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Acute phosphate nephropathy (APN) is an acute renal failure secondary to the use of oral sodium phosphate (OSP) laxatives, with a high risk of progression to chronicity. We report a 60-year-old woman with mixed connective tissue disease whose serum creatinine increased up to 2.0 mg/dL in her regular control tests, without an evident causative factor. Kidney biopsy showed numerous intratubular calcium phosphate deposits, consistent with APN. She had a history of OSP laxative intake, and a sodium phosphate enema was used before a colonoscopy performed six months earlier. The temporal association between the use of OSP laxatives and acute kidney injury, should lead to the suspicion of APN. The urine sediment is generally normal or with mild to moderate proteinuria. The diagnosis is confirmed with a kidney biopsy. Until now, there is no specific treatment for APN, thus prevention is essential. In high-risk patients for developing APN, the administration of these laxatives should be avoided.

Background Acute phosphate nephropathy (APN) is a disease that can occur when exposed to high doses of phosphate. The most common cause of APN is the use of oral sodium phosphate for bowel cleansing preparations. However, there are other less commonly known sources of phosphate that are equally important. To date, our literature search did not identify any report of excessive dietary phosphate as a cause of APN. Case summary We report an unusual case of a 39-year-old diabetic male who presented with epigastric pain and oliguria. Work-up showed elevated serum creatinine, potassium, and calcium-phosphate product, and metabolic acidosis. The patient was admitted in the intensive care unit and received emergent renal replacement therapy. Kidney biopsy revealed tubular cell injury with transparent crystal casts positive for Von Kossa staining, which established the diagnosis of APN. Conclusion This case confirmed that APN may occur with other sources of phosphorus, highlighting the importance of good history taking and kidney biopsy in patients with predisposing factors for APN. Raising awareness on the possibility of APN and its timely recognition and management is imperative so that appropriate measures can be instituted to prevent or delay its progression to end stage renal disease.

Acute phosphate nephropathy (APN) is a form of kidney injury that classically occurs following the use of bowel purgatives and enemas that contains oral sodium phosphate (OSP). We present here an unusual case occurring in the setting of OSP replacement use in a patient without pre-existing renal impairment.

Acute Phosphate Nephropathy is a clinical and pathological finding characterized by acute and subsequent chronic renal failure following the use of intestinal cleansers containing sodium phosphate. The pathophysiology of Acute Phosphate Nephropathy occurs due to the increase of sodium and water absorption in the proximal tubules due to hypovolemia, and the accumulation of calcium phosphate load in the distal tubules in the collector and distal canals. Renal biopsy findings include acute and chronic tubular damage with tubular and interstitial calcium phosphate deposits. Prevention of Acute Phosphate Nephropathy can be achieved by hydration before and after the use of calcium phosphate in risky patients, minimizing the sodium phosphate dose, and having 12-hour intervals between sodium phosphate applications. In this article, we aimed to present the patients who used sodium phosphate for colonoscopy and developed Acute Phosphate Nephropathy.

Background and study aims Colonoscopy is a widely used diagnostic procedure which requires prior cleansing of the bowel. Many different bowel cleansing preparations have been developed, all of which have specific advantages and disadvantages. This review compares two low-volume high-osmolarity bowel cleansing preparations, oral phosphate salts and oral sulphate salts, with a particular focus on risk of nephrotoxicity.Patients and methods An electronic search of the Medline database was performed using the search terms “(phosphates OR sulfates) AND cathartics [MeSH Term] AND kidney” restricted to humans with a cut-off date of December 31, 2016.Results Introduction of oral phosphate salts offered the advantage of low intake volume and low risk of bowel irritation compared to previous options. However, phosphate salts have been associated with renal toxicity (acute phosphate nephropathy [APN]), thought to arise due to perturbations of calcium and phosphate homeostasis as a consequence of increases in serum phosphate. This results in high concentrations of calcium phosphate in the distal tubule and collecting ducts of the kidney, where it may precipitate. Although APN is rare, it may lead to permanent kidney damage. For this reason, phosphate salts are contraindicated in vulnerable patient groups. As an alternative to phosphate salts, oral sulphate salts have recently been introduced. Because sulphate absorption from the intestinal tract is saturable, serum sulphate concentrations increase only minimally after ingestion. Furthermore, excretion of sulphate in the kidney is not accompanied by calcium excretion and urine calcium levels are unchanged. For these theoretical reasons, use of sulphate salts as bowel cleansing solutions is not expected to lead to calcium precipitation in the nephron.Conclusions Oral phosphate salts are no longer recommended for routine use as bowel cleansing preparations as they carry significant risk of kidney damage and a safer alternative is available in the form of oral sulphate solutions. To date, use of sulphate salts has not been associated with elevations in serum creatinine or other markers of renal impairment, nor with clinical manifestations of kidney injury. Nonetheless, experience with sulphate salts in everyday practice is limited and physicians should be vigilant in detecting potential safety issues.

