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Acute phosphate nephropathy

Acute phosphate nephropathy
Authors:
Glen S Markowitz, MD
Mark A Perazella, MD, FACP
Section Editor:
Paul M Palevsky, MD
Deputy Editor:
Eric N Taylor, MD, MSc, FASN
Literature review current through: Dec 2022. | This topic last updated: Feb 11, 2021.

INTRODUCTION — Acute phosphate nephropathy is a form of kidney injury that occurs following the use of bowel purgatives that contain oral sodium phosphate (OSP) and has been reported following the administration of sodium phosphate-containing enemas [1,2]. OSP was formerly sold without prescription under the brand name "Fleet Phospho-soda" (C.B. Fleet Inc). Fleet no longer distributes OSP; however, generic versions of OSP are still available without prescription. OSP is also available by prescription in a pill form (Visicol, OsmoPrep). In both pill and liquid form, OSP is a hyperosmotic laxative that acts by drawing water into the gastrointestinal tract. Although long used as a laxative, OSP began to be used as a purgative for colonoscopy in 1990 [3]. It is frequently given in favor of standard polyethylene glycol (PEG)-based lavage solutions because of the smaller required volume, which results in better patient compliance and improved colonic cleansing [4-6].

However, there have been multiple cases of OSP-induced acute kidney injury (AKI) with defining histologic features on biopsy [7-11]. This clinicopathologic entity has been referred to as acute phosphate nephropathy.

In 2006, in response to published reports, the US Food and Drug Administration (FDA) issued a warning regarding the potential for AKI in patients who received OSP [12]. The warning was incorporated into a consensus document on bowel preparation by the American Society of Colon and Rectal Surgeons (ASCRS), the American Society of Gastrointestinal Endoscopy (ASGE), and the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) [13]. In December 2008, the FDA required that a boxed warning be added to labeling of Visicol and OsmoPrep, which are still available by prescription [14]. At the same time, following the recommendation of the FDA, over-the-counter preparations that contain OSP were voluntarily withdrawn from the market by Fleet; but, as noted above, generic versions are still available. In 2014, the FDA issued another warning that using more than one dose in 24 hours of OSP to treat constipation can cause "rare but serious harm to the kidneys and heart, and even death" [15].

This topic provides a review of the clinical features of acute phosphate nephropathy. AKI associated with an increased phosphate load has also been described in tumor lysis syndrome, especially with alkalinization of the urine by bicarbonate-containing intravenous (IV) fluids. Tumor lysis syndrome is discussed elsewhere. (See "Tumor lysis syndrome: Pathogenesis, clinical manifestations, definition, etiology and risk factors".)

PATHOGENESIS — The mechanism underlying acute phosphate nephropathy most likely relates to a transient but potentially severe increase in serum phosphate coupled with volume depletion, both of which may occur following the administration of bowel purgatives that contain oral sodium phosphate (OSP).

Hyperphosphatemia — Hyperphosphatemia occurs in a large number of patients following OSP ingestion [1,16,17]. In one study, 28 percent of patients who underwent elective colonoscopy had serum phosphate concentrations >8 mg/dL (2.6 mmol/L; normal range 2.5 to 4.5 mg/dL [0.8 to 1.5 mmol/L]) following OSP administration [16].

The high rate of hyperphosphatemia following the use of OSP as a bowel purgative reflects the ingestion of a large amount of phosphate over a short period of time; this leads to a marked increase in phosphate absorption since the intestinal sodium-phosphate cotransporters that mediate absorption cannot be rapidly downregulated [18,19].

Until reports were published describing acute phosphate nephropathy, the recommended dose as a bowel preparation provided 11.6 grams of phosphorus within 24 hours, an amount that far exceeds the usual dietary intake of 1 g/day. Subsequent to reports of kidney injury, a phosphate dose reduction of 17 to 20 percent has been instituted [20].

Hyperphosphatemia is more likely to occur in patients with kidney function impairment, who have decreased excretion of phosphate [17,20-23]. As a result, OSP is contraindicated in patients with clinically significant acute or chronic impairment in kidney function.

