Sevelamer hydrochloride, as a phosphate binder that contains neither aluminum nor calcium, is expected to improve the prognosis of dialysis patients. However, sevelamer hydrochloride has been reported to lower the serum bicarbonate level. In the present study, we performed a retrospective study on the potential influences of sevelamer hydrochloride on metabolic acidosis in hemodialysis patients. The subjects were 72 patients who underwent hemodialysis at our hospital. Thirty-six patients taking sevelamer hydrochloride and 36 patients matched for sex, diabetes mellitus, age and duration of dialysis who were not taking sevelamer hydrochloride were studied. We assigned the 36 patients who had been taking sevelamer hydrochloride to the 'sevelamer group', and the 36 patients not taking sevelamer hydrochloride were the control group. Statistical significance was evaluated by a t-test and Pearson's correlation coefficient. In the sevelamer group, the mean levels of bicarbonate, base excess and pH decreased significantly after administration, compared with the values before administration, but in the control group, aggravation of acidosis was not seen. The levels of bicarbonate, base excess and pH after the medication of sevelamer hydrochloride were found to be significantly and negatively correlated with the daily dose of sevelamer hydrochloride. The levels were also found to be significantly and negatively correlated with the cumulative dose of sevelamer hydrochloride; however, the value of the mean levels of chlorine and the anion gap did not increase with sevelamer hydrochloride. Sevelamer hydrochloride caused metabolic acidosis in a dose-dependent manner in hemodialysis patients without hyperchloremia.
US-guided block of individual branches of the brachial plexus at the axilla achieved effective anesthesia using small amounts of local anesthetic. An advanced selective nerve block in the upper arm allows minimum necessary anesthesia and provides safe and efficient analgesia for VA surgery in the forearm.
Hemodialysis patients frequently develop upper limb pain, especially following ipsilateral arteriovenous access (AVA). Various etiologies of AVA-related pain include needle ABSTRACT Introduction: Arteriovenous access (AVA)-related pain treated successfully with runoff-venous decompression of the causative nerve, following ultrasound (US)-assisted preoperative evaluation, has never been reported. Case presentation: A 57-year-old man suffering from constant exhausting pains along the outflow cephalic vein of the radiocephalic arteriovenous fistula at the wrist and the antecubital fossa, was treated surgically after the diagnosis of AVA-related pain derived from cephalic vein compression on two peripheral cutaneous nerves, the superficial radial nerve (SRN) and the lateral antebrachial cutaneous nerve (LACN). Technique: The SRN and LACN, which ran along and/or provided sensory innervation to the painful regions in the upper limb, were traced using ultrasonography in the short axis and proved to be compressed by and in contact with veins where the pain existed, at the wrist and the antecubital fossa. Once diagnostic US-guided blocks of both were performed and pain disappeared, they were identified as the causative nerves. The cephalic venous decompression surgeries that separated and transposed the veins away from the SRN and the LACN were performed sequentially under pneumatic tourniquet inflation to improve nerve visualization. Results: The pains disappeared after the operations. An adequate length of the runoff cephalic vein was maintained for needle cannulations during hemodialysis. Conclusions: Outflow venous compression to the peripheral nerves may be a cause of AVA-related pain. USguided assessments of the nerves may improve the safety and efficiency of venous decompression surgeries to treat AVA-related pains.
To elucidate the precise mechanism of carpal tunnel syndrome (CTS), serum hyaluronic acid (HA), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) were measured in 71 chronic hemodialysis patients with or without CTS and/or shoulder pain. Patients were divided into two groups: Group 1 (n = 40) was the control group, and Group 2 (n = 31) patients had carpal tunnel syndrome, shoulder pain, or both. None of the patients had liver disease, rheumatoid arthritis, other inflammatory disease, or cancer. Serum HA concentrations in Groups 1 and 2 were 106.0 +/- 77.5 and 442.6 +/- 564.7 ng/dl (mean +/- SD), respectively. The difference between the groups was significant (p < 0.01). The serum concentrations of IL-6 in Group 1 were significantly lower than in Group 2 (p < 0.05); however, there was no significant difference in serum IL-1 beta and TNF-alpha levels. The mechanisms regulating in vivo synthesis of HA was obscure; however, in vitro studies suggest that inflammatory cytokines may stimulate an increased production of HA. In this study, CTS might be associated with increased serum concentrations of HA, and HA production might be mediated by IL-6.
The objective of this study was to investigate changes in oxidative stress associated with the cleaning of the dialysate. Thirty-six dialysis patients were studied. Changes in soluble CD-14 (sCD-14), malondialdehyde-low-density lipoprotein (MDA-LDL), and oxidized-LDL (Ox-LDL) were monitored for 1 year before and 1 year after dialysate cleaning. The mean endotoxin (ET) level in the dialysate had previously been confirmed to decrease from 39.0 EU/L to an undetectable level after the cleaning. The mean levels of sCD-14, MDA-LDL, and Ox-LDL decreased significantly after the cleaning (sCD-14, P < 0.0001; MDA-LDL, P < 0.001; Ox-LDL, P < 0.001). One year after the cleaning, six cases still showed high levels of MDA-LDL and Ox-LDL. Cardiovascular events occurred in four of those six cases within 2.8 years after the cleaning. These four patients suffered from strong oxidative stress during dialysis, even after the cleaning. We therefore concluded that high levels of MDA-LDL and Ox-LDL are improved in dialysis patients by cleaning of the dialysate. These results indicate that even a dialysate containing 50 EU/L or less ET may stimulate monocytes and cause oxidative stress. They also suggest that even low levels of ET may aggravate arteriosclerosis in dialysis patients. Thus, in order to prevent cardiovascular events in dialysis patients, it is necessary to purify the dialysate.
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