Current Understanding of the Role of Randall’s Plaque

Abstract

The mechanisms by which urinary calculi develop in humans are not entirely understood. In the 1930s, Randall described white plaques on the papillae of cadaveric kidneys from patients with calculi and postulated that this was the site of stone formation in all stone formers. His theory was not well received and for many years was abandoned. It is now known that in certain subsets of stone formers (idiopathic calcium oxalate stone formers), stone formation does occur by overgrowth on Randall’s plaque. However, many other types of stone formers do not demonstrate evidence of classic Randall’s plaque and must therefore possess a different mechanism for stone formation. Careful endoscopic assessment and renal tissue biopsies from unique stone-forming patients (i.e., those with cystinuria, primary hyperparathyroidism, renal tubular acidosis, and primary hyperoxaluria) has revealed evidence of crystalline plugging within dilated ducts of Bellini with associated inflammation and cell injury. These findings are not identified in idiopathic calcium oxalate stone formers and lead one to believe that alternate pathways to the development of nephrolithiasis must be at play. In this chapter we review the composition and anatomic location of Randall’s plaque as well as describe the stone-plaque interface and mechanism of stone overgrowth. Additionally, we review the specific endoscopic and histologic abnormalities in stone-forming patients with cystinuria, brushite stone disease, gastric bypass, ileostomy, primary hyperparathyroidism, renal tubular acidosis, and primary hyperoxaluria and propose potential mechanisms for stone formation.