It is known that oral sodium phosphate, used as bowel preparation for colonoscopy, can cause acute phosphate nephropathy, a potentially severe and irreversible form of acute kidney injury. Due to these safety concerns, guidelines have advised against the routine use of this agent for a decade. We present a case report and biopsy series that demonstrate that oral sodium phosphate is still being used and that cases of APN are still occurring, in Australia.

Background and objectives Screening colonoscopy with polipectomy reduces colonorectal cancer incidence and mortality. An adequate bowel cleansing is one of the keys to achieving best results with this technique. Oral sodium phosphate solution (OSP) had a widespread use in the 90s decade. Its efficacy was similar to polyethylene glycol (PEG) solution, but with less cost and convenient administration. Series of patients with acute renal failure due to OSP use have been reported. However, large cohorts of patients found no difference in the incidence of renal damage between these two solutions. Methods From 2006 to 2009 we identified twelve cases of phosphate nephropathy after colonoscopy prepared with OSP. All patients were followed up to six months. All patients had received just a single dose. Results We analyzed 12 cases with phosphate nephropathy; three patients debuted with AKI and nine patients had chronic renal injury. Four cases were confirmed with renal biopsy. One patient with AKI needed hemodialysis at diagnosis without subsequent recovery. Two patients (both with chronic damage) fully recovered their previous renal function. The remaining patients (nine) had an average loss of estimated glomerular filtration rate of 24 ml/min/1.73 m2. Conclusions The use of OSP can lead to both acute and chronic renal damage. However, chronic injury was the most common pattern. Both forms of presentation imply a significant and irreversible loss of renal function. Further studies analyzing renal damage secondary to bowel cleaning should consider these two different patterns of injury.

A 63-year-old woman presented with intestinal disorder, alternating between obstipation and diarrhoea. Sodium phosphate/diphosphate (Fleet®) was used in preparation for colonoscopy. Within 24 h the patient developed severe hyperphosphatemia and oliguric acute kidney failure with the need of renal replacement therapy. This case illustrates the rare event of phosphate nephropathy after colonoscopy.

Protocols are commonly used in the hospitals around the world and enable health care organizations to put evidence into practice and provide a framework for the management of the individual patient. Such standardization of practice is felt to reduce variations in practice and improve quality of care. However, the protocols have advantages and disadvantages. I present a case where activation of the protocols for “Electrolyte, phosphate and magnesium replacement” at the time of admission to the hospital, resulted in harm to the patient because of inappropriate timing of the test(s) with a resulting action to correct the expected laboratory abnormality. Timing of tests and administration of various medications including antibiotics in hospitalized dialysis patients is important, and both the physicians and the nursing staff require vigilance when requesting/performing tests and ordering/administering medications to dialysis patients.

