Proposed mechanisms in renal tubular crystal retention.
The production of concentrated urine inevitably leads to the precipitation of poorly soluble waste salts in the renal tubular fluid. These crystallization processes are physiologic and without consequences as long as all crystals are excreted with the urine. The retention of crystals in the renal tubules, however, may lead to tubular nephrocalcinosis. Here, we present a brief survey of the possible mechanisms involved in this process, which seems to depend predominantly on the presence of regenerating/(re)differentiating cells in the renal tubules. Crystal binding to the surface of these cells can be mediated by a number of luminal membrane molecules, including acidic fragment of nucleolin-related protein, annexin-II, osteopontin, and hyaluronan.
Verkoelen
C F
CF
Department of Urology, Josephine Nefkens Institute, Erasmus Medical Center Rotterdam, Rotterdam, The Netherlands. c.verkoelen@erasmusmc.nl
Verhulst
A
A
D000818:Animals; D017306:Annexin A2 / Q000502:physiology; D002129:Calcium Oxalate / Q000378:metabolism; D002135:Calcium-Binding Proteins / Q000502:physiology*; D002454:Cell Differentiation / Q000502:physiology; D003460:Crystallization; D006801:Humans; D006820:Hyaluronic Acid / Q000502:physiology; D007686:Kidney Tubules, Distal / Q000473:pathology / Q000503:physiopathology*; D009397:Nephrocalcinosis / Q000473:pathology / Q000503:physiopathology*; D053495:Osteopontin / Q000502:physiology
D017306:Annexin A2; D002135:Calcium-Binding Proteins; D053495:Osteopontin; D002129:Calcium Oxalate; D006820:Hyaluronic Acid