However, hyperphosphatemia also occurs in patients with normal kidney function, as illustrated in a study of 70 patients with creatinine clearances >70 mL/min [17]. After OSP administration, 37 percent had serum phosphate levels >8 mg/dL (2.6 mmol/L). In this study, there was a strong correlation between patient age and the degree of hyperphosphatemia, suggesting that age-related factors (including decreased total body water, abnormal bowel motility, enhanced gastrointestinal absorption) unrelated to kidney function promote hyperphosphatemia. As a result, advanced age may increase the risk for the development of acute phosphate nephropathy. (See 'Risk factors' below.)

Hyperphosphatemia is more likely to occur in patients who have impaired gastrointestinal motility, which leads to increased phosphate absorption. Gastrointestinal obstruction is a contraindication to the use of OSP.

Nephrocalcinosis — The mechanism by which hyperphosphatemia causes kidney injury is not known, although hypotheses have been raised based on observed histology. The predominant (though not exclusive) finding on kidney biopsy is widespread deposition of calcium phosphate in tubular lumina, tubular epithelia, and the interstitium. There is also evidence of tubular epithelial injury and inflammation. (See 'Pathology' below.)

One hypothesis to explain the pathogenesis is that transient hyperphosphatemia leads to an increased intratubular phosphate concentration, resulting in the precipitation and tissue deposition of calcium phosphate salts that cause luminal obstruction, direct tubular epithelial injury, and activation of the immune response [20,24].

Although tubular injury is noted in all nephron segments, calcium phosphate deposition is limited to the distal tubule and collecting duct [25]. The delivery of phosphate to these sites is enhanced by the decrease in proximal tubular phosphate absorption that occurs within minutes of OSP ingestion.

Volume depletion — The intraluminal calcium phosphate deposition is probably worsened by volume depletion, which often results from the OSP-induced osmotic diarrhea in the setting of reduced oral intake prior to the procedure. Conditions that cause effective volume depletion, such as heart failure and ascites, are contraindications to the use of OSP.

True or effective volume depletion results in increased sodium chloride and water reabsorption in the proximal tubule. This effect, combined with ongoing water reabsorption in the descending limb of the loop of Henle, raises the calcium phosphate product within the tubular lumen in the fluid presented to the ascending limb and distal tubule [26]. Volume depletion may also increase the adherence of calcium phosphate crystals to the distal tubule epithelium via an increase in surface expression of hyaluronan and osteopontin [27].

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers — Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) enhance the development of acute phosphate nephropathy from OSP. This is because ACE inhibitors and ARBs worsen the prerenal state by promoting the loss of angiotensin II-mediated efferent arteriolar constriction, which then reduces glomerular filtration [8,28,29]. In addition, ACE inhibitors and ARBs decrease angiotensin II-dependent proximal tubule bicarbonate reabsorption, which leads to an increase in distal tubular bicarbonate concentration. The increase in intraluminal pH promotes precipitation of calcium phosphate crystals [30,31].

PATHOLOGY — The chief pathologic characteristic of acute phosphate nephropathy is extensive deposition of calcium phosphate in the tubular lumina, within tubular epithelial cells, and, less commonly, in the peritubular interstitium [25]. Calcium phosphate deposits are distinguished from calcium oxalate deposits by positive staining with the "von Kossa stain" and the absence of birefringence under polarized light (picture 1).

Other findings observed on kidney biopsy depend upon the elapsed time between oral sodium phosphate (OSP) exposure and the time at which the biopsy was performed. Early biopsies show tubular degenerative changes similar to those seen in acute tubular necrosis [25]. These changes include luminal ectasia, cytoplasmic simplification, loss of brush border, shedding of cell fragments into the lumina, and enlarged nuclei with prominent nucleoli. The tubular degenerative changes and calcifications are accompanied by interstitial edema and mild to moderate interstitial inflammation that is not typically associated with significant tubulitis.

