Previous studies have shown that magnesium deficiency accelerates renal tubular calcium oxalate monohydrate deposition in rats on chronic hyperoxaluric, lithogenic protocols. The present study was conducted to investigate the effect of magnesium deficiency on intratubular calcium oxalate formation in rats from the 1st day of administration of a hyperoxaluric agent. The objectives were to delineate early ultrastructural features of the formation, mechanisms of retention, and development of renal tubular crystal deposits and to characterize the crystalluria in rats on the hyperoxaluric/hypomagnesuric protocol. Intratubular calcium oxalate monohydrate deposits were found in magnesium deficient rats after only 24 hours of ad libitum administration of 1 per cent ethylene glycol drinking water. Animals on regular food diet did not display renal tubular deposition after 11 days of ethylene glycol administration. Strand- and sheet-like organic material emanating from the luminal wall of the tubules was adherent to the crystals, thereby serving to immobilize them within the tubule. Calcium oxalate monohydrate crystals predominated in the urines of hyperoxaluric/hypomagnesuric animals with intratubular deposits while dihydrate crystals were the primary constituent of urines from rats administered ethylene glycol alone (no intratubular deposition). The results support the supposition that under certain conditions magnesium deficiency is a significant risk factor for intrarenal calcium oxalate deposition and stone formation. Furthermore the identification of calcium oxalate monohydrate crystalluria may be an important indicator of the propensity toward intranephronic calcium oxalate formation and urolithiasis.