A 65-year-old woman was admitted to the hospital with an elevated serum creatinine concentration associated with leukocyturia and erythrocyturia. Past medical history analysis revealed that four months before current hospitalization she had been subjected to colonoscopy preceded by the administration of oral sodium phosphate solution (OSP) as preparation for this procedure. Kidney biopsy revealed mild chronic tubulo-interstitial inflammation and scarring with prominent cortical tubular calcium phosphate deposits. The diagnosis of phosphate nephropathy, most probably secondary to OSP ingestion was made. During follow-up the renal function remained impaired but stable with eGFR of 25 ml/min/1.73 m². The patient is currently under the care of the nephrology clinic.

Nephrocalcinosis is characterized by aberrant deposition of calcium in the kidneys and is seen in phosphate nephropathy, primary hyperparathyroidism, and distal renal tubular acidosis. To further evaluate the specific pathophysiologic role of T cells in ectopic calcification, we used DBA/2 mice that are prone to develop nephrocalcinosis and dystrophic cardiac calcinosis. Female DBA/2 mice were depleted of T cells ( n = 10) or regulatory T cells (Tregs) ( n = 15) using either an anti-CD3ɛ or an anti-CD25 monoclonal antibody and compared with isotype-treated controls ( n = 9; n = 15), respectively. After this immunomodulation, the DBA/2 mice were given a high-phosphate diet for 9 days and the degree of calcification was assessed by microcomputed tomography. Successful depletion was confirmed by flow cytometry of splenocytes. In DBA/2 mice, the high-phosphate diet induced a phenotype of nephrocalcinosis and dystrophic cardiac calcinosis. T-cell depletion significantly increased renal calcification in microcomputed tomography ( P = 0.022). Concordantly, Treg depletion significantly deteriorated acute phosphate nephropathy ( P = 0.039) and was associated with a significantly increased mortality rate ( P = 0.004). Immunomodulation had no impact on the amount of cardiac calcification. Semiquantitative histopathologic evaluations with Alizarin Red staining independently confirmed the respective radiologic measurements. In summary, our data suggest a pivotal role of T cells, particularly Tregs, in the progression of nephrocalcinosis and emphasize the fact that inflammation deteriorates the outcome in acute phosphate nephropathy.

An 86-year-old woman developed acute kidney injury after colonoscopy. A renal biopsy showed diffuse tubular injury with minimal calcium phosphate deposits (CPDs), which were thought to be caused by an oral sodium phosphate bowel purgative before colonoscopy. According to these findings, she was diagnosed with acute phosphate nephropathy (APhN). In contrast to previous reports of diffuse tubular injury associated with tubular CPDs in APhN, this case demonstrated diffuse tubular injury despite a limited distribution of CPDs, suggesting that calcium phosphate can cause tubular injury without deposition. This case thus supports the hypothesis that urinary calcium phosphate crystals may cause tubular injury via other mechanisms, including inflammatory cytokines.

Oral sodium phosphate solutions can cause acute phosphate nephropathy, resulting in acute kidney injury and chronic kidney disease. A recent cohort study suggests that phosphate enemas may also be associated with a decline in glomerular filtration rate, but further study is needed to establish a causal relationship.

An adolescent with acute lymphoblastic leukemia developed an early and severe tumor lysis syndrome with acute kidney injury after a low and single dose of steroids. Renal dysfunction was attributed primarily to phosphate nephropathy with nephrocalcinosis due to extreme elevations of phosphate in blood. Urinary alkalinization probably contributed to this development. We used peritoneal dialysis with resolution of nephrocalcinosis and normalization of creatinine clearance.

