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Correspondence

Acute Phosphate Nephropathy and Renal Failure

N Engl J Med 2003; 349:1006-1007September 4, 2003

Article

To the Editor:

Phosphate-based cathartic agents are commonly prescribed for bowel cleansing before colonoscopy. They may have serious side effects, including seizures and acute renal failure. Although the latter complication has been reported on at least three occasions,1-3 the pathophysiology and histologic lesion underlying it remain unknown. In this report, we describe a case of phosphosoda-induced acute renal failure that was evaluated by biopsy.

Two weeks after ingesting a cathartic agent, a 71-year-old woman presented with nonspecific malaise. The serum creatinine level was 4.5 mg per deciliter (as compared with 1.0 mg per deciliter 10 weeks earlier), and both the results of urinalysis and a renal ultrasound image were normal. Examination of the renal-biopsy specimen showed numerous intratubular deposits, all positive on von Kossa's staining and nonbirefringent under polarized light (Figure 1Figure 1Histologic and Mineralogic Features of a Renal Biopsy Specimen Obtained Two Weeks after a 71-Year-Old Woman Ingested 90 ml of a Phosphosoda Preparation.). Scanning electron microscopy and energy-dispersive x-ray microanalysis indicated that these deposits contained calcium and phosphate ions assembled as hydroxyapatite crystals. Additional tests performed several months after the biopsy showed that the patient had no risk factors for nephrocalcinosis. The serum creatinine level remained elevated (1.7 mg per deciliter) one year later.

An important facet of this case is that it provides key information about the pathophysiology and management of acute renal failure associated with phosphate loads. Indeed, the nature and localization of the lesions strongly suggest that phosphosoda ingestion led to obstructive calcium-phosphate crystalluria, followed by intratubular nephrocalcinosis. On the basis of these findings, one might postulate that analogous lesions were the cause of acute renal failure in the other reported cases.1-3 It is also interesting to speculate that similar lesions may occur in tumor lysis syndromes, which are generally complicated by hyperphosphatemia or hyperphosphaturia.4 Accordingly, alkalinizing agents should probably not be used after the use of phosphosoda preparations. Alkalinizing agents should also not be used to treat or prevent uric acid nephropathy, since the threshold for calcium phosphate precipitation decreases in alkaline urine.5

Another important facet of this case is that the patient's acute renal failure was followed by chronic renal impairment. Because a similar outcome was observed in another patient,1 and because high phosphate loads could induce some degree of calcium phosphate crystalluria in certain persons, it is possible that the prevalence of long-term renal damage caused by phosphosodas far exceeds that reported in the published cases. This is a matter of concern because such agents are administered to thousands of patients each year. We suggest that additional studies be performed to determine the safety of phosphate-based cathartic agents.

In conclusion, this case of biopsy-proven, phosphosoda-induced nephrocalcinosis provides strong evidence that renal lesions can be induced by a high phosphate load as the sole causative factor. We propose the term “phosphate nephropathy” as a nosologic designation for this entity.

Simon Desmeules, M.D.
Marc J. Bergeron, M.Sc.
Paul Isenring, M.D., Ph.D.
L'Hôtel-Dieu de Québec Research Centre, Quebec, QC G1R 2J6, Canada

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