ReviewJournal of the American Society of Nephrology : JASN2014
Reduced renal calcium excretion in the absence of sclerostin expression: evidence for a novel calcium-regulating bone kidney axis.
Review in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- Thermodynamic and Kinetic Aspects of Calcium Oxalate Crystallization and Renal Lithiasis.Biomolecules · 2025Article
- Gut-X Axis and Its Role in Poultry Bone Health: A Review.Microorganisms · 2025Review
- Between a Rock and a Short Place-The Impact of Nephrolithiasis on Skeletal Growth and Development Across the Lifespan.Current osteoporosis reports · 2024Review
- Renal Endothelial Single-Cell Transcriptomics Reveals Spatiotemporal Regulation and Divergent Roles of Differential Gene Transcription and Alternative Splicing in Murine Diabetic Nephropathy.International journal of molecular sciences · 2024Article
- The hidden cross talk between bone and tissues through bone turnover.Advances in laboratory medicine · 2024Article
- Article
- Urinary Calcium Is Associated with Serum Sclerostin among Stone Formers.Journal of clinical medicine · 2023Article
- 24-h Urinary Calcium Excretion and Renal Outcomes in Hospitalized Patients with and without Chronic Kidney Disease.Journal of clinical medicine · 2023Article
- Sclerostin and Osteocalcin: Candidate Bone-Produced Hormones.Frontiers in endocrinology · 2021Review
- Sclerostin: a new biomarker of CKD-MBD.International urology and nephrology · 2020Review
- Calcitriol and FGF-23, but neither PTH nor sclerostin, are associated with calciuria in CKD.International urology and nephrology · 2019Article
- The Use of Vitamin D Metabolites and Analogues in the Treatment of Chronic Kidney Disease.Endocrinology and metabolism clinics of North America · 2017Review
- Vitamin D-Mediated Hypercalcemia: Mechanisms, Diagnosis, and Treatment.Endocrine reviews · 2016Review
- Modeling hypercalciuria in the genetic hypercalciuric stone-forming rat.Current opinion in nephrology and hypertension · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The kidneys contribute to calcium homeostasis by adjusting the reabsorption and excretion of filtered calcium through processes that are regulated by parathyroid hormone (PTH) and 1α,25-dihydroxyvitamin D3 (1α,25[OH]2D3). Most of the filtered calcium is reabsorbed in the proximal tubule, primarily by paracellular mechanisms that are not sensitive to calcium-regulating hormones in physiologically relevant ways. In the distal tubule, however, calcium is reabsorbed by channels and transporters, the activity or expression of which is highly regulated and increased by PTH and 1α,25(OH)2D3. Recent research suggests that other, heretofore unrecognized factors, such as the osteocyte-specific protein sclerostin, also regulate renal calcium excretion. Clues in this regard have come from the study of humans and mice with inactivating mutations of the sclerostin gene that both have increased skeletal density, which would necessitate an increase in intestinal absorption and/or renal reabsorption of calcium. Deletion of the sclerostin gene in mice significantly diminishes urinary calcium excretion and increases fractional renal calcium reabsorption. This is associated with increased circulating 1α,25(OH)2D3 levels, whereas sclerostin directly suppresses 1α-hydroxylase in immortalized proximal tubular cells. Thus, evidence is accumulating that sclerostin directly or indirectly reduces renal calcium reabsorption, suggesting the presence of a novel calcium-excreting bone-kidney axis.
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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.