Ultrasound-guided endovascular treatment for vascular access malfunction: results in 4896 cases.

PURPOSE: For the protracted maintenance of vascular access, countermeasures against stenosis are important. Between March 2004 and October 2011 superficial ultrasound-guided percutaneous transluminal angioplasty (PTA) was performed in our hospital for arteriovenous fistula malfunction in 4869 cases in 1011 patients, and the utility of the treatment was assessed on the basis of early results. In cases where vascular intervention was deemed necessary, the procedure was conducted under ultrasound guidance as first option, with fluoroscopy and radiography used additionally as necessary.
 METHODS: The ultrasound apparatus used was primarily the 11 MHz linear-type probe (GE-Yokogawa Logiq S6). For subclavian and brachiocephalic veins, the microconvex-type probe was used to visualize the lesion through the intercostal space. In obstruction cases, ultrasound-guided PTA was performed after superficial ultrasound-guided aspiration or thrombus removal. 
 RESULTS: In stenosis cases, early success (technical and clinical) was obtained in 4288 of 4414 cases (97.1%). In obstruction cases, early success was obtained in 443 cases and 91.9% for obstruction cases. Assistance by intra-operative fluoroscopy or radiography was required in 55 cases, and surgical reconstruction was required in 42 cases. Serious complications occurred in 12 of 4869 cases (0.2%).
 CONCLUSIONS: Ultrasound-guided PTA for arteriovenous fistula malfunction could be used as a substitute for fluoroscopy-guided PTA, and enables the use of safe and rapid intervention techniques.

The influences of method of calcium correction and the timing of blood collection on application of the K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Japan.

We investigated the treatment of renal osteodystrophy (ROD) in Japan and problems concerning the K/DOQI Guidelines. The subjects were 3698 hemodialysis patients (2328 males and 1370 females) with a mean age of 61.4 years. On average, they had been on hemodialysis for 8.34 years. The serum phosphorus level was <3.5 mg/dL in 5% of the subjects, 3.5-5.5 mg/dL in 49%, 5.6-7.0 mg/dL in 33%, and >7.0 mg/dL in 13%. The serum calcium level was <8.4 mg/dL in 16% of the subjects, 8.4-9.5 mg/dL in 47%, 9.5-10.2 mg/dL in 22%, and >10.2 mg/dL in 15%. The intact PTH level was <150 pg/mL in 57%, 150-300 pg/mL in 27%, and >300 pg/mL in 16% of the patients. The first problem is that correcting Ca is not always performed in clinical fields. The uncorrected calcium level was 9.14+/-0.92 mg/dL, while the corrected calcium level [Ca = Ca + 0.8 x (4-Alb)] was 9.26+/-0.93 mg/dL (P < 0.05). The second problem is that the timing of blood collection is not described in the K/DOQI Guidelines. Subjects with a serum phosphorus level >7.0 mg/dL at 3 days after the previous dialysis were selected for assessment. In these patients, the midweek serum phosphorus level (7.13+/-0.15 mg/dL) at was significantly lower than that (8.11+/-0.15 mg/dL) at the beginning of the next week (P < 0.001). These results suggest that it is necessary to specify the timing of measurement and the method of Ca correction when guidelines for management of ROD are established in the future.

The oxalate level in ultrafiltrate fluid collected from a dialyzer is useful for estimating the plasma oxalate level in hemodialysis patients.

BACKGROUND: Patients on chronic hemodialysis are likely to develop secondary hyperoxalemia. It is, however, difficult to measure plasma oxalate levels. To measure plasma oxalate levels, rapid plasma separation, deproteinization, and acidification are essential in preventing the formation of oxalate and the deposition of calcium oxalate within the test tube. The present study was undertaken to examine whether the oxalate level in dialyzer ultrafiltrate is potentially useful for estimating plasma oxalate levels. METHODS: In nine patients on chronic hemodialysis, the plasma, after deproteinization with a filter, and the ultrafiltrate from the dialyzer before hemodialysis were acidified to a pH level of less than 3, followed by the measurement of oxalate levels by ion chromatography. Also, oxalate levels were compared between acidified and non-acidified ultrafiltrates from the dialyzer. In the second part of the study, seven patients on chronic hemodialysis receiving erythropoietin therapy, in whom the ferritin level was more than 300 ng/ml and transferrin saturation was less than 25%, were intravenously administered ascorbic acid, 100 mg, three times a week, after each dialysis session to facilitate the utilization of stored iron. This treatment was continued until the serum ferritin level decreased to a level below 300 ng/ml (for 3 months, at a maximum). The oxalate level in the dialyzer ultrafiltrate after this treatment was compared with that before treatment. RESULTS: The mean +/- SE oxalate level in the dialyzer ultrafiltrate was 45 +/- 6 micromol/l, essentially equal to the plasma oxalate level (46 +/- 7 micromol/l). The plasma oxalate level had a significant positive correlation with the dialyzer ultrafiltrate oxalate level (plasma oxalate level = 0.99 x dialyzer ultrafiltrate oxalate level + 1.5; r = 0.95; P < 0.0001). The oxalate level in the acidified ultrafiltrate (45 +/- 6 micromol/l) did not differ significantly from that in the non-acidified ultrafiltrate (45 +/- 6 micromol/l). The mean +/- SE duration of ascorbic acid administration was 64 +/- 13 days. The hemoglobin level remained unchanged at 9.6 +/- 0.4 g/dl, whereas the serum iron level increased significantly, from 34 +/- 2 microg/dl to 43 +/- 4 microg/dl (P < 0.05), and serum ferritin levels decreased significantly, from 645 +/- 219 ng/ml to 231 +/- 30 ng/ml after the treatment (P < 0.05). The oxalate level in the acidified ultrafiltrate showed no significant change after ascorbic acid administration (31 +/- 8 micromol/l vs 47 +/- 7 micromol/l). CONCLUSIONS: In patients on chronic hemodialysis, the oxalate level in acidified ultrafiltrate from the dialyzer was found to be useful for estimating the plasma level of non-protein-bound oxalate. When administering ascorbic acid to hemodialysis patients, the plasma oxalate level can be monitored using this method.