In contrast, kidney biopsies performed more than three weeks following OSP use show chronic changes, including tubular atrophy and interstitial fibrosis. The tubular degenerative changes are less severe and more localized and resemble changes seen in repeat kidney biopsies from patients with nonresolving acute tubular necrosis.

INCIDENCE — There are no reliable data on the incidence of acute phosphate nephropathy in patients with previously intact kidney function. A number of retrospective studies have examined this issue by evaluating the frequency or magnitude of reduction in estimated glomerular filtration rate (eGFR) at 6 to 12 months after the administration of bowel purgatives that contain oral sodium phosphate (OSP) [28,29,32,33].

However, all of these studies are limited in a variety of ways, including lack of confirmation of the diagnosis by kidney biopsy. This is an important issue since many patients who develop acute kidney injury (AKI) following OSP administration do not have acute phosphate nephropathy. (See 'Acute and reversible kidney injury' below.)

The following observations illustrate the range of findings:

The largest study is an observational analysis of 9799 Department of Defense beneficiaries who underwent colonoscopy between 2002 and 2006 [32]. AKI, defined as a >50 percent increase in serum creatinine from baseline within one year following colonoscopy, was observed in 114 patients. After adjusting for putative risk factors, OSP was the strongest risk factor for AKI (risk ratio [RR] 2.35, 95% CI 1.51-3.66).

A retrospective case-control study evaluated 2237 patients who had outpatient colonoscopy [29]. AKI, defined as a 25 percent or a 0.5 mg/dL (44.2 micromol/L) increase in serum creatinine over six months postcolonoscopy, was identified in 141 patients (6.3 percent). An association between OSP and AKI was only seen in patients who received an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB).

However, interpretation of this study is limited by the small sample size and the permissive definition of AKI [34]. When a stricter definition of AKI (which required an increase in creatinine of 1 mg/dL [88.4 micromol/L]) was employed, the number of cases of kidney injury fell from 116 to 3.

Risk factors — The following potential risk factors for the development of acute phosphate nephropathy have been identified. However, since only the series from Columbia University had biopsy confirmation of the disease [8], one cannot be certain how many of the patients with impaired kidney function in other series had acute phosphate nephropathy.

Phosphate dosing – The degree of hyperphosphatemia is directly related to the total amount of administered OSP, and a greater degree of hyperphosphatemia is likely to increase the risk of acute phosphate nephropathy [3,35-37]. A wider interval between the administration of the two doses of OSP (ie, 24 versus 12 hours) is associated with a lesser degree of hyperphosphatemia and, therefore, is likely to be safer [20,34].

Chronic kidney disease (CKD) – Reduced GFR increases the risk of hyperphosphatemia following OSP administration. A retrospective study on the safety of bowel preparations in patients with an eGFR <60 mL/min/1.73 m2 found an adjusted relative risk of AKI for OSP-exposed patients of 12.6 relative to polyethylene glycol (PEG)-exposed patients [38]. OSP is contraindicated in patients with a clinically significant impairment in kidney function.

ACE inhibitors and ARBs – In the series from Columbia, 14 of 21 patients with acute phosphate nephropathy were being treated with one of these two agents [8]. The increased risk conferred by these agents has been confirmed in observational studies [28,29].

Age – Advanced age has been identified as an independent risk factor in multiple studies [17,32,33,39]. An absolute age at which the risk is increased has not been determined.

Drugs – The use of diuretics, nonsteroidal anti-inflammatory agents (NSAIDs), and lithium has been suggested as a possible risk factor [20,39].

Female sex – The majority of reported cases of acute phosphate nephropathy have occurred in women [8,29]. A possible contributing factor is that female subjects are generally smaller and have a lower GFR than men but receive the same dose of OSP.

Comorbid conditions – Hypertension and diabetes have been suggested as risk factors by several studies [8,28,33].

Risk with sodium phosphate enemas — Acute phosphate nephropathy also has been rarely reported following the administration of sodium phosphate enemas (SPEs), although the majority of these reports have followed the use of excessive doses [40-42].