The U.S. Congress [PL 107–188] amended the Safe Drinking Water Act and required each community water system serving more than 3,000 people to conduct vulnerability assessments. These assessments address potential circumstances that could compromise the safety and reliability of municipal water. The present evaluation concerns the concentrations of the blended phosphates (also known as polyphosphates, condensed complex phosphates, polyphosphate glassy balls, and pyrophosphates) intended to aid regulatory agencies in decisions to avoid contact with affected water. Polyphosphates are direct food additives and they are used to treat municipal drinking water, but depending upon the concentration and duration of exposure these substances can induce chemical burns. Ingested polyphosphates are degraded by phosphatase enzymes to monophosphates, substances that are over-the-counter bowel purgatives. High oral doses of the monophosphates can induce transient hyperphosphatemia in older and susceptible young people, which can lead to acute phosphate nephropathy. In some patients, the condition is fatal. Based on the acute diarrhea after the ingestion of a single oral dose of monobasic (NaH2PO4) and dibasic (Na2HPO4) monophosphates in adults, a do not consume concentration of 600 mg PO4/L can be derived. Based on mild local irritation after topical application of 1.0% sodium metaphosphate [(NaPO3)6 • H2O] to intact skin of sensitive volunteers, a do not use concentration of 8,000 mg PO4/L can be assigned. Given the lack of eye irritation in rabbits after direct instillation of 0.2% (NaPO3)6 • H2O, an acute ocular contact limit of 50 mg PO4/L serves as the overall do not use level.

Aim Sodium-phosphate-containing colonoscopy preparations cause renal failure by the development of calcium phosphate nephropathy. Although Fleet’s Phospho-Soda has been removed from the US market, sodium phosphate tablets sold as OsmoPrep and Visicol remain available. Our aim was to analyse renal risks of the sodium phosphate tablets. Method We conducted a retrospective study using the US Food and Drug Administration Adverse Event Reporting System, a voluntary reporting system available for public access. Renal adverse events were identified using search terms including renal impairment, increased blood urea nitrogen, increased creatinine, renal failure, acute renal failure, chronic renal failure, acute phosphate nephropathy, nephrocalcinosis, renal tubular necrosis, haemodialysis, nephropathy toxic, dialysis, peritoneal dialysis, renal injury, renal tubular disorder, decreased glomerular filtration rate and decreased creatinine clearance. Patient age, gender and body weight were compared with data for the general population in the National Health and Nutrition Examination Survey (NHANES). Results In total 2 097 223 files were extracted from the US Food and Drug Administration website for 2004–2008 and the first 9 months of 2009. Of these, 178 patients on tablet preparations (71% women) were identified, with increasing numbers of renal adverse drug reactions reported from tablet preparations each year. The mean weight for women with renal complications from tablet preparations was 68.57 ± 1.78 kg, significantly lower than the national average weight of 74 ± 0.5 kg for the same age group (P = 0.003) in NHANES. Conclusion Renal adverse drug reactions from sodium phosphate tablets are more common in women with a mean body weight lower than the national average weight.

We established a murine model of phosphate nephropathy with secondary hyperparathyroidism. db/db mice, which develop obesity and type 2 diabetes mellitus, were uninephrectomized at the age of 6 weeks and were fed either standard chow or a phosphorus-rich diet during the next 8 weeks. Thereafter, renal cryosections showed abundant tubular casts with a strong histochemical von Kossa reaction in all db/db mice on the phosphorus-rich diet but none in the controls. X-ray diffraction and Raman spectroscopy proved that these tubular casts consist mostly of hydroxyapatite Ca 5 (PO 4 ) 3 (OH). These intraluminal precipitations were located in distal tubuli and collecting ducts and were associated with degenerative tubular changes and peritubular infiltration of T cells and macrophages. In line, kidneys of db/db mice on the phosphorus-rich diet displayed significantly increased mRNA expression of the T H 1 cytokines interferon γ, IL-6, and tumor necrosis factor α. In addition, mice developed signs of secondary hyperparathyroidism as shown by elevated serum phosphate, decreased serum calcium, and increased parathyroid hormone, osteopontin, and fibroblast growth factor 23 levels. db/db mice on the phosphorus-rich diet also presented with significantly lower body weight, lower homeostasis model assessment of insulin resistance index, and hypertrophic cardiomyopathy. Thus, we provide a murine model of phosphate nephropathy and secondary hyperparathyroidism, which can be used for future pharmacologic and pathophysiologic studies to analyze the effect of hyperphosphatemia on renal, metabolic, and cardiovascular phenotypes.

