Eight decades ago, Alexander Randall identified calcium phosphate deposits at the tip of renal papillae as the origin of renal calculi. The awareness that these " Randall's plaque " promote renal stone formation has been amplified during the past years by the development of endoscopic procedures allowing the in situ visualization of these plaques. Recent studies based upon kidney biopsies evidenced that apatite deposits at the origin of these plaque originate from the basement membranes of thin loops of Henle and then spread in the surrounding interstitium. In addition, scanning electron microscopy examination of calcium oxalate stones developed on Randall's plaque evidenced that plaque may also be made of tubules obstructed by calcium phosphate plugs. Hypercalciuria has been associated to Randall's plaque formation. However, several additional mechanisms may be involved resulting in increased tissular calcium phosphate supersaturation and the role of macromolecules in plaque formation remains elusive. At last, apatite crystals are the main mineral phase identified in plaques, but other calcium phosphates and various chemical species such as purines have been evidenced, revealing thereby that several mechanisms may be responsible for plaque formation.