One report highlights the occurrence of acute phosphate nephropathy following the use of a 250 mL dose of SPEs in older patients. In this report, 11 older patients with a mean age of 80 years (range 61 to 89 years) developed AKI following the administration of Fleet enemas; of these, three individuals had received large doses of 500 to 798 mL, and eight had received standard doses of 250 to 266 mL. Four patients had normal baseline kidney function (defined as eGFR >60 mL/min/1.73 m2), and seven had reduced kidney function (eGFR between 25 to 57 mL/min/1.73 m2). Although kidney functional outcomes are not provided, five patients expired. Histologic confirmation of the diagnosis of acute phosphate nephropathy was available for a single patient in whom tubular calcium phosphate deposits were found at autopsy [2]. Of note, fluid volume and phosphorus content of the SPE used in this study are substantially greater than the Fleet SPE that is marketed in the US (133 mL).

In a retrospective cohort study that included 70,499 Veterans Affairs (VA) patients who underwent colonoscopy, compared with PEG oral solution alone (n = 64,092), the use of SPE (with or without oral PEG; n = 6407) was associated with increased risk for a 50 percent increase in serum creatinine within 15 months of use (odds ratio [OR] 1.3, 95% CI 1.2-1.5) [42]. There was no difference between groups in the risk for an acute eGFR decline (ie, over six weeks).

However, in the absence of an increased risk for an acute decline in eGFR, the causal relationship of sodium phosphate-containing enemas to a decline in eGFR is not clear [43]. In addition, SPE alone was not associated with either acute or long-term eGFR changes in a sensitivity analysis in which the subjects were broken into three groups: PEG (90.9 percent), PEG and SPE (8.1 percent), and SPE alone (1 percent). The authors may have obtained misleading results by using variables in their multivariate model that were in the causal pathway between exposure and outcome (ie, baseline CKD and anemia) and by using variables that are not associated with eGFR decline (ie, asthma and chronic obstructive pulmonary disease [COPD]).

The impact of SPE on eGFR is unclear. Further studies are required to address this issue.

CLINICAL PRESENTATION AND PROGNOSIS — Two different clinical patterns of kidney injury have been described following the administration of bowel purgatives that contain oral sodium phosphate (OSP): an acute form that is reversible and may not represent acute phosphate nephropathy, and a delayed onset that is due to acute phosphate nephropathy and is generally irreversible [44].

Acute and reversible kidney injury — In some patients, acute kidney injury (AKI) occurs within hours of the administration of OSP. This presentation is mainly associated with excessive dosing of OSP or other risk factors for hyperphosphatemia [44-46]. AKI occurs in the setting of severe hyperphosphatemia and hypocalcemia, leading to tetany, cardiac arrest, and, in some cases, death. Patients who survive the immediate event typically return to normal or near-normal kidney function. As a result, kidney biopsy is not usually performed.

It appears likely that the AKI in these patients was due to prerenal factors or acute tubular necrosis rather than acute phosphate nephropathy. (See "Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults".)

Acute phosphate nephropathy — In contrast, acute phosphate nephropathy is characterized by increases in serum creatinine that occur in asymptomatic patients and are documented days to months following OSP administration. The serum phosphate and calcium concentrations are typically normal when kidney injury is discovered. The majority of reports of acute phosphate nephropathy have been confirmed by kidney biopsy.

The largest series on acute phosphate nephropathy is a retrospective review of biopsies processed by the kidney pathology laboratory at Columbia University from 2000 to 2004 [8]. This study identified 21 patients who had biopsy-confirmed acute phosphate nephropathy and a compatible history of OSP ingestion. The following observations were noted:

Seventeen of the 21 were White patients, 17 were female, and the mean age was 64 years. Sixteen patients had a history of hypertension, and 14 of the 16 were taking either an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB). (See 'Risk factors' above.)

