I found this paper on PubMed.... it is a severe issue connected to dialysis and renal disease:
Quote:
J Neurol Sci. 1976 Oct;29(2-4):343-9.
Peripheral neuropathy complicating primary hyperoxaluria.
Hall BM, Walsh JC, Horvath JS, Lytton DG.
Abstract
A patient with chronic renal disease due to primary hyperoxaluria developed a rapidly progressing motor neuropathy with marked impairment of nerve conduction. Pathological studies demonstrated the presence of both axonal degeneration and segmental demyelination, together with the presence of oxalate crystals within axons. It is suggested that the development of peripheral neuropathy complicating hyperoxaluria is a consequence of the increased life-span mad possible by haemodialysis.
PMID:
185338
[PubMed - indexed for MEDLINE]
|
and:
Quote:
Can J Neurol Sci. 1976 Feb;3(1):63-7.
Peripheral neuropathy in oxalosis. A case report with electron microscopic observations.
Bilbao JM, Berry H, Marotta J, Ross RC.
Abstract
A 61 year old man had chronic renal failure because of oxaluria and renal calculi. Two years before death, while on hemodialysis, he developed severe progressive peripheral neuropathy. At autopsy calcium oxalate crystals were found in the peripheral nerves and other tissues. Nerve lesions included segmental demyelination, axonal degeneration and crystalline deposits within the myelin sheath. Ultrastructurally there were foci of osmiophilic granular material within myelin lamellae and endoneurium, and pleomorphic lamellar bodies in the perinuclear Schwann cell cytoplasm. It is probable that chronic hemodialysis favors the deposition of oxalate in the Schwann cells and the development of neuropathy in patients with primary hyperoxaluria and renal failure.
PMID:
175908
[PubMed - indexed for MEDLINE]
|
Now oxalate can accumulate in the blood and the kidneys can have problems eliminating it. People who do not have an organism in the bowel, that complexes oxalate, will absorb more and place a load on the kidneys as a result. This organism is called:
http://en.wikipedia.org/wiki/Oxalobacter_formigenes
B6 is thought to help reduce oxalate loads:
Quote:
Urology. 2011 May;77(5):1054-8. Epub 2011 Feb 19.
Pyridoxine and dietary counseling for the management of idiopathic hyperoxaluria in stone-forming patients.
Ortiz-Alvarado O, Miyaoka R, Kriedberg C, Moeding A, Stessman M, Monga M.
Source
Department of Urologic Surgery, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Abstract
OBJECTIVES:
To examine the effects of dietary manipulation and pyridoxine medical management for idiopathic hyperoxaluria in patients with nephrolithiasis.
METHODS:
A retrospective longitudinal study of the patients treated in our stone clinics from July 2007 to February 2009 was performed. All patients were evaluated with pre- and postintervention 24-hour urine collection and met a registered dietician. Recommendations to keep urine volume above 2 L per day, sodium restriction, protein moderation, increased calcium intake with meals and low oxalate diet combined with oral pyridoxine were given. Initial dosage ranged from 50 to 100 mg per day depending on the baseline oxalate level, and was titrated to a maximum of 200 mg daily. Subjects with at least two 24-hour urine collections were included in the study.
RESULTS:
Of 314 patients with complete metabolic and urinary profile evaluation, 95 subjects were identified with idiopathic hyperoxaluria. Mean follow-up was 18.4 ± 14.8 months and mean age was 50.3 ± 12.8 years. In patients treated with the combination of dietary counseling and pyridoxine, there was a significant change in urinary parameters in 75% of patients with a significant decrease in urinary oxalate excretion (58.26 ± 27.05 to 40.61 ± 15.04, P < .0001). In all, 39% of the patients had a decrease from a high urine oxalate levels (>40 mg/d) to a normal range urine oxalate (55.30 ± 22.04 to 33.45 ± 3.93, P = .0004). No peripheral neuropathy was reported.
CONCLUSIONS:
Dietary management and medical treatment using pyridoxine may be an effective first-line therapy to decrease hyperoxaluria in patients who form stones.
Copyright © 2011 Elsevier Inc. All rights reserved.
PMID:
21334732
[PubMed - indexed for MEDLINE]
|
The bolded statement re: "no neuropathy was reported" I think pertains to the high B6 doses used in this study.
Based on the lack of papers concerning neuropathy in general... I would think at this point you'd have to have HIGH oxalates to get those effects.
Where did you hear about this? Do you mind sharing that? |
