Abnormal dietary habits that lead to hypercalciuria, hyperoxaluria, hypereruricosuria, and hypocitraturia do not always result in nephrolithiasis. A concept is emerging according to which, to account for renal stone formation in the face of the aforementioned biochemical disorders, one must search for underlying conditions in patients with the disease. Work carried out over the past few years and reviewed herein definitely supports this idea and includes the following processes: 1) interleukin-1 production by monocytes to augment the impact of dietary hypercalciuria; 2) disturbed activation of pyridoxine to pyridoxal 5'-phosphate to aggravate dietary hyperoxaluria; 3) abnormal intestinal transport of citrate to aggravate dietary hypocitraturia; 4) molecular abnormalities of glycoprotein inhibitors to aggravate the promotive effect of the diet on urinary crystallization; and 5) renal tubular lesions to favor particle retention and stone formation. This article reviews the most recent literature and discusses the author's "powder keg and tinderbox" theory of idiopathic calcium stone disease.