Theoretically, the blood sugar level will not be less than the dialysate glucose concentration during dialysis. Therefore, evaluation of the relation between blood sugar kinetics and erythrocytes is considered in this study. For 120min, saline 1,000mL was recirculating to the dialyzer blood compartment (100mL/min) and dialysate flow was 500mL/min during evaluation of glucose diffusion in the dialyzer. The measured of glucose concentration in blood and dialysate compartment of the dialyzer. The dialysate glucose concentration showed three values (0, 100, and 150mg/dL), and the dialyzer used was an APS-15. Forty-two CKD (NIDDM group:18, IDDM group:6, and CGN group:18) was used for interaction between glucose and erythrocytes. The dialysate glucose concentration was 150mg/dL, dialysate flow was 500mL/min, blood flow 150~200mL/min, and the dialyzer was an APS-15. Blood samples were serially collected from dialyzer inlet pre-dialysis, and 2 hours after dialysis started. Then 0.5% glucose solution infusion (0.5mL) was centrifuged to collect erythrocytes from whole blood. These samples were incubated at 37°C and blood sugar levels were measured. The blood sugar levels at the dialyzer inlet and outlet were also measured to determine blood sugar kinetics in the dialyzer. At 0mg/dL, dialysate glucose concentration did not diffuse glucose between blood and dialysate compartment. At 100 and 150mg/dL, the glucose concentration in the blood and dialysate compartment were similar 30 minutes after the start of dialysis. Blood sugar levels in 0.5% glucose containing erythrocytes were 1.8% NIDDM, -4.5% IDDM, and 4.1% CGN, showing different changes in glucose levels compared to those pre HD. Two hrs after HD started, 0.5% glucose containing erythrocytes demonstrated values of -3.8% NIDDM, 4% IDDM, and -4.3% CGN. The three groups showed dialyzer outlet blood sugar levels that were less than dialysate glucose concentration. In conclusion, CKD blood sugar kinetics with erythrocytes differed between NIDDM, IDDM, and CGN. Erythrocyte intervention was considered the mechanism that decreased the blood sugar level in CKD.

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Leukocyte adsorptive apheresis (L-CAP and G-CAP) is an effective treatment for ulcerative colitis (UC). We reported that leukocyte absorption might influence blood dendritic cell subsets constitution in UC patients ¹⁾. In this study, we aimed to clarify how DC subsets change during the leukocyte adsorptive apheresis session against active UC. Twelve active UC patients were enrolled in this study. These patients received either 6 or 11 sessions of leukocyte adsorptive apheresis and 3,000mL of whole blood was evenly processed at each leukocyte absorption session. All patients received prednisolone at a dose of 30±10mg/body before leukocyte adsorptive apheresis and each dose did not change during the whole leukocyte adsorptive apheresis session. Peripheral blood samples were examined at every first, 3rd, 6th and 11th leukocyte adsorptive apheresis session. Using 4 colors FACS, total DC were captured as negative for Lineage marker (CD3, CD14, CD16, CD19, CD20 and CD56) and positive for HLA-DR. Next, total DC were divided into DC subsets as DC1, DC2 and less-differentiated DC (ldDC) by reactivity of CD11C and CD123 antibody. Above 50 points decreases by Seo activity index was evaluated as the effective group. Therapeutic effectiveness was obtained in 8 of 12 UC patients and the DC subsets were compared to those of healthy volunteers, the leukocyte adsorptive apheresis-effective group and leukocyte adsorptive apheresis-ineffective group. Total DC, DC1 and DC2 did not significantly differ between healthy volunteers and UC patients, and did not significantly change during the leukocyte adsorptive apheresis session. However, the ldDC concentration before leukocyte adsorptive apheresis was significantly higher in UC patients than in healthy volunteers (p<0.03) and significantly decreased toward the healthy control level after the final leukocyte adsorptive apheresis session in the leukocyte adsorptive apheresis-effective group. These outcomes indicate that leukocyte adsorptive apheresis reduces less-differentiated dendritic cells (ldDC), which are increased in active ulcerative colitis.