The mean baseline (within four months of the procedure) serum creatinine was 1.0 mg/dL (88.4 micromol/L). In contrast, the mean value at the time of presentation with AKI was 3.9 mg/dL (345 micromol/L) at a median of one month after colonoscopy.

At the time of AKI, serum calcium levels were normal in all 20 patients with available data. Hyperphosphatemia was noted in 7 of 16 patients and was more common in patients with a shorter interval between OSP administration and onset of AKI.  

The urinalysis was bland in 13 patients; hematuria was observed in three patients and pyuria in five patients. Twenty-four-hour protein excretion was <600 mg/day in 13 of 14 patients in whom quantification was performed. In the seven other patients, urinalysis showed 0 to 1+ proteinuria on dipstick testing. Protein excretion exceeded 1 g/day in only one patient who had concurrent diabetic glomerulosclerosis on kidney biopsy.

Most patients appear to have taken OSP at the correct dose and in the absence of clear contraindications.

At mean follow-up of 16.7 months, four patients progressed to end-stage kidney disease, and the remaining 17 patients had a decline in serum creatinine to a mean of 2.4 mg/dL (212 micromol/L). No patient returned to baseline kidney function. Similar findings have been noted by others; complete recovery of kidney function, if it occurs, appears to be a rare event [44,47-49]. In the Department of Defense study cited above, 16 percent of patients returned to their baseline serum creatinine [32]. However, kidney biopsies were not performed, and some or many of these patients may have had acute tubular necrosis rather than acute phosphate nephropathy.

Given the poor prognosis, identification of patients at risk and preventive measures are important.

DIAGNOSIS — The diagnosis of acute phosphate nephropathy is suggested by the temporal association between acute kidney injury (AKI) and the administration of bowel purgatives that contain oral sodium phosphate (OSP). However, some patients present late after the exposure with chronic kidney disease (CKD).

The diagnosis of phosphate nephropathy is supported by a benign sediment on urinalysis and modest proteinuria. By definition, all patients with phosphate nephropathy should be normocalcemic prior to receiving OSP. (See "Nephrocalcinosis".)

There are no reports of the use of imaging to demonstrate nephrocalcinosis in acute phosphate nephropathy. As a result, the diagnosis can be confirmed only by kidney biopsy, which may not be required in patients with AKI diagnosed shortly after using an OSP purgative. (See 'Pathology' above.)

Differential diagnosis — For the patient who presents days to months following colonoscopy with an elevated creatinine, minimal proteinuria, and a relatively bland urine sediment, the differential diagnosis includes acute and chronic tubular and interstitial diseases. These include acute and chronic forms of interstitial nephritis, ischemic and toxic forms of acute tubular necrosis, and myeloma cast nephropathy, to name a few. (See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)

Once a kidney biopsy is obtained, all causes of nephrocalcinosis should be considered, including conditions associated with hypercalcemia, hypercalciuria without hypercalcemia, or hyperphosphatemia with hyperphosphaturia. (See 'Nephrocalcinosis' above.)

PREVENTION AND TREATMENT — The single, most important preventive strategy is to identify patients who are at higher risk for the development of acute phosphate nephropathy and then avoid the administration of bowel purgatives that contain oral sodium phosphate (OSP), if possible. Specific recommendations for the choice of bowel preparation are discussed elsewhere. (See 'Risk factors' above and "Bowel preparation before colonoscopy in adults".)

There is no specific treatment for established acute phosphate nephropathy. However, acute hemodialysis is likely to be beneficial in the infrequent patient who is diagnosed within 12 to 24 hours after OSP administration and still has marked hyperphosphatemia. As noted above, most patients are diagnosed later, and, since complete recovery of kidney function is rare, these patients should be treated the same as others with chronic kidney disease (CKD). (See 'Acute phosphate nephropathy' above and "Overview of the management of chronic kidney disease in adults".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute kidney injury in adults".)

