialysis patients, we attempted to perform planned hemodialyses applying this method. As a result, a close linear correlation was found between the Kt/V(x) input before the hemodialysis session and that (y) attained after the session (y=1.01x-0.03, r=0.973). Moreover, there was no significant difference between the Kt/V (1.15±0.21) input before the hemodialysis session and that (1.14±0.22) attained after the session. This method may allow hemodialysis with a higher blood flow rate, a lower dialysis fluid flow rate without changing Kt/V level. Thus, we examined whether or not the clearances for phosphate and β₂-microglobulin change when the blood flow rate is increased and the dialysis fluid flow rate is decreased on the condition that the urea clearance remains the same. We found that the clearance for phosphate did not change, whereas the clearance for β₂-microglobulin was increased by this manipulation of hemodialysis treatment.

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Cinacalcet is an agent used to treat secondary hyperparathyroidism. This drug acts on calcium-sensing receptors in the parathyroid gland to suppress secretion of parathyroid hormone. In past clinical trials, gastrointestinal symptoms and hypocalcemia were the major adverse events reported with cinacalcet. In this study, we surveyed adverse events associated with cinacalcet, in 93 dialysis patients. Cinacalcet significantly decreased the median serum intact-parathyroid hormone (i-PTH) level, from 519 pg/mL at baseline to 193 pg/mL at 21-24 weeks. Adverse events related to cinacalcet were reported in 51 of 93 patients (55%). Gastrointestinal symptoms were the most frequent and were reported in 34 patients, while hypocalcemia was detected in 18 patients. In 17 of the 34 patients, gastrointestinal symptoms occurred within a week after commencing cinacalcet. Various gastrointestinal medications were used to treat symptoms in 12 patients, and cinacalcet was discontinued in 7 patients. Fifteen of 18 patients with hypocalcemia, demonstrated hypocalcemia within 4 weeks after commencing cinacalcet. Most of these hypocalcemic events were managed by increasing the dosage of vitamin D sterols or calcium carbonate, without the need to discontinue cinacalcet. Our findings indicate that cinacalcet treatment is well tolerated, but gastrointestinal symptoms are frequent, especially in the early stages of commencing or increasing the cinacalcet dosage. Coadministration of vitamin D sterols or calcium carbonate in the early stages could prevent most hypocalcemic events.

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【Objective】Among dialysis patients, those who are diabetic or elderly require longer term hospitalization and may develop serious complications. ADL was compared between outpatients and inpatients receiving hemodialysis. Comparison was made using FIM, which has been established in the field of rehabilitation, and the causes of decreased ADL among dialysis patients were examined. 【Methods】Seventy-one patients (31 outpatients and 40 inpatients) receiving hemodialysis care and rehabilitation at our hospital were investigated. Basic information on patients, primary disease causing chronic renal failure, complications and FIM were investigated. 【Results】A greater proportion of inpatients showed diabetes mellitus as the primary disease compared to that among outpatients. Among diabetics, the probability of being hospitalized due to complications was high. There was significant locomotor rehabilitation in 87% of outpatients. However, there was a marked incidence of cerebrovascular disease and rehabilitation for disuse atrophy in 65% of inpatients (p<0.0001). FIM of inpatients was 65±33 points compared with 124±4 points in outpatients and the difference was highly significant (p<0.0001). There were 16 patients with stroke (infarction 8, hemorrhage 7, anoxia encephalosis 1), and palsy significantly decreased ADL when complications of inpatients were examined. Orthopedic conditions were noted in 8 patients (femur the neck bone fracture 4, lumbar spine compression fracture 4). ASO was found in 7 patients (unilateral below knee amputation 2, bilateral above knee/bilateral below knee/unilateral above knee amputation each 1, intractable ulcer 2). Six anima patients were diagnosed (cyclophrenia 1, mental retardation 2, serious affiliation symptom 3). There were 3 seriously ill patients (poorly controlled diabetes mellitus 2, cardiac decompensation 1). However, there were several inpatients with good ADL. 【Conclusion】FIM of inpatients showed more extreme problems than that of outpatients. Complications significantly deteriorate ADL, and long-term admission promotes deterioration. Accordingly, prevention of the complications indicated above is important to maintain dialysis. It is thought that promoting body control and maintenance of ADL by exercise therapy is necessary. Rationalization of dialysis care and Long Term Care Insurance, institutions that accept dialysis patient further augmentation of connections among dialysis hospitals and institutions are immediately necessary.

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The mechanisms involved in thrombus formation at or near the arterio-venous shunt (a-v shunt) prepared for hemodialysis are necessarily rather complicated because blood access is quickly shifted from the high shear stress on the arterial side to medium or low shear stress on the venous side. However, the mechanisms involving shear stress and arterial sclerotic lesions at the a-v shunt in thrombus formation are not yet fully understood. In this study, we analyzed the behavior of blood coagulation and fibrinolysis-related molecular markers in blood samples obtained at the locus of a-v shunt in patients with PTA-treatment and found that SF specifically related to the early stage of thrombus formation was extremely elevated in 4 of 15 patients. The thrombin-antithrombin complex (TAT), an established molecular marker appearing at the early stage of thrombus formation was also elevated, but did not correlate with the level of SF, suggesting that the mechanisms by which these two molecular markers formed were not necessarily interrelated with each other even at the early stage of thrombus formation at or near the a-v shunt. SF is proposed to be a tri-molecular complex composed of 1 molecule of fibrin monomer (formed when a pair of fibrinopeptide A is cleaved from fibrinogen by thrombin) and 2 molecules of native fibrinogen. We previously reported that thrombin further cleaved the paired alpha C domain attached to the central E domain of the fibrin monomer, and exposed the RGD domain present at the alpha(95-97) segment on the molecular surface. Thus, the exposed RGD domain is allowed to interact with α₅ β₁ integrin that functions as a fibrinogen receptor and αvβ₃integrin that functions as vitronectin receptor on the cell surface, and thus promotes cell attachment and extension. In this regards, SF must be considered to contribute to the attachment of platelets to the endothelial cell surface of blood vessels as well as functioning as a molecular marker of accelerated blood coagulation. In 4 patients with elevated SF in the local blood (SF-elevated group), the pulse wave velocity (PWV), a marker of arteriosclerosis, was significantly increased as compared with that in the group without SF elevation. Furthermore, the annual incidence of shunt occlusion was also high in the group with SF elevation compared with that in the group without such elevation. Thus, SF is expected to function as a molecular marker not only for accelerated blood coagulation but also for early recognition of shunt occlusion and its prognosis.

