Abstract
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.
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Methodist Hospital Institute for Kidney Stone Disease, Indiana University School of Medicine, International Kidney Stone Institute, Indianapolis, Indiana and Nephrology Section, University of Chicago, Chicago, Illinois
