Acute phosphate nephropathy (APhN) is a clinical pathological entity characterized by acute and subsequent chronic renal failure following exposure to oral sodium phosphate (OSP) bowel purgatives. Renal biopsy findings include acute and chronic tubular injury with prominent tubular and interstitial calcium phosphate deposits. Risk factors for APhN include older age, female gender, hypertension, chronic kidney disease (CKD), and treatment with angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and diuretics. The pathomechanism of APhN involves hypovolemia-induced avid proximal salt and water reabsorption, delivery of a large phosphate load to the distal nephron, and precipitation of calcium phosphate in the distal tubule and collecting duct. To date, 37 cases of biopsy-proven APhN have been reported, and epidemiologic studies have produced inconsistent results regarding the incidence of acute kidney injury (AKI) following the use of OSP purgatives. OSP solution was withdrawn from the market in December of 2008, but OSP tablets, offered by prescription only, remain available. Prevention of APhN is best achieved by avoiding OSP in high-risk patients, aggressive hydration before, during, and after OSP administration, minimizing the dose of OSP, and maintaining a minimum of a 12 h interval between OSP administrations.