Subclavian steal syndrome in a hemodialysis patient after percutaneous transluminal angioplasty of arteriovenous access.

INTRODUCTION: We describe a hemodialysis patient who developed subclavian steal syndrome via an arteriovenous fistula after percutaneous transluminal angioplasty. CASE DESCRIPTION: A 55-year-old female with end-stage renal failure due to polycystic kidney disease had been treated with hemodialysis for 10 years. Because of an autologous arteriovenous fistula stenosis, percutaneous transluminal angioplasty was performed. After successful treatment with percutaneous transluminal angioplasty, the patient developed dizziness. Magnetic resonance imaging with angiography of the brain and neck revealed normal bilateral subclavian and carotid arteries. However, flow in the left vertebral artery was not detected in time-of-flight magnetic resonance angiography. The left vertebral artery showed completely reversed blood flow as detected by color duplex ultrasound. We also confirmed anterograde flow in the left vertebral artery by color duplex ultrasound with arteriovenous fistula compression. Arteriovenous flows before the arteriovenous fistula stenosis and post-percutaneous transluminal angioplasty were 1146 and 2239 mL/min, respectively. These findings suggested high-flow arteriovenous fistula led to the subclavian steal syndrome. The patient was subsequently treated by a flow reduction in the high-flow arteriovenous access using a modified graft inclusion technique. We decreased the arteriovenous fistula flow to 851 mL/min, which remained under 850 mL/min, 1 year later. The brain natriuretic peptide level and right-ventricular pressure also decreased after treatment. A modified graft inclusion technique was successful in decreasing the high flow of the arteriovenous fistula, and improved subclavian steal syndrome symptom and cardiac overload. CONCLUSION: This case shows that percutaneous transluminal angioplasty for an arteriovenous fistula may induce subclavian steal syndrome, and a modified graft inclusion technique was useful in improving the high flow of an arteriovenous fistula.

Efficacy of continuous oral administration of lanthanum carbonate over 24 months.

To examine the efficacy of long-term administration of lanthanum carbonate, changes in serum Ca, phosphate, whole parathyroid hormone (wPTH), and ALP were examined in 40 patients who were able to tolerate dosage of lanthanum carbonate over a continuous period of 24 months. Concurrently, concomitant administration of other phosphate binders, cinacalcet, vitamin D, etc., was also examined. After 24 months, serum phosphorus levels (P levels) had decreased to within management target of guidelines, from 6.16 ± 1.44 mg/dL to 5.58 ± 1.15 mg/dL, and this effect was maintained for 2 years. There were no changes in Ca level. wPTH did not change significantly but tended to increase at 12 months. The dose of concomitantly administered calcium carbonate and sevelamer hydrochloride was reduced. The P-lowering function of lanthanum carbonate still held steady at 24 months following the start of dosage. Because of the rising trend seen in wPTH, dose of cinacalcet and/or vitamin D need to be modulated. Reducing the number of concomitantly administered phosphate binder tablets was desirable from the standpoint of patient adherence.

Elimination of lipid peroxide during hemodialysis.

BACKGROUND/AIMS: This study is aimed to show the antioxidative effect of hemodialysis (HD) by demonstrating the elimination of toxic lipid peroxides. METHODS: Blood samples were obtained from patients on regular maintenance HD before and 15, 30, 60, 120 and 240 min after the start of each HD session. Plasma cholesteryl ester hydroperoxide (CE-OOH), phosphatidylcholine hydroperoxide (PC-OOH), and eliminators of lipid peroxides (LOOH) such as apolipoprotein A-I (apoA-I) and lecithin:cholesterol acyltransferase (LCAT) were investigated. The hydroxyl radical scavenging activity was measured for the evaluation of the pro-oxidative side. RESULTS: CE-OOH and PC-OOH were elevated in patients with chronic kidney disease both on and not on HD, while these values were much higher in HD patients. CE-OOH quickly dropped during the first 30 min of HD, then gradually decreased until 240 min. CE-OOH concentrations were related to those of apoA-I. In contrast, PC-OOH showed an increase 30 min after the start of HD, a change which resembled that of LCAT and was the reverse of the hydroxyl radical scavenging activity. CONCLUSION: These results demonstrate the antioxidative action through CE-OOH elimination involving apoA-I. The pro- and antioxidative effects of HD on LOOH are not uniform but PC-OOH is mainly influenced prooxidatively.

Oxidative stress during leukocyte absorption apheresis.

Leukocyte absorption apheresis absorbs leukocytes to the apheresis columns involving leukocyte activation. This process is regarded as bioincompatible and avoided in hemodialysis or other extracorporeal circulation processes. Thus, leukocyte apheresis has a potential risk to exacerbate in vivo oxidative stress. We evaluated the changes in plasma oxidative stress during leukocyte apheresis. Patients diagnosed as ulcerative colitis (UC) and treated with leukocyte apheresis were studied. Adacolumn (celluloseacetate beads) or Cellsorba EX (polyethylenephtarate fiber) was used for the leukocyte absorption device. Oxidative stress was measured by thiobarbituric acid reactive substances (TBARS) and hydroxyl radical ((*)OH) scavenging activity. Plasma samples were collected from the pre- and post-column sampling port at the start, and from the pre-column sampling port at the end of the treatment. The (*)OH signal intensities (OHRI) significantly increased during a column passage, indicating a loss of plasma (*)OH scavenging activity. However, OHRI was reduced at the end, suggesting a recovery of radical scavenging activity during leukocyte apheresis. Significant decreases of OHRI and TBARS were only observed in the early phase of the therapeutic course. No differences of OHRI and TBARS levels were observed between the two columns. These results indicate that though the plasma antioxidant activity was diminished by a column passage, plasma antioxidant activity recovers during the procedure. This efficient antioxidative effect is limited to the early phase of the therapeutic course.