Eight decades ago, Al exander 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.
Urolithiasis August 2014 Date: 07 Aug 2014
Randall’s plaque as the origin of calcium oxalate kidney stones
Michel Daudon, Dominique Bazin, Emmanuel Letavernier
http://link.springer.com/article/10.1007/s00240-014-0703-y
Congrats for your publication. Its a great area of research as many people are suffering from renal calculi. The etiology shows mainly deposition of calcium phosphate and calcium oxalate which later on forms the stone. There are several food products which are rich in these chemicals and its excess in the body leads into its deposition.
Randall plaque as nidus former of urolithiasis, has been hypothesized but yet not proved definitely, these plaque often made up of calcium apatite, but after deposition on the base membrane of tubules and damage to vasa recta at papilla results in depostion of other supersaturated ingredient such as calcium oxalate, however as mentioned in Campbell's urology, Randall's plaque incidence in normal population (non stone former) is about 34% but in calcium oxalate stone burden rises to 73%, so its existence is not an enough reason to promote as a stone former kidney.
Do you think acid uric stones which are related to diabetus type II have a Relationship with randall ' plaque ?
Take care
Dominique
Thanks Dominique for your manuscript for the special issue. It is an excellent article. But I am not sure that we can look at the
It is impossible to read your interesting publication in its entirety. Could you send it to us in a different way?
(I think this is the problem announced by Mr Khan)
For anyone interested, the publication of Prof. Bazin over Randall's plaque formation is available in its entirety on ResearchGate in its publications list. Thank you.
Article gives good information. however, while investigating a Stone disease patient , a high Super-saturation index gives useful information whether individual is forming stone or not. This is irrespective of values of urinary calcium, oxalates etc. I mean for example even if urinary calcium or other components are abnormal and supersaturation is not high, then person is not forming stones
For Urolab India
What do you suggest as a simple procedure to consider a supersaturation? In practice, using my knowledge, one use the concentration of Ca, Mg, uric acid, oxalic acid and citric acid in urine.
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