Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Acute phosphate nephropathy Frank P. Hurst a,b and Kevin C. Abbott a,b Introduction Acute phosphate nephropathy (APN) was first described in 2003 in a 71-year-old female patient who developed acute kidney injury (AKI) after ingestion of oral sodium phosphate (OSP). She presented with nonspecific malaise 2 weeks after exposure to OSP with a serum creatinine of 4.5 mg/dl up from a prior baseline of 1.0 mg/ dl. Renal biopsy showed numerous intratubular deposits containing calcium and phosphate ions assembled as hydroxyapatite crystals (Fig. 1). On the basis of appear- ance of the biopsy, the authors postulated that OSP ingestion led to obstructive calcium phosphate crystal- luria and intraluminal nephrocalcinosis. This insult resulted in chronic kidney disease (CKD) in that the patient’s renal function did not return to prior baseline 1 year later (serum creatinine 1.7 mg/dl) [1]. Later, a large biopsy case series described more histo- pathologic cases of APN, strengthening the association of OSP ingestion to this pathologic finding. The authors reviewed biopsies over a 5-year period, searching for cases with the triad of unexplained AKI, OSP exposure, and nephrocalcinosis (with normal serum calcium). A total of 21 cases met criteria out of 7349 biopsies (0.29%). The renal biopsy findings showed abundant calcium phosphate deposits in the distal tubules and collecting ducts often accompanied by tubular atrophy and interstitial fibrosis. Most patients had normal renal function prior to OSP exposure [mean baseline serum creatinine of 1.0 mg/dl (range 0.6–1.7 mg/dl)], though some patients had preexisting CKD. After a mean of 16.7 months of follow-up, no patient returned to baseline creatinine [mean 2.4 mg/dl (range 1.3–3.4)], and 19% were on permanent hemodialysis [2]. This study helped to confirm prior suspicions that APN may be an underrecognized cause of both AKI and CKD. With increased recognition of this disease and increasing numbers of reported cases, the US Food and Drug Administration (FDA) issued an alert in May 2006 describing APN as a rare but serious event associated with the use of OSP for bowel cleansing. Cases continued to surface, and several epidemiologic studies were pub- lished in an attempt to quantify the risk of AKI with the use of OSP. On 11 December 2008, the FDA issued a boxed warning on prescription OSP products and directed manufacturers to develop a risk evaluation a Nephrology Service, Walter Reed Army Medical Center, Washington, District of Columbia and b Uniformed Services University of Health Sciences, F. Edward Hebert School of Medicine, Bethesda, Maryland, USA Correspondence to Dr Frank P. Hurst, MD, Department of Nephrology, Walter Reed Army Medical Center, 6900 Georgia Ave. NW, Washington, DC 20307, USA Tel: +1 202 782 6462; fax: +1 202 782 0185; e-mail: frank.hurst@us.army.mil Current Opinion in Nephrology and Hypertension 2009, 18:513–518 Purpose of review Acute phosphate nephropathy (APN) has been identified in renal biopsy specimens of patients exposed to oral sodium phosphate (OSP) bowel purgatives. Biopsy confirmed cases presented with bland urinary sediment, low-grade proteinuria, and varying degrees of creatinine elevation. Prospective identification of APN is difficult in that definitive diagnosis requires renal biopsy, and biopsy is rarely performed for patients with this clinical presentation. Recent findings Observational studies evaluating acute kidney injury after OSP exposure using interval changes in creatinine as a surrogate for APN have reported conflicting results. Although these studies have produced estimates of disease occurrence, they have been unable to definitively quantify the overall risk of APN with OSP as compared with alternative bowel-cleansing agents. Summary On the basis of association of APN and OSP, the US Food and Drug Administration issued a boxed warning and manufacturers have ceased production and distribution of some OSP products. As this is a temporary solution, more studies are needed to delineate the pathophysiology of this disease and to better identify the subset of the population at risk for APN. Keywords acute kidney injury, colonoscopy, nephrocalcinosis, phosphate nephropathy Curr Opin Nephrol Hypertens 18:513–518 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins 1062-4821 1062-4821 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins DOI:10.1097/MNH.0b013e32833096af