Many in vitro and in vivo studies on the mechanisms underlying calcium nephrolithiasis have provided evidence of a frequently associated condition, i.e., a microscopic renal crystal deposition that can occur within the tubular lumen (intratubular nephrocalcinosis) or in the interstitium (interstitial nephrocalcinosis). Medullary nephrocalcinosis is the typical pattern seen in 98% of cases of human nephrocalcinosis, with calcification clustering around each renal pyramid. It is common in patients with metabolic conditions that predispose them to renal calcium stones. Cortical nephrocalcinosis is rare and usually results from severe destructive disease of the cortex. It has been described in chronic glomerulonephritis, but often in association with another factor, such as an increased calcium ingestion, acute cortical necrosis, chronic pyelonephritis or trauma. The most accredited hypothesis to explain the onset of interstitial nephrocalcinosis is purely physicochemical, relating to spontaneous Ca2PO4 crystallization in the interstitium due to oversaturation of Ca2PO4salts in this milieu. The theory that nephrocalcinosis is a process driven by osteogenic cells was first proposed by our group. We review nephrocalcinosis in terms of its definition, genetic associations, and putative mechanisms, pointing out how much evidence in the literature suggests that it may have some features in common with, and pathogenic links to vascular calcification.
Part of the book: Updates and Advances in Nephrolithiasis