Hypophosphatemia is a common complication after kidney transplant, affecting >90% of patients. However, no specific recommendations for phosphate repletion exist for transplant recipients. We report a case of a 70-year-old highly sensitized woman with end-stage renal disease caused by diabetic nephropathy who underwent deceased donor kidney transplant. Four weeks later, she was noted to have hypophosphatemia with undetectable serum phosphate levels, and she reported mild diarrhea. She was started on oral phosphate supplementation. On a routine visit 2 weeks later, she was found to have an acute increase in serum creatinine level and kidney biopsy was performed. We discuss the causes, management, and complications of hypophosphatemia in kidney transplant.

Efficient cleansing of the colon before a colonoscopy or a radiological examination is essential. The osmotically acting cathartics (those given the Anatomical Therapeutic Chemical code A06AD) currently used for this purpose comprise products based on three main substances: sodium phosphate, combinations of polyethylene glycol and electrolyte lavage solutions (PEG-ELS), and magnesium citrate. All these preparations give adequate cleansing results and have similar profiles in terms of the frequency and type of mild to moderate adverse effects. However, serious adverse events, such as severe hyperphosphatemia and irreversible kidney damage owing to acute phosphate nephropathy, have been reported after use of sodium‑phosphate‑based products. The aim of this Review is to provide an update on the potential safety issues related to the use of osmotically acting cathartics, especially disturbances of renal function and water and electrolyte balance. The available evidence indicates that PEG-ELS ‑based products are the safest option. Magnesium‑citrate‑based, hypertonic products should be administered with caution to elderly individuals and patients who are prone to develop disturbances in water and electrolyte balance. Sodium‑phosphate‑based products can occasionally cause irreversible kidney damage and should not be routinely used in bowel‑cleansing procedures.

We report a case of APN after OSP use in a patient with nephrotic syndrome (NS). Renal biopsy revealed minimal change disease with multifocal calcium phosphate deposits within the tubules and in the interstitium. The serum level of fetuin-A, a systemic calcification inhibitor, was low during severely proteinuric state but normalized after remission of NS. To verify whether fetuin-A levels are low in NS patients, serum fetuin-A levels were determined in 10 patients with NS and 10 with asymptomatic microscopic hematuria (H). The mean serum fetuin-A levels were significantly lower in the NS group compared to the H group (p < 0.01). This finding suggests that a lower serum fetuin-A level may be associated with APN after OSP use in patients with NS, thus careful attention should be paid when colonoscopy using OSP is scheduled in this population.

Fleet enemas are hypertonic solutions with an osmotic action and a high concentration of phosphate. When retained in the human body they have a great toxic potential, causing severe hydro-electrolyte disorders in children, especially in newborns. We report the case of a previously healthy 8-day-old newborn who needed neonatal intensive care treatment after the inadvertent administration of an osmotically active hypertonic phosphate enema. Taking into account that phosphate removal by peritoneal dialysis (PD) strongly depends on total dialysate turnover, we chose continuous flow PD (CFPD) as the treatment option, with a successful outcome. Clinical experience with this dialytic modality is limited to a few case reports in pediatric and adult patients. To the best of our knowledge, we report here the first description of CFPD in the setting of acute phosphate nephropathy in the neonatal period. The modality of PD described here has potential as an alternative management option as it is a highly efficient, methodologically simple, and low-cost method without any need for sophisticated equipment. Physicians and parents should be aware of the adverse effects of a hypertonic phosphate enema and should never use these medications in infants and newborns.

Acute phosphate nephropathy following a large phosphate load is a potentially irreversible cause of kidney failure. Here, we report on the unfavorable graft outcome in two recipients of deceased donor kidneys from a donor who had evolving acute phosphate nephropathy at the time of organ procurement. The donor, a 30-year-old with cerebral infarction, developed hypophosphatemia associated with diabetic ketoacidosis and was treated with intravenous phosphate resulting in a rise in serum phosphorus from 0.9 to 6.1 mg/dL. Renal biopsies performed on both recipients for suboptimal kidney function revealed acute tubular injury and diffuse calcium phosphate microcrystal deposits in the tubules, which were persistent in subsequent biopsies. A retrospective review of preimplantation biopsies performed on both kidneys revealed similar findings. Even though initial renal histology in both recipients was negative for BK virus, they eventually developed BK viremia with nephropathy but both had a substantive virologic response with therapy. The first patient returned to dialysis at 6 months, while the other has an estimated glomerular filtration rate of 12 mL/min, 17 months following his transplant. We conclude that unrecognized acute phosphate nephropathy in a deceased donor contributed substantially to poor graft outcome in the two recipients.

