Abstract
Nephrocalcinosis is the deposition of calcium salts in renal parenchyma and can be intratubular or interstitial. Animal model studies indicate that intratubular nephrocalcinosis is a result of increased urinary supersaturation. Urinary supersaturation with respect to calcium oxalate (CaOx) and calcium phosphate (CaP) are generally achieved at different locations in the renal tubules. As a result experimental induction of hyperoxaluria in animals with CaP deposits does not lead to growth of CaOx over CaP. Interstitial nephrocalcinosis has been seen in mice with lack of crystallization modulators Tamm-Horsfall protein and osteopontin. Sodium phosphate co-transporter or sodiumhydrogen exchanger regulator factor-1 null mice also produced interstitial nephrocalcinosis. Crystals plug the tubules by aggregating and attaching to the luminal cell surface. Structural features of the renal tubules also play a role in crystal retention. The crystals plugging the terminal collecting ducts when exposed to the metastable pelvic urine may promote the formation of stone.