SUMMARY AND RECOMMENDATIONS

Acute phosphate nephropathy is a clinicopathologic entity that results from colonic cleansing with bowel purgatives that contain oral sodium phosphate (OSP). Acute phosphate nephropathy has also been reported following the administration of sodium phosphate-containing enemas. Acute phosphate nephropathy is usually detected days to months following OSP administration. This entity is complicated by the development of chronic kidney disease (CKD). (See 'Introduction' above.)

The pathogenesis of acute phosphate nephropathy is related to volume depletion and transient OSP-induced hyperphosphatemia and involves precipitation of calcium phosphate crystals in the distal tubule. (See 'Pathogenesis' above.)

Kidney biopsy reveals an acute and chronic tubulointerstitial nephropathy with the distinctive finding of abundant tubular and interstitial deposits of calcium phosphate. In biopsies performed within three weeks of OSP exposure, findings of acute tubular injury predominate and resemble changes seen in acute tubular necrosis. Later biopsies exhibit findings of chronicity, including tubular atrophy and interstitial fibrosis. (See 'Pathology' above.)

The incidence of acute phosphate nephropathy remains unknown. Acute phosphate nephropathy can occur in patients with normal kidney function. (See 'Incidence' above.)

Apparent risk factors for acute phosphate nephropathy include advanced age, hypertension, kidney dysfunction, volume depletion, and the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs). Possible additional risk factors include the use of diuretics, nonsteroidal antiinflammatory agents (NSAIDs) or lithium, the presence of diabetes, and female sex. (See 'Risk factors' above.)

Careful review of all contraindications to the use of OSP should be done prior to selection of a bowel purgative for an individual patient. (See 'Prevention and treatment' above.)

Specific recommendations for the choice of bowel preparation are discussed elsewhere. (See "Bowel preparation before colonoscopy in adults".)