An oral sulfate salt solution (OSS), under development as a bowel cleansing agent for colonoscopy in humans, is studied in rats and dogs. In rats, amaximumpractical oral OSS dose (5 g/kg/d) is compared with an oral sodium phosphate (OSP) solution, both at about 7 times the clinical dose. OSS induces the intended effects of loose stools and diarrhea. In rats, higher urine sodium and potassium accompany higher clearance rates, considered adaptive to the osmotic load of OSS. OSS for 28 days is well tolerated in rats and dogs. In contrast, OSP causes increased mortality, reduced body weight and food consumption, severe kidney tubular degeneration, and calcium phosphate deposition in rats. These are accompanied by mineralization in the stomach and aorta, along with cardiac and hepatic degeneration and necrosis. The greater safety margin of OSS over OSP at similarmultiples of the clinical dose indicates its suitability for human use.

Background Acute phosphate nephropathy (APN) is a clinicopathological entity causing renal failure, after ingestion of oral sodium phosphate solution (OSPS). Approximately 25 cases have been described, but OSPS is still widely used. This study reports a further 5 cases and discusses the ever-growing significance of APN. Methods Five cases of APN were included, 3 retrospectively whereas 2 were diagnosed prospectively. In all, use of OSPS was established, and other causes of nephrocalcinosis were excluded. Results Average age was 67.4 ± 7.0 years, with a female preponderance (4:1). All patients had hypertension. Baseline serum creatinine: 0.7 to 1.2 mg/dL (creatinine clearance: 52 to 77 mL/min). Time from colonoscopy to presentation was 56 ± 36 days. Serum creatinine levels at presentation: 1.4 to 3.6 mg/dL. Time from colonoscopy to renal biopsy was 123 ± 88 days. Urinalysis showed minimal proteinuria, leucocyturia, and hematuria. One patient had renal glucosuria. All patients were anemic (hemoglobin 8.8–11.4 gr/dL). Serum calcium and phosphate were normal. One required hemodialysis. Mean follow-up was 36 ± 17 months. Serum creatinine levels at end of follow-up were 1.3 to 3.1 mg/dL. Renal function did not recover completely in any patient. Four required long-term erythropoietin treatment. The prominent histopathological findings were calcium–phosphate tubular depositions (100%), interstitial fibrosis (80%), hypertensive changes (80%), and acute tubular degenerative and regenerative changes (60%). Conclusions APN is a serious, irreversible renal complication of OSPS. It is probably under-recognized. Risk factors include female gender, older age, hypertension, and renal failure, although it may occur with preexisting normal renal function.

Acute phosphate nephropathy after bowel preparation with oral sodium phosphate (OSP) for colonoscopy has emerged as an important clinical entity. In 2004, five cases of nephrocalcinosis and irreversible renal failure after bowel preparation with OSP were reported. More recently, several retrospective studies have shown that the incidence of acute kidney injury after OSP use is in the range of 1-4%, similar to the incidence of contrast nephropathy in the general population. The degree of renal failure is not generally as severe as in the first reported cases, but irreversible damage can still occur. Millions of people worldwide undergo screening colonoscopies for colon and rectal cancer after the age of 50, so careful patient selection and monitoring for possible complications is essential when OSP is used. In addition to educating patients about the possibility of renal damage, physicians should routinely watch for considerable weight loss during bowel preparation and correct the fluid deficit as needed. Carrying out a renal function panel, which includes serum phosphorus level, is prudent after colonoscopy. Alternative bowel cleansing agents are needed because calcium phosphate precipitation is inevitable after OSP use even in the normal kidney.

