ArticlePloS one2016
Phosphocalcic Markers and Calcification Propensity for Assessment of Interstitial Fibrosis and Vascular Lesions in Kidney Allograft Recipients.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Serum Calcification Propensity Represents a Good Biomarker of Vascular Calcification: A Systematic Review.Toxins · 2022Pooled it
- Calcium Crystal Deposits in Kidney Allografts: The Interplay of PTH Levels and Phosphaturia.Kidney medicine · 2026Article
- Post-transplantation management of hyperparathyroidism and its association with kidney graft survival and fibrosis.Clinical and experimental nephrology · 2025Article
- Hydroxyproline in Urine Microvesicles as a Biomarker of Fibrosis in the Renal Transplant Patient.Biomedicines · 2024Article
- Treatment of Hypercalcemic Hyperparathyroidism After Kidney Transplantation Is Associated With Improved Allograft Survival.The oncologist · 2024Article
- Accelerated calciprotein crystallization time (T50) is correlated with impaired lung diffusion capacity in systemic sclerosis.Frontiers in immunology · 2024Article
- Calcification Propensity (T50) Predicts a Rapid Decline of Renal Function in Kidney Transplant Recipients.Journal of clinical medicine · 2023Article
- Hyperparathyroidism Is an Independent Risk Factor for Allograft Dysfunction in Pediatric Kidney Transplantation.Kidney international reports · 2023Article
- Targeting a Silent Disease: Vascular Calcification in Chronic Kidney Disease.International journal of molecular sciences · 2022Review
- Calciprotein Particles and Serum Calcification Propensity: Hallmarks of Vascular Calcifications in Patients with Chronic Kidney Disease.Journal of clinical medicine · 2020Review
- Overexpression of BMP‑7 reverses TGF‑β1‑induced epithelial‑mesenchymal transition by attenuating the Wnt3/β‑catenin and TGF-β1/Smad2/3 signaling pathways in HK‑2 cells.Molecular medicine reports · 2020Article
- Personalized Management of Bone and Mineral Disorders and Precision Medicine in End-Stage Kidney Disease.Seminars in nephrology · 2018Review
- Phosphate, Calcification in Blood, and Mineral Stress: The Physiologic Blood Mineral Buffering System and Its Association with Cardiovascular Risk.International journal of nephrology · 2018Review
- Review
- Hope for CKD-MBD Patients: New Diagnostic Approaches for Better Treatment of CKD-MBD.Kidney diseases (Basel, Switzerland) · 2017Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal interstitial fibrosis and arterial lesions predict loss of function in chronic kidney disease. Noninvasive estimation of interstitial fibrosis and vascular lesions is currently not available. The aim of the study was to determine whether phosphocalcic markers are associated with, and can predict, renal chronic histological changes. We included 129 kidney allograft recipients with an available transplant biopsy in a retrospective study. We analyzed the associations and predictive values of phosphocalcic markers and serum calcification propensity (T50) for chronic histological changes (interstitial fibrosis and vascular lesions). PTH, T50 and vitamin D levels were independently associated to interstitial fibrosis. PTH elevation was associated with increasing interstitial fibrosis severity (r = 0.29, p = 0.001), while T50 and vitamin D were protective (r = -0.20, p = 0.025 and r = -0.23, p = 0.009 respectively). On the contrary, fibroblast growth factor 23 (FGF23) and Klotho correlated only modestly with interstitial fibrosis (p = 0.045) whereas calcium and phosphate did not. PTH, vitamin D and T50 were predictors of extensive fibrosis (AUC: 0.73, 0.72 and 0.68 respectively), but did not add to renal function prediction. PTH, FGF23 and T50 were modestly predictive of low fibrosis (AUC: 0.63, 0.63 and 0.61) but did not add to renal function prediction. T50 decreased with increasing arterial lesions (r = -0.21, p = 0.038). The discriminative performance of T50 in predicting significant vascular lesions was modest (AUC 0.61). In summary, we demonstrated that PTH, vitamin D and T50 are associated to interstitial fibrosis and vascular lesions in kidney allograft recipients independently of renal function. Despite these associations, mineral metabolism indices do not show superiority or additive value to fibrosis prediction by eGFR and proteinuria in kidney allograft recipients, except for vascular lesions where T50 could be of relevance.
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