  1. Markowitz GS, Perazella MA. Acute phosphate nephropathy. Kidney Int 2009; 76:1027.
  2. Ori Y, Rozen-Zvi B, Chagnac A, et al. Fatalities and severe metabolic disorders associated with the use of sodium phosphate enemas: a single center's experience. Arch Intern Med 2012; 172:263.
  3. Vanner SJ, MacDonald PH, Paterson WG, et al. A randomized prospective trial comparing oral sodium phosphate with standard polyethylene glycol-based lavage solution (Golytely) in the preparation of patients for colonoscopy. Am J Gastroenterol 1990; 85:422.
  4. Cohen SM, Wexner SD, Binderow SR, et al. Prospective, randomized, endoscopic-blinded trial comparing precolonoscopy bowel cleansing methods. Dis Colon Rectum 1994; 37:689.
  5. Golub RW, Kerner BA, Wise WE Jr, et al. Colonoscopic bowel preparations--which one? A blinded, prospective, randomized trial. Dis Colon Rectum 1995; 38:594.
  6. Tan JJ, Tjandra JJ. Which is the optimal bowel preparation for colonoscopy - a meta-analysis. Colorectal Dis 2006; 8:247.
  7. Desmeules S, Bergeron MJ, Isenring P. Acute phosphate nephropathy and renal failure. N Engl J Med 2003; 349:1006.
  8. Markowitz GS, Stokes MB, Radhakrishnan J, D'Agati VD. Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure. J Am Soc Nephrol 2005; 16:3389.
  9. Markowitz GS, Whelan J, D'Agati VD. Renal failure following bowel cleansing with a sodium phosphate purgative. Nephrol Dial Transplant 2005; 20:850.
  10. Demoulin N, Jadoul M, Cosyns JP, Labriola L. An easily overlooked iatrogenic cause of renal failure. Clin Nephrol 2008; 70:176.
  11. Steinman TI, Samir AE, Cornell LD. Case records of the Massachusetts General Hospital. Case 27-2008. A 64-year-old man with abdominal pain, nausea, and an elevated level of serum creatinine. N Engl J Med 2008; 359:951.
  12. Oral sodium phosphate (OSP) products for bowel cleansing. US Government Printing Office; Center of Drug Evaluation Research, DC 2006.
  13. American Society of Colon and Rectal Surgeons (ASCRS), American Society for Gastrointestinal Endoscopy (ASGE), Society of American Gastrointestinal and Endoscopic Surgeons (SAGES), et al. A consensus document on bowel preparation before colonoscopy: prepared by a task force from the American Society of Colon and Rectal Surgeons (ASCRS), the American Society for Gastrointestinal Endoscopy (ASGE), and the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES). Surg Endosc 2006; 20:1147.
  14. Oral sodium phosphate (OSP) products for bowel cleansing (marketed as Visicol and OsmoPrep), and oral sodium phosphate products available without a prescription. US Govenrment Printing Office; Center of Drug Evaluation Research. US Food and Drug Administration, Washington, DC 2008.
  15. http://www.fda.gov/Drugs/DrugSafety/ucm380757.htm?source=govdelivery&utm_medium=email&utm_source=govdelivery.
  16. Lieberman DA, Ghormley J, Flora K. Effect of oral sodium phosphate colon preparation on serum electrolytes in patients with normal serum creatinine. Gastrointest Endosc 1996; 43:467.
  17. Gumurdulu Y, Serin E, Ozer B, et al. Age as a predictor of hyperphosphatemia after oral phosphosoda administration for colon preparation. J Gastroenterol Hepatol 2004; 19:68.
  18. Murer H, Hernando N, Forster L, Biber J. Molecular mechanisms in proximal tubular and small intestinal phosphate reabsorption (plenary lecture). Mol Membr Biol 2001; 18:3.
  19. Forster IC, Hernando N, Biber J, Murer H. Proximal tubular handling of phosphate: A molecular perspective. Kidney Int 2006; 70:1548.
  20. Heher EC, Thier SO, Rennke H, Humphreys BD. Adverse renal and metabolic effects associated with oral sodium phosphate bowel preparation. Clin J Am Soc Nephrol 2008; 3:1494.
  21. Mishra R, Kaufman D, Mattern J 3rd, Dutta SK. Severe hyperphosphatemia and hypocalcemia caused by bowel preparation for colonoscopy using oral sodium phosphate in end-stage renal disease. Endoscopy 2005; 37:1259.
  22. Wechsler A, Schneider R, Sapojnikov M, et al. Bowel cleansing in patients with chronic renal failure--an often overlooked hazard. Nephrol Dial Transplant 2006; 21:1133.
  23. Fass R, Do S, Hixson LJ. Fatal hyperphosphatemia following Fleet Phospo-Soda in a patient with colonic ileus. Am J Gastroenterol 1993; 88:929.
  24. Hebert LA, Lemann J Jr, Petersen JR, Lennon EJ. Studies of the mechanism by which phosphate infusion lowers serum calcium concentration. J Clin Invest 1966; 45:1886.
  25. Markowitz GS, Nasr SH, Klein P, et al. Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleansing. Hum Pathol 2004; 35:675.
