ArticleBMC urology2013
Renal papillary calcification and the development of calcium oxalate monohydrate papillary renal calculi: a case series study.
Article in BMC urology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Ex Vivo Removal of Stones in Donor Kidneys by Flexible Ureteroscopy Prior to Renal Transplantation: A Case Report.The American journal of case reports · 2017Article
- Endoscopic description of renal papillary abnormalities in stone disease by flexible ureteroscopy: a proposed classification of severity and type.World journal of urology · 2016Article
- Biomimetic Randall's plaque as an in vitro model system for studying the role of acidic biopolymers in idiopathic stone formation.Urolithiasis · 2015Article
- A new device for simple and accurate urinary pH testing by the Stone-former patient.SpringerPlus · 2014Article
- Vascular Calcification and Stone Disease: A New Look towards the Mechanism.Journal of cardiovascular development and diseaseArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe objective of this study is to determine in a case series (four patients) how calcified deposits in renal papillae are associated with the development of calcium oxalate monohydrate (COM) papillary calculi.
methodsFrom the recently collected papillary calculi, we evaluated retrospectively patients, subjected to retrograde ureteroscopy, with COM papillary lithiasis.
resultsThe COM papillary calculi were found to result from subepithelial injury. Many of these lesions underwent calcification by hydroxyapatite (HAP), with calculus morphology and the amount of HAP in the concave zone dependent on the location of the calcified injury. Most of these HAP deposits grew, eroding the epithelium covering the renal papillae, coming into contact with urine and starting the development of COM calculi. Subepithelial HAP plaques may alter the epithelium covering the papillae, resulting in the deposit of COM crystals directly onto the epithelium. Tissue calcification depends on a pre-existing injury, the continuation of this process is due to modulators and/or crystallization inhibitors deficiency.
conclusionsSince calculus morphology and the amount of detected HAP are dependent on the location and widespread of calcified injury, all types of papillary COM calculi can be found in the same patient. All patients had subepithelial calcifications, with fewer papillary calculi, demonstrating that some subepithelial calcifications did not further evolve and were reabsorbed. A high number of subepithelial calcifications increases the likelihood that some will be transformed into COM papillary calculi.
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