ArticleInternational urology and nephrology2016
The renal mitochondrial dysfunction in patients with vascular calcification is prevented by sodium thiosulfate.
Article in International urology and nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Review
- Vascular Calcification in Chronic Kidney Disease: An Update and Perspective.Aging and disease · 2022Article
- Mitochondria Homeostasis and Vascular Medial Calcification.Calcified tissue international · 2021Review
- Renal mitochondria can withstand hypoxic/ischemic injury secondary to renal failure in uremic rats pretreated with sodium thiosulfate.Indian journal of pharmacologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeVascular calcification (VC) is an impact of calcium accumulation in end-stage renal diseases, normally initiated in the mitochondria. Sodium thiosulfate (STS) is effective in rescuing mitochondrial function in the neurovascular complications associated with VC, but has limitation in protecting the cardiac mitochondria. However, the STS efficacy in restoring the renal mitochondrial function has not been studied, which is the primary focus of this study.
methodsWistar rats (n = 6/group) were administered 0.75 % adenine in the diet for 28 days to induce renal failure. STS (400 mg/kg) was given in two regimens STS_Pre (preventive: along with adenine for 28 days) and STS_Cur (curative: 29th to 49th day). Renal failure was assessed by plasma and urinary markers. The effectiveness of treatment was assessed from oxidative stress, DNA damage, mitochondrial physiology and enzymology in the renal tissue.
results0.75 % adenine diet caused renal medullary swelling, tubular interstitial nephropathy and impaired renal function (creatinine, urea, uric acid and ALP), which were recovered after STS treatment. The renal failure was due to oxidative stress as measured by elevated malondialdehyde (29 %) and lowered reduced glutathione (27 %) levels. STS reduced the lipid peroxidation and significantly (p < 0.05) elevated the antioxidant enzymes. Further, it improved renal mitochondrial respiratory capacity by maintaining the hyperpolarized membrane potential and restored the complex enzyme activities. Absence of renal DNA fragmentation supports the above findings.
conclusionSTS protects the kidney by preserving renal mitochondria, in experimental adenine-induced vascular calcified rats. The efficacy was prominent when given after induction, i.e., in STS_Cur group.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.