Experimental data reported by studies performed using different models of kidney injury, such as chronic glomerulonephritis [37,38,39,40], diabetic nephropathy [41,42], Lupus Nephritis [43], crystalline nephropathy [44,45,46,47] and hypertensive nephropathy [48,49,50], have shown that NLRP3 inflammasome activation participates in the underlying pathogenetic events involved in the onset and progression of kidney damage, regardless of the aetiology of kidney disease. This evidence concerns the gene NLRP3 and Nephropathy.