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The patient was a 79-year-old woman. Hemodialysis was introduced in April 2004. Then it was switched to CAPD because of vascular access failure and heart failure. The patient developed persistent eosinophilia of unknown etiology lasting for 6 months. The PD catheter was implanted in the peritoneal cavity on May 20, 2008. Thereafter, the peripheral blood eosinophil ratio increased from 10.1% to 22.3% six days later. CAPD was introduced after a standby period of two weeks. Unexpectedly WBC and eosinophil count in the peritoneal effluent increased on the 22nd day. We diagnosed the patient as having eosinophilic peritonitis because of negative growth on culture of peritoneal effluent and the lack of either abdominal pain or fever. During careful observation of the course, the cloudy effluent disappeared naturally. She was discharged from hospital on the 49th day. Peripheral blood eosinophil ratio decreased to 5.5% on the 56th day. Regarding the etiology, it remains uncertain whether the CAPD system was the cause of eosinophilic peritonitis. The prior increase of peripheral blood eosinophil count before CAPD introduction appears to have been associated with the onset of eosinophilic peritonitis during the course in this patient.

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A 67-year-old male underwent aorto-bifemoral bypass to treat arteriosclerosis obliterans in June 2003. The patient underwent artificial blood vessel replacement because of a pseudoaneurysm in the artificial blood vessel of the abdominal aorta. Stent grafting was also performed because of the recurrence of pseudoaneurysm. Thereafter, hemodialysis was initiated due to the progression of renal dysfunction in March 2006. On November 20, 2006, the patient was admitted to our department due to right femoral pain and swelling. Computed tomography scans demonstrated a hematoma in the right femoral region. Angiography showed 2 bleeding points probably due to rupture of the right femoral circumflex aneurysm, and therefore, embolization was performed at these sites. Thirty-seven days after admission, rupture of the pseudoaneurysm in the artificial blood vessel occurred again, and closure of the rupture site was successfully achieved. Dialysis patients have a high risk of arteriosclerotic diseases. When lower limb pain or swelling is observed in dialysis patients, aneurysmal rupture of the lower limb should also be taken into consideration as a disease requiring differentiation.

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A 54-year-old man was admitted because the serum creatinine level had increased from 1.2 mg/dL to 5.15 mg/dL within 10 months. Histological examination of renal biopsy demonstrated crescentic glomerulonephritis with deposit of immunoglobulin A in the mesangial area. He was diagnosed as immunoglobulin A nephropathy associated with proteinase3-antineutrophil cytoplasmic antibody (PR3-ANCA) -associated glomerulonephritis. He was followed in our outpatient clinic without medications such as steroids or immunosuppressive drugs. Two months after discharge, his serological test also showed the elevation of myeloperoxidase (MPO) -ANCA level. Four months later, he was admitted again with complaints of low grade fever, anorexia, anemia, body weight loss, and general malaise. His laboratory investigation showed elevations of creatinine and CRP. Chest X-ray demonstrated pleural effusion and cardiomegaly. Hemodialysis was initiated. Chest CT scan on the second admission showed bilateral supraclavicular, mediastinal, and paraaortic lymphadenopathy. Light microscopic examination of the left supraclavicular lymph node, “Virchow-Troisier's node” biopsy demonstrated necrotizing granulomatous inflammation with Langerhans type giant cells. Polymerase chain reaction assay of the tissue sample was positive for Mycobacterium tuberculosis. This patient was diagnosed as having extrapulmonary lymph node tuberculosis and treated with the anti-tuberculous drugs, rifampin, isoniazid, ethambutol and pyrazinamide, resulting in a reduction in the sizes of all lymph nodes. When ANCA level increases again or reappearsed in patient with end stage renal disease, active tuberculosis should be considered in the differential diagnosis, because it is possible that tuberculosis causes a positive serological test for ANCA.

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A 78-year-old man who had been receiving hemodialysis (HD) for 2 years was admitted to our hospital due to right-sided pleural effusion that had been nonresponsive to HD. The pleural effusion was hemorrhagic and exudative ; however, various examinations could not demonstrate the specific cause of pleural effusion. Despite the administration of antibiotics and antituberculosis drugs as an empirical therapy, pleural effusion persisted. When left pleural effusion also developed, we performed pleural biopsy under CT-guidance and video-assisted thoracoscopy. The biopsy sample demonstrated nonspecific pleuritis without any finding of infectious disease or malignancy. The patient died of respiratory failure in November 2007, and was autopsied. The findings at autopsy demonstrated pleural fibrosis and pleuritis. Then he was finally diagnosed as having uremic pleuritis on the basis of the clinical and pathological features. There may be relatively many cases of uremic pleuritis among patients on maintenance HD. However, such cases may often be overlooked. It was interesting to note in the present case that no specific cause such as infectious diseases or malignancy were detected even after autopsy. Therefore uremic pleuritis should be taken into consideration as a likely candidate for the cause of refractory pleural effusion in pateients on HD.

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