Bowel preparations containing oral so− dium phosphate have gained increased favor among gastroenterology endosco− pists in preference to the traditional poly− ethylene glycol, likely due to greater pa− tient tolerability and improved cleansing and compliance [1]. Despite the availabil− ity of reports in the literature concerning life−threatening metabolic and cardiac abnormalities associated with the use of oral sodium phosphate in patients with renal insufficiency, less than half of re− spondents in a recent survey among gas− trointestinal endoscopists reported its ex− clusion in this patient population [2]. We report two cases of severe hyperphospha− temia and secondary hypocalcemia due to administration of an oral sodium phos− phate−containing bowel preparation in patients with chronic renal insufficiency.The first patient, a 51−year−old woman with end−stage renal disease requiring peritoneal dialysis, was evaluated for gen− eralized weakness, perioral tingling, elici− table Chvostek s sign, and a prolonged QT interval. The patient had ingested two 45− ml doses of Fleet s Phospho−Soda solution the previous night, in preparation for a screening colonoscopy. Laboratory evalu− ation revealed abnormal levels of calcium and phosphate in comparison with base− line values (Figure 1). Clinical symptoms and laboratory abnormalities of hypocal− cemic tetany resolved rapidly after the pa− tient received intravenous calcium and peritoneal dialysis. The patient subse− quently underwent colonoscopy without any complications and continued to be asymptomatic on follow−up.The second patient was a 57−year−old man with diabetes mellitus and chronic renal insufficiency who presented with hema− tochezia. Laboratory values on admission were unremarkable except for a serum creatinine of 2.1 mg/dl. At 2 days after in− gesting two doses of 45 ml of oral sodium phosphate for a colonoscopy, his metabol− ic profile demonstrated serum calcium and phosphate of 6.5 mg/dl and16.9 mg/ dl, respectively (Figure 1). He remained asymptomatic and received oral calcium acetate to bind phosphate. The patient was discharged in a stable condition with serum calcium and phosphate of 6.7 mg/ dl and 14.4 mg/dl, respectively. No fol− low−up information was available.Similar abnormalities in serum calcium and phosphate, associated with oral so− dium phosphate ingestion, have been re− ported in the absence of renal insufficien− cy. This may, however, be related to the dosage of oral sodium phosphate admi− nistered (greater than 90 ml) or to im− paired bowel motility leading to pro− longed intestinal transit time [3]. A 45− ml bottle of oral sodium phosphate con− tains approximately 6 g of inorganic phos− phate, while a person with normal renal function can handle an intake of phos− phate up to 4 g over a 24−hour period, due to reduced proximal tubular reab− sorption of phosphate [4]. A rise in serum phosphate is thought to be the primary etiology of hypocalcaemia in these pa− tients [5].Previously published literature does not report the magnitude of renal...