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Blood flow rate through the dialysis circuit is an important factor affecting the dialyzer performance especially for removal of relatively low molecular weight substances. Actual blood flow rate, however, sometimes varies during dialysis treatment due to the condition of the patient's vascular access even though the blood flow rate on the blood pump remains at a constant setting. We developed a new method of measuring the actual blood flow rate through the circuit based on two point hematocrit values (CRIT-2 Point Method). Using two hematocrit monitors, CRIT-LINE (JMS Co. Ltd.), this method estimates the actual blood flow rate based on the difference in hematocrit values between the inlet and outlet of the dialyzer, caused by removal of water from the blood flowing through the dialyzer. In vitro experiments using bovine blood were carried out to evaluate the accuracy of this method. Initially, there was a relative error of the hematocrit value between the CRIT-LINE monitors and a method of correcting the error between monitors was added in order to estimate the actual blood flow rate. The blood flow rate obtained from the CRIT-2 Point Method after error correction (Q_B-crit) was compared with the actual blood flow rate measured directly using a measuring cylinder (Q_B-actual). A good correlation between the Q_B-crit and Q_B-actual values was obtained, indicating the high accuracy of this method. The percent error of the Q_B-crit to Q_B-actual was within±10%. A dialysis machine equipped with the CRIT-2 Point Method to measure the actual blood flow rate will be available in the near future in order to facilitate a safe and adequate dialysis treatment for each patient.

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Objectives : Hemodialysis (HD) using relatively low sodium dialysate (LSHD) has been used to control high blood pressure (BP). However, circulation volume-independent mechanisms of the anti-hypertensive effect have yet been not clearly elucidated. Methods : Twenty-five maintenance HD patients with hypertension underwent regular-HD for 12 weeks followed by LSHD for 12 weeks. Twenty-four-hour ambulatory blood pressure monitoring and echocardiography were performed at the end of each phase. Results : Significant decline in both systolic BP (178±17mmHg to 157±19mmHg, p<0.01) and diastolic BP (91±10mmHg to 84±11mmHg, p<0.01) were observed. Left ventricular chamber volumes did not demonstrate any significant difference between the 2 phases despite the equal dry-weight settings. The effective arterial elastance decreased with LSHD (2.07±0.75mmHg/mL to 1.65±0.49mmHg/mL, p<0.01). Conclusions : Reduced vascular resistance due to amelioration of sympathetic overactivity could be partly involved with the anti-hypertensive mechanisms of LSHD.

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For end stage renal failure (ESRD) patients associated with bone marrow failure syndrome, thrombocytopenia and defective thrombocyte function can cause fatal hemorrhagic complications on initiation of dialysis therapy. In this paper, we report two elderly patients with ESRD complicated by bone marrow failure syndrome, such as myelodysplatic syndrome (MDS) or myelofibrosis (MF). These two patients have been well maintained by peritoneal dialysis (PD) for the treatment of ESRD with periodic administration of blood transfusion and erythropoietin. Prior to the PD-catheter insertion operation, platelet transfusion was performed to prevent hemorrhagic problems. After the initiation of PD therapy, there was improvement of symptoms caused by uremia and volume overload as well as anemia. Moreover, performance status and quality of life could be improved because of the diminished symptoms associated with uremia and anemia.

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A 64-year-old female with systemic lupus erythematosus (SLE) was admitted to our hospital. Disease activity had been controlled by oral administration of prednisolone (9mg/day) for recent years. In April 2005, she developed a high fever that did not respond to standard therapy with antipyretics and antibiotics. Therefore, she consulted our hospital and was admitted. After hospitalization, renal function rapidly failed and she finally became oliguric on the 4th day. She was considered to have developed rapidly progressive glomerulonephritis (RPGN) and a combination of hemodialysis (HD), steroid pulse therapy and cyclophophosphamide administration was started. Since serological data on the 9th day demonstrated that serum anti-glomerular basement membrane (GBM) antibody titer was elevated to 300EU, plasma exchange therapy was added. On the 25th day, she suddenly developed pulmonary bleeding followed by acute respiratory failure requiring artificial ventilation. At this point, her disease was clinically diagnosed as Goodpasture's syndrome. Combined therapy consisting of plasma exchange, HD, and steroid pulse was continued and the patient made a good recovery, except for kidney function. She is now doing well on maintenance HD therapy. This is a rare patient who developed Goodpasture's syndrome during the stable course of SLE.

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