  26. Asplin JR, Mandel NS, Coe FL. Evidence of calcium phosphate supersaturation in the loop of Henle. Am J Physiol 1996; 270:F604.
  27. Verhulst A, Asselman M, De Naeyer S, et al. Preconditioning of the distal tubular epithelium of the human kidney precedes nephrocalcinosis. Kidney Int 2005; 68:1643.
  28. Khurana A, McLean L, Atkinson S, Foulks CJ. The effect of oral sodium phosphate drug products on renal function in adults undergoing bowel endoscopy. Arch Intern Med 2008; 168:593.
  29. Brunelli SM, Lewis JD, Gupta M, et al. Risk of kidney injury following oral phosphosoda bowel preparations. J Am Soc Nephrol 2007; 18:3199.
  30. Tenenhouse HS, Gauthier C, Martel J, et al. Na+ -phosphate cotransport in mouse distal convoluted tubule cells: evidence for Glvr-1 and Ram-1 gene expression. J Bone Miner Res 1998; 13:590.
  31. Hesse A, Heimbach D. Causes of phosphate stone formation and the importance of metaphylaxis by urinary acidification: a review. World J Urol 1999; 17:308.
  32. Hurst FP, Bohen EM, Osgard EM, et al. Association of oral sodium phosphate purgative use with acute kidney injury. J Am Soc Nephrol 2007; 18:3192.
  33. Russmann S, Lamerato L, Marfatia A, et al. Risk of impaired renal function after colonoscopy: a cohort study in patients receiving either oral sodium phosphate or polyethylene glycol. Am J Gastroenterol 2007; 102:2655.
  34. Markowitz GS, Radhakrishnan J, D'Agati VD. Towards the incidence of acute phosphate nephropathy. J Am Soc Nephrol 2007; 18:3020.
  35. Barclay RL. Safety, efficacy, and patient tolerance of a three-dose regimen of orally administered aqueous sodium phosphate for colonic cleansing before colonoscopy. Gastrointest Endosc 2004; 60:527.
  36. Hookey LC, Depew WT, Vanner SJ. A prospective randomized trial comparing low-dose oral sodium phosphate plus stimulant laxatives with large volume polyethylene glycol solution for colon cleansing. Am J Gastroenterol 2004; 99:2217.
  37. Rostom A, Jolicoeur E, Dubé C, et al. A randomized prospective trial comparing different regimens of oral sodium phosphate and polyethylene glycol-based lavage solution in the preparation of patients for colonoscopy. Gastrointest Endosc 2006; 64:544.
  38. Russmann S, Lamerato L, Motsko SP, et al. Risk of further decline in renal function after the use of oral sodium phosphate or polyethylene glycol in patients with a preexisting glomerular filtration rate below 60 ml/min. Am J Gastroenterol 2008; 103:2707.
  39. Ainley EJ, Winwood PJ, Begley JP. Measurement of serum electrolytes and phosphate after sodium phosphate colonoscopy bowel preparation: an evaluation. Dig Dis Sci 2005; 50:1319.
  40. Martin RR, Lisehora GR, Braxton M Jr, Barcia PJ. Fatal poisoning from sodium phosphate enema. Case report and experimental study. JAMA 1987; 257:2190.
  41. Korzets A, Dicker D, Chaimoff C, Zevin D. Life-threatening hyperphosphatemia and hypocalcemic tetany following the use of fleet enemas. J Am Geriatr Soc 1992; 40:620.
  42. Schaefer M, Littrell E, Khan A, Patterson ME. Estimated GFR Decline Following Sodium Phosphate Enemas Versus Polyethylene Glycol for Screening Colonoscopy: A Retrospective Cohort Study. Am J Kidney Dis 2016; 67:609.
  43. Markowitz GS, Bomback AS, Perazella MA. Phosphate enemas and GFR decline: it's premature to sound the alarm. Kidney Int 2016; 90:13.
  44. Gonlusen G, Akgun H, Ertan A, et al. Renal failure and nephrocalcinosis associated with oral sodium phosphate bowel cleansing: clinical patterns and renal biopsy findings. Arch Pathol Lab Med 2006; 130:101.
  45. Fine A, Patterson J. Severe hyperphosphatemia following phosphate administration for bowel preparation in patients with renal failure: two cases and a review of the literature. Am J Kidney Dis 1997; 29:103.
  46. Orias M, Mahnensmith RL, Perazella MA. Extreme hyperphosphatemia and acute renal failure after a phosphorus-containing bowel regimen. Am J Nephrol 1999; 19:60.
  47. Manley P, Somerfield J, Simpson I, et al. Bilateral uraemic optic neuritis complicating acute nephrocalcinosis. Nephrol Dial Transplant 2006; 21:2957.
  48. Aasebø W, Scott H, Ganss R. Kidney biopsies taken before and after oral sodium phosphate bowel cleansing. Nephrol Dial Transplant 2007; 22:920.
  49. Beyea A, Block C, Schned A. Acute phosphate nephropathy following oral sodium phosphate solution to cleanse the bowel for colonoscopy. Am J Kidney Dis 2007; 50:151.
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