The Role of Randall’s Plaques in the Pathogenesis of Calcium Stones
Purpose
Knowledge of the inciting lesion in kidney stone formation has remained rudimentary until quite recently. Randall theorized that areas of apatite plaque on the renal papillae would be an ideal site for an overgrowth of calcium oxalate to develop into a calculus. We reviewed in vivo data that have further defined the role of Randall’s plaques in stone disease.
Materials and Methods
We examined a set of literature that tested 2 hypotheses, that is 1) Randall’s plaques are a specialized disease that begins as apatite in a unique region of the kidney due to local driving forces and anatomy, and 2) stones that arise from causes different from common calcium oxalate stones do not necessarily arise on plaque.
Results
Intraoperative papillary and cortical biopsy specimens obtained during percutaneous nephrolithotomy from the kidneys of 3 types of stone formers (idiopathic calcium stone formers, patients with stones due to bariatric procedures and brushite stone formers) showed unique histopathological findings.
Conclusions
The metabolic and surgical pathological findings in 3 distinct groups of stone formers demonstrate that the histology of the renal papillae from a stone former is particular to the clinical setting.
Key Words: kidney, kidney calculi, calcium oxalate, brushite, nephrostomy, percutaneous
Abbreviations and Acronyms: PNL, percutaneous nephrolithotomy, TEM, transmission electron microscopy
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Supported by National Institutes of Health Grants PO1 DK56788 and PO1 DK43881, and an American Foundation for Urologic Diseases Scholarship (BRM).
PII: S0022-5347(06)02172-0
doi:10.1016/j.juro.2006.08.088
© 2007 American Urological Association. Published by Elsevier Inc. All rights reserved.