Oral sodium phosphate (OSP) is a commonly used purgative before colonoscopy. There have been numerous reports of acute phosphate nephropathy attributed to the use of OSP. This study evaluated the association between the use of OSP and acute kidney injury (AKI) in an observational, retrospective, cohort study. Of 9799 patients who underwent colonoscopy and had serum creatinine values recorded within 365 days before and after the procedure, AKI, defined as > or =50% increase in baseline serum creatinine, was identified in 114 (1.16%). After adjustment for significant covariates in a multiple logistic regression model, the use of OSP was associated with increased risk for AKI (odds ratio 2.35; 95% confidence interval 1.51 to 3.66; P < 0.001) with an adjusted number need to harm of 81. Age was also independently associated with AKI in this cohort; therefore, until larger, prospective studies define the population at risk for acute phosphate nephropathy, the use of polyethylene glycol-based purgatives should be considered for older patients and possibly for those with comorbid medical conditions.

Acute phosphate nephropathy is an accepted complication of the use of phosphate preparations in patients about to undergo colonoscopy. Age, renal failure, and the ongoing use of medications, such as angiotensin-converting enzyme inhibitors and/or angiotensin-receptor blockers, are now recognized as risk factors for the development of phosphate nephropathy. The presence of any of these risk factors necessitates careful attention to avoiding excessive dehydration in the process of bowel cleansing. In so doing, the likelihood of acute phosphate nephropathy occurring can be lessened.

A74-year-old woman presented with a 2-day history of abdominal pain and nausea, 1 week after undergoing upper and lower endoscopies. Her comorbidities included hypertension, dyslipidaemia, sigmoid diverticulosis, transient ischaemic attack, peripheral vascular disease and mild valvular heart disease.

Sodium phosphate purgatives are used for bowel preparation before endoscopic or radiologic examination and occasionally for treatment of severe obstipation. Generally, they are well tolerated and effective; however, safety concerns exist regarding serious renal injury and electrolyte disturbances after administration of these drugs.The review presents complications associated with the use of agents containing sodium phosphate with regard to electrolyte disorders and renal impairment, namely acute phosphate nephropathy (APhN). This paper discusses the pathophysiology, histopathological findings, clinical symptoms, diagnosis and treatment of APhN. Additionally, it examines the epidemiology of adverse renal events and the safety of using sodium phosphate preparations prior to colonoscopy.Because of safety concerns, sodium phosphate purgatives are not recommended for routine bowel cleansing. Despite some serious and even fatal adverse events associated with these drugs when used with at-risk patients, available data suggest that administration of sodium phosphate purgatives is relatively safe in nonrisk individuals(i.e., in adequately hydrated, otherwise healthy adults, younger than 55 years with evidence of normal renal function).

Prior to colonoscopy, bowel cleansing is performed for which frequently oral sodium phosphate (OSP) is used. OSP results in significant hyperphosphatemia and cases of acute kidney injury (AKI) referred to as acute phosphate nephropathy (APN; characterized by nephrocalcinosis) are reported after OSP use, which led to a US-FDA warning. To improve the safety profile of OSP, it was evaluated whether the side-effects of OSP could be prevented with intestinal phosphate binders. Hereto a Wistar rat model of APN was developed. OSP administration (2 times 1.2 g phosphate by gavage) with a 12h time interval induced bowel cleansing (severe diarrhea) and significant hyperphosphatemia (21.79 ± 5.07 mg/dl 6h after the second OSP dose versus 8.44 ± 0.97 mg/dl at baseline). Concomitantly, serum PTH levels increased fivefold and FGF-23 levels showed a threefold increase, while serum calcium levels significantly decreased from 11.29 ± 0.53 mg/dl at baseline to 8.68 ± 0.79 mg/dl after OSP. OSP administration induced weaker NaPi-2a staining along the apical proximal tubular membrane. APN was induced: serum creatinine increased (1.5 times baseline) and nephrocalcinosis developed (increased renal calcium and phosphate content and calcium phosphate deposits on Von Kossa stained kidney sections). Intestinal phosphate binding (lanthanum carbonate or aluminum hydroxide) was not able to attenuate the OSP induced side-effects. In conclusion, a clinically relevant rat model of APN was developed. Animals showed increased serum phosphate levels similar to those reported in humans and developed APN. No evidence was found for an improved safety profile of OSP by using intestinal phosphate binders.

