Sodium Thiosulfate Pharmacokinetics in Hemodialysis Patients and Healthy Volunteers

Farese, Stefan; Stauffer, Emilie; Kalicki, Robert M.; Hildebrandt, Tatjana M.; Frey, Brigitte M.; Frey, Felix J.; Uehlinger, Dominik E.; Pasch, Andreas

doi:10.2215/cjn.10241110

Cited by 54 publications

(53 citation statements)

References 42 publications

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“…clinical settings to treat caliciphylaxis, extravasations during chemotherapy or cyanide poisoning (50), and is also a component of the transsulfuration pathway. Used as a substrate for rhodanaselike enzymes, thiosulfate could also be a source of targeted persulfidation, as recently proposed by Mishanina et al (31).…”

Section: Treatment With Sodium Thiosulfate Reduces Eye Degeneration Imentioning

confidence: 99%

Overexpression of Cystathionine γ-Lyase Suppresses Detrimental Effects of Spinocerebellar Ataxia Type 3

Snijder

Baratashvili

Grzeschik

et al. 2015

Mol Med

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Spinocerebellar ataxia type 3 (SCA3) is a polyglutamine (polyQ) disorder caused by a CAG repeat expansion in the ataxin-3 (ATXN3) gene resulting in toxic protein aggregation. Inflammation and oxidative stress are considered secondary factors contributing to the progression of this neurodegenerative disease. There is no cure that halts or reverses the progressive neurodegeneration of SCA3. Here we show that overexpression of cystathionine γ-lyase, a central enzyme in cysteine metabolism, is protective in a Drosophila model for SCA3. SCA3 flies show eye degeneration, increased oxidative stress, insoluble protein aggregates, reduced levels of protein persulfidation and increased activation of the innate immune response. Overexpression of Drosophila cystathionine γ-lyase restores protein persulfidation, decreases oxidative stress, dampens the immune response and improves SCA3-associated tissue degeneration. Levels of insoluble protein aggregates are not altered; therefore, the data implicate a modifying role of cystathionine γ-lyase in ameliorating the downstream consequence of protein aggregation leading to protection against SCA3-induced tissue degeneration. The cystathionine γ-lyase expression is decreased in affected brain tissue of SCA3 patients, suggesting that enhancers of cystathionine γ-lyase expression or activity are attractive candidates for future therapies.

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Section: Treatment With Sodium Thiosulfate Reduces Eye Degeneration Imentioning

confidence: 99%

Overexpression of Cystathionine γ-Lyase Suppresses Detrimental Effects of Spinocerebellar Ataxia Type 3

Snijder

Baratashvili

Grzeschik

et al. 2015

Mol Med

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“…Cicone et al first reported that administration of sodium thiosulfate (STS) may be useful in treating CUA (15). Although the exact mechanism of action is unknown (16,17), several case reports and small case series have been published on STS administration for CUA (17). However, published data on STS have been mixed, with some demonstrating beneficial effects (18)(19)(20) and others showing no benefit (21,22).…”

Section: Introductionmentioning

confidence: 99%

Sodium Thiosulfate Therapy for Calcific Uremic Arteriolopathy

Nigwekar

Brunelli

Meade

et al. 2013

Clinical Journal of the American Society of Nephrology

185

136

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SummaryBackground and objective Calcific uremic arteriolopathy (CUA) is an often fatal condition with no effective treatment. Multiple case reports and case series have described intravenous sodium thiosulfate (STS) administration in CUA, but no studies have systematically evaluated this treatment.Design, setting, participants, & measurements This study included 172 patients undergoing maintenance hemodialysis who had CUA and were treated with STS between August 2006 and June 2009 at Fresenius Medical Care North America. Of these, 85% completed STS therapy. Clinical, laboratory, and mortality data were abstracted from clinical information systems. Responses to survey questionnaires sent to treating physicians regarding patient-level outcomes were available for 53 patients. Effect on CUA lesions and mortality were summarized as CUA outcomes. Relevant laboratory measures, weight (using pairwise comparisons of values before, during, and after STS), and adverse events were summarized as safety parameters.Results Mean age of the cohort was 55 years, and 74% of patients were women. Median STS dose was 25 g, and median number of doses was 38. Among surveyed patients, CUA completely resolved in 26.4%, markedly improved in 18.9%, improved in 28.3%, and did not improve in 5.7%; in the remaining patients (20.8%), the response was unknown. One-year mortality in patients treated with STS was 35%. Adverse events, laboratory abnormalities, and weight-related changes were mild. Significant reductions in serum phosphorous (P=0.02) and parathyroid hormone (P=0.01) were noted during STS treatment in patients who completed the therapy.Conclusions Although conclusive evidence regarding its efficacy is lacking, a majority of patients who received STS demonstrated clinical improvement in this study.

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“…Intravenous and intraperitoneal administration of STS in hemodialysis and peritoneal dialysis patients are well tolerated and adverse events are mild [66][67][68] . STS is readily cleared by dialysis [69] . In two preliminary studies in hemodialysis patients, STS was able to delay the progression of CAC after 4-5 mo of twice weekly intravenous administration but with a decline of hip bone mineral density in one study [67,70] .…”

Section: Sodium Thiosulfatementioning

confidence: 99%

Lowering vascular calcification burden in chronic kidney disease: Is it possible?

Disthabanchong

2013

WJN

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High prevalence of atherosclerosis and arterial calcification in chronic kidney disease is far beyond the explanation by common cardiovascular risk factors such as aging diabetes, hypertension and dyslipidemia. The magnitude of coronary artery calcification is independently and inversely associated with renal function. In addition to cardiovascular risk factors, other chronic kidney diseaserelated risks such as phosphate retention, excess of calcium and prolonged dialysis vintage also contribute to the development of vascular calcification. Strategies to lower vascular calcification burden in chronic kidney disease population should include minimizing chronic kidney disease and atherosclerotic risk factors. Current therapies available are non-calcium containing phosphate binders, low dose active vitamin D and calcimimetic agent. The role of bisphosphonates in vascular calcification in chronic kidney disease population remains unclear. Preliminary data on sodium thiosulfate are promising, however, larger studies on efficacy and patient outcomes are necessary. Several large randomized controlled trials have confirmed the lack of benefit of statin in attenuating the progression of vascular calcification.

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Sodium Thiosulfate Pharmacokinetics in Hemodialysis Patients and Healthy Volunteers

Cited by 54 publications

References 42 publications

Overexpression of Cystathionine γ-Lyase Suppresses Detrimental Effects of Spinocerebellar Ataxia Type 3

Overexpression of Cystathionine γ-Lyase Suppresses Detrimental Effects of Spinocerebellar Ataxia Type 3

Sodium Thiosulfate Therapy for Calcific Uremic Arteriolopathy

Lowering vascular calcification burden in chronic kidney disease: Is it possible?

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