Also, this does not only hold true for hyperoxaluria-induced nephrocalcinosis, but for a variety of other renal inflammatory models and conditions, e.g., thioglycolate-induced peritonitis (58), inflammatory response and albuminuria in response to albumin-overload (59), anti-GBM glumerulonephritis (60) as well as response to nephrotoxins (61). This evidence concerns the gene ALB and Hyperoxaluria.