Acute phosphate nephropathy is a form of acute kidney injury (AKI) due to oral sodium phosphate (ONaP) purgatives used for bowel cleansing before colonoscopy. Usually, 45 ml ONaP is given two times daily 12-24 hours prior to colonoscopy. Intestinal absorption is followed by transient hypocalcemia and hyperphosphatemia in almost all patients. In addition, severe hyperphosphatemia, symptomatic hypocalcemia, hypernatremia, hypocalcemia, hyponatremia, hypokalemia, high anion gap metabolic acidosis and AKI can be seen. The patient presented in this paper is a 65-year-old female. She was diagnosed with type 2 diabetes mellitus and hypertension. Colonoscopy was performed in order to investigate the etiology of iron deficiency anemia. ONaP was administered for preparation of colonoscopy and AKI which was clinically compatible with APN developed after the procedure. KEY wORdS: Acute phosphate nephropathy, Colonoscopy, Oral sodium phosphate doi: 10.5262/tndt.2013.1001.19 Yazisma Adresi: omer Celal ElCIOglu Saglik Bakanligi Istanbul Medeniyet Universitesi, Goztepe Egitim ve Arastirma Hastanesi, Nefroloji, Bilim Dali, Istanbul, Turkiye Tel : 0 212 570 92 87 E-posta : o.c.elcioglu@gmail.com Gelis Tarihi : 09.07.2012 Kabul Tarihi : 05.08.2012 dir. Ayrica ciddi hiperfosfatemi, semptomatik hipokalsemi, hipernatremi, semptomatik hiponatremi; hipokalemi, yuksek anyon acikli metabolik asidoz ve ABH gorulebilmektedir. Bu yazida ONaP ile kolonoskopi hazirligi yapildiktan sonra ABH gelismis bir

Intratubular calcification is a common finding in renal allografts. However, possible harmful effect of this calcification is not well recognized, and allograft failure purely due to this condition has not been reported. We report a kidney transplant recipient who suffered from severe secondary hyperparathyroidism and unexplained early allograft failure. A diagnosis of acute phosphate nephropathy was made subsequently based on serial allograft biopsy findings. This case calls for a high index of suspicion to look for this rare cause of allograft dysfunction among high-risk patients. It also highlights the importance of good calcium–phosphate control before renal transplantation.

Liver or gastrointestinal (GI) disease may sometimes be a cause or a consequence of CKD. Symptoms or signs of liver or GI tract disease may thus be a clue to CKD etiology. We review some etiologies: they include among others glomerulonephritis induced by the hepatitis B or C virus and oxalate nephropathy from steatorrhea due to small bowel or pancreatic disease. Liver or GI tract disease may also be more prevalent (associated with) or the consequence of CKD. We first discuss the reasons for the increased prevalence of hepatitis B and C virus in CKD, their implications, and the management of chronic hepatitis in CKD. Similarly, angiodysplasia is more prevalent too in CKD and should be given priority in the differential diagnosis of GI tract hemorrhage in CKD. We further discuss the role of drugs in the onset of GI tract symptoms in CKD patients. Indeed, both nausea/vomiting and bowel movement disturbances can be drug-induced. Several classes of drugs used frequently in CKD may be incriminated. These include phosphate binders, potassium-binding resins, iron preparations, immunosuppressants, etc. Finally, we emphasize 2 recent KDIGO recommendations: oral phosphate-containing bowel preparations should not be used in people with a GFR