Acute Phosphate Nephropathy

By Donna J. Lager, M.D.

Case History

A 60 year old woman presented with progressive renal insufficiency and a serum creatinine of 2.5 mg/dl, which was increased from 0.9 mg/dl five months prior. Her history is significant for hypertension and ulcerative colitis. She underwent colonoscopy one month prior to presentation.

Diagnosis: Acute Phosphate Nephropathy

Acute phosphate nephropathy is a term first proposed in 2003 to describe a syndrome of renal failure in patients receiving oral sodium phosphate solution (OSPS) for bowel preparation prior to colonoscopy (1). It is characterized by calcium phosphate deposition in the kidney with associated tubular damage, interstitial inflammation and fibrosis, and renal dysfunction (1- 4). The  phosphate composition of the crystals can be confirmed with a von Kossa stain.

The kidney is important in maintaining calcium and phosphorus homeostasis such that as the phosphate level increases, the calcium level decreases and vice versa. It has been long recognized that the administration of elemental phosphorus to patients with hypercalcemia will result in a decrease in serum calcium and an increase in serum creatinine (5). A number of reports have subsequently described hyperphosphatemia and hypocalcemia as well as nephrocalcinosis in patients receiving OSPS (3, 6). The first biopsy documented case of phosphate nephropathy was that of a 71 year old woman who had ingested 90 ml of a phosphosoda preparation. The composition of the crystals was confirmed using x-ray dispersion (1). Several reports have since appeared describing isolated examples and series of patients developing phosphate nephropathy following OSPS administration (2-4, 7, 8).

Risk factors for the development of phosphate nephropathy include (4, 9):

• Older age

• Female gender

• Significantly reduced gut motility

• Decreased intravascular volume

• Reduced renal function

• Use of ACE inhibitors, angiotensin receptor blockers (ARB) and NSAIDs

• Excessive dosing

• Inadequate hydration

Most patients with phosphate nephropathy develop progressive renal dysfunction with end-stage renal failure in approximately 25% (4). Because of the rising number of reports of phosphate nephropathy following the use of OSPS, the FDA issued an alert in May 2005 urging caution in those patients at increased risk. A safe and increasingly used alternative to OSPS as a bowel purgative is polyethylene glycol-electrolye lavage solution (PEG-ELS) (10).

References:

1. Desmeules S, Bergeron MJ, Isenring P. Acute Phosphate Nephropathy and Renal Failure. N Engl J Med 349(10): 1006-1007, 2003.
2. Aasebo W, Scott H, Ganss R. Kidney biopsies taken before and after oral sodium phosphate bowel cleansing. Nephrol Dial Transplant 22:920-922, 2007.
3. Gonlusen G, Akgun H, Ertan A, Olivero J, Truong LD. Renal Failure and Nephrocalcinosis Associated with Oral Sodium Phosphate Bowel Cleansing. Clinical Patterns and Renal Biopsy Findings. Arch Pathol Lab Med 130:101106, 2006.
4. Markowitz GS, Stokes MB, Radhakrishnan J, D’Agati VD. Acute Phosphate Nephropathy following Oral Sodium Phosphage Bowel Purgative: An Underrecognized Cause of Chronic Renal Failure. J Am Soc Nephrol 16:3389-3396, 2005.
5. Ayala G, Chertow BS, Shah JH, Williams GA, Kukreja SC. Acute Hyperphosphatemia and Acute Persistent Renal Insufficiency Induced by Oral Phosphate Therapy. Ann Int Med 83(4):520-521, 1975.
6. Ullah N, Yeh R, Ehrinpreis M. Fatal Hyperphosphatemia from a Phosphosoda Bowel Preparation. J Clin Gastroenterol 34(4):457-458, 2002.
7. Carl DE, Sica DA. Acute Phosphate Nephropathy Following Colonoscopy Preparation. Am J Med Sci 334(3):151-154, 2007.
8. Beyea A, Block C, Schned A. Acute Phosphate Nephropathy Following Oral Sodium Phosphate Solution to Cleanse the Bowel for Colonoscopy. Am J Kid Dis 50(1):151-154, 2007.
9. Sica DA, Carl D, Zfass AM. Acute Phosphate Nephropathy—An Emerging Issue. Am J Gastroenterol 102:1844-1847, 2007.
10. Burke CA, Church JM. Enhancing the quality of colonoscopy: the importance of bowel purgatives. Gastrointest Endo66(3):565-573, 2007.

Date of last revision: September 2009.