[Comparison of intravenous ascorbic acid versus intravenous iron for functional iron deficiency in hemodialysis patients].

The effect of intravenous ascorbic acid was compared with that of intravenous iron in the treatment of functional iron deficiency, as defined as serum ferritin levels over 300 ng/ml and serum iron levels below 50 microg/dl, in patients on chronic hemodialysis. Thirteen patients on chronic hemodialysis with functional iron deficiency received intravenous injections of ascorbic acid, 100 mg, three times a week, after hemodialysis. The therapy was continued until serum ferritin decreased to below 300 ng/ml (3 months at the maximum). The iron and control group were composed of patients who had serum iron levels below 50 microg/dl within 3 months after serum ferritin rose to over 300 ng/ml. Seven patients with the iron group received more than a total of 10 intravenous injections of saccharated ferric oxide (40 mg/dose) after hemodialysis, and seven patients with the control group received no iron preparation during the 3 months. In the ascorbic acid group, while hemoglobin did not change from 10.9 +/- 0.5 g/dl (mean +/- SE) during the three-month period, serum iron increased significantly from 37 +/- 4 microg/dl to 49 +/- 4 microg/dl after one month (p<0.01), and remained elevated until the end of the three-month period. Serum ferritin decreased significantly from 607 +/- 118 ng/ml to 354 +/- 30 ng/ml after 3 months (p<0.01). In the iron group, hemoglobin and serum iron increased significantly from the respective pre-treatment levels during the 2-month period, and serum ferritin rose significantly after 3 months. In the control group, hemoglobin, serum iron and ferritin levels decreased significantly from the respective pre-treatment levels during the 3 months. The recombinant erythropoietin dose remained stable for three months in the ascorbic acid, iron, and control groups, respectively. These results suggest that in hemodialysis patients with a functional iron deficiency, treatment with intravenous ascorbic acid can prevent iron overload due to treatment with intravenous iron, and provide a useful adjuvant means of maintaining hemoglobin and serum iron levels.

[The clinical evaluation of maxacalcitol on therapy for secondary hyperparathyroidism of chronic hemodialysis patients].

The spectrum of bone disease in end-stage renal failure is changing, but secondary hyperparathyroidism is still a troublesome complication. The vitamin D3 analog, maxacalcitol, has reduced calcemic action compared to vitamin D3, but show equivalent suppression of parathyroid hormone(PTH) secretion. In the first step of the study, we investigated the severity of secondary hyperparathyroidism in 670 chronic hemodialysis patients, whose age, sex(male/female), and duration on dialysis were 63.5 +/- 12.4 years, 383/287, and 7.3 +/- 6.0 years, respectively. The number of patients with serum intact-PTH concentrations over 300 pg/ml was 118. Most patients in this group(87.3%) were already being prescribed oral vitamin D3 analog. In the second step, maxacalcitol was administered intravenously, instead of the oral vitamin D3 analog, to 92 patients selected from the above-described group. The age, sex(male/female), and duration of dialysis were 59.4 +/- 11.5 years, 56/36, and 7.3 +/- 6.0 years, respectively. Serum intact-PTH concentration and alkaline phosphatase activity decreased significantly, from 612.3 +/- 32.7 to 414.2 +/- 26.8 pg/ml, and from 329.3 +/- 17.3 to 277.0 +/- 12.5 IU/l, respectively. Serum calcium phosphorous concentration increased significantly, and maxacalcitol administration was interrupted because of hypercalcemia in 17 patients(18.5%). Serum intact-PTH concentration did not decrease in patients with serum Ca concentrations of 10.5 mg/dl or more before maxacalcitol therapy. In conclusion, maxacalcitol suppressed PTH secretion more effectively in hemodialysis patients with secondary hyperparathyroidism than did oral active vitamin D3 therapy, especially in patients with serum Ca concentrations lower than 10.5 mg/dl.