ArticleKidney international2026
Uremia and parathyroid hormone have distinct effects on bone protein and gene expression.
Article in Kidney international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
introductionChronic kidney disease (CKD)-associated osteoporosis is highly prevalent and increases the risk of fractures. Current therapy aims to preserve normal bone turnover, by maintaining parathyroid hormone (PTH) at relatively adequate levels. However, these patients continue to experience fractures.
methodsTo assess potential adverse effects of PTH on bone, we examined bone histology and osteocytic gene and protein expression in 76 patients receiving hemodialysis compared to that of 33 control individuals.
resultsUsing bulk bone tissue RNAseq, we observed that CKD is associated with enhanced inflammatory signaling, increased cell death, impaired osteoblastic differentiation, and reduced bone mass, consistent with low osteocyte count and increased apoptosis. Patients with elevated PTH levels showed an attenuation of these alterations, but exhibited increased expression of genes related to fibrosis, matrix apposition, and bone remodeling, leading to increased cortical porosity.
conclusionsCKD induces inflammation and cell death in bone. However, elevated PTH levels exhibited dual effects that were both protective and detrimental to bone tissue quality and strength. Our findings suggest that combining anabolic agents with relatively low PTH levels may be a potential approach to improve bone quality in CKD. This hypothesis warrants further investigation in future studies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.