Acute Phosphate Nephropathy Research Articles

A Case of Acute Phosphate Nephropathy after Colonoscopy

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

Emergency do not consume/do not use concentrations for blended phosphates in drinking water

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 (NaH2PO(4)) and dibasic (Na2HPO(4)) monophosphates in adults, a do not consume concentration of 600 mg PO(4)/L can be derived. Based on mild local irritation after topical application of 1.0% sodium metaphosphate [(NaPO(3))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% (NaPO(3))6 • H2O, an acute ocular contact limit of 50 mg PO4/L serves as the overall do not use level.

A case of biopsy-proven chronic kidney disease on progression from acute phosphate nephropathy

Acute phosphate nephropathy (APhN) following oral sodium phosphate solution (OSP) ingestion as a bowel purgative has been frequently reported. It was recently suggested that APhN could progress to chronic kidney disease (CKD) and a history of APhN might be considered as one of the causes of CKD. However, there are few reports proving APhN as a cause of CKD. Here, we report a case of APhN that progressed to CKD, as proven by renal biopsy.

Renal risks of sodium phosphate tablets for colonoscopy preparation: a review of adverse drug reactions reported to the US Food and Drug Administration

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. 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). 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. Renal adverse drug reactions from sodium phosphate tablets are more common in women with a mean body weight lower than the national average weight.

Fire extinguisher: an imminent threat or an eminent danger?

Acute phosphate toxicity following rectal administration of phosphate-containing preparations was documented earlier. However, acute phosphate toxicity due to inhalation of monoammonium phosphate (MAP) is rarely reported. The present report describes the systemic toxicity following intentional inhalation of MAP, a dry chemical powder present in fire extinguishers, in a 25-year-old healthy man with normal renal function resulting in hyperphosphatemia (11.0 mg/dL), hypocalcemia (ionized calcium, 1.18 mg/dL; total calcium, 3.6 mg/dL), hypomagnesemia (1.2 mg/dL), seizures, and 4 episodes of pulseless polymorphic ventricular tachycardia requiring defibrillation. In view of the easy accessibility of fire extinguishers and its likely use for suicidal or homicidal purposes, physicians and practitioners working in emergency departments should be aware of this entity. Early recognition, removal of phosphate by hemodialysis, and supportive care have prevented this case from acute phosphate nephropathy and further complications.

Hypophosphatemia in Kidney Transplant Recipients: Report of Acute Phosphate Nephropathy as a Complication of Therapy

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.

Lower body weight and female gender: Hyperphosphatemia risk factors after sodium phosphate preparations

Casais et al have reported an inverse correlation between serum phosphate and body weight after administration of sodium phosphate at a dose of 60 g. Our group has already described the relationship between body weight and hyperphosphatemia with these preparations, although our study was not quoted by Casais. We performed a pharmacokinetic study involving 13 volunteers who were divided into two groups on the basis of body weight: group I consisting of seven women with a median weight of 60 kg and group II consisting of five men and one woman with a median weight of 119.2 kg. Group I developed higher peak phosphate levels and maintained these levels above the subjects in Group II for a prolonged time period despite adequate hydration being ensured with frequent monitoring of weight, fluid intake and total body weight. Our study demonstrated that adequate hydration does not protect against the secondary effects of hyperphosphatemia. In the study by Casais et al, 66% of the study subjects were women, the correlation between serum phosphate and gender in their data also appears to be important. Women are at higher risk of acute phosphate nephropathy due to a diminished volume of distribution of the high dose of ingested phosphate. Decreased volume of distribution in women is due to diminished body weight. This is further compounded by decreased creatinine clearance in females.

Incidence and Outcome of Acute Phosphate Nephropathy in Iceland

BackgroundOral sodium phosphate solutions (OSPS) are widely used for bowel cleansing prior to colonoscopy and other procedures. Cases of renal failure due to acute phosphate nephropathy following OSPS ingestion have been documented in recent years, questioning the safety of OSPS. However, the magnitude of the problem remains unknown.Methodology/Principal FindingsWe conducted a population based, retrospective analysis of medical records and biopsies of all cases of acute phosphate nephropathy that were diagnosed in our country in the period from January 2005 to October 2008. Utilizing the complete official sales figures of OSPS, we calculated the incidence of acute phosphate nephropathy in our country. Fifteen cases of acute phosphate nephropathy were diagnosed per 17,651 sold doses of OSPS (0.085%). Nine (60%) were women and mean age 69 years (range 56–75 years). Thirteen patients had a history of hypertension (87%) all of whom were treated with either ACE-I or ARB and/or diuretics. One patient had underlying DM type I and an active colitis and one patient had no risk factor for the development of acute phosphate nephropathy. Average baseline creatinine was 81.7 µmol/L and 180.1 at the discovery of acute renal failure, mean 4.2 months after OSPS ingestion. No patient had a full recovery of renal function, and at the end of follow-up, 26.6 months after the OSPS ingestion, the average creatinine was 184.2 µmol/L. The average eGFR declined from 73.5 ml/min/1.73 m2 at baseline to 37.3 ml/min/1.73 m2 at the end of follow-up. One patient reached end-stage renal disease and one patient died with progressive renal failure.Conclusion/SignificanceAcute phosphate nephropathy developed in almost one out of thousand sold doses of OSPS. The consequences for kidney function were detrimental. This information can be used in other populations to estimate the impact of OSPS. Our data suggest that acute phosphate nephropathy may be greatly underreported worldwide.

The safety of osmotically acting cathartics in colonic cleansing

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.

A case of acute phosphate nephropathy in a patient with nephrotic syndrome and decreased serum fetuin-A

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.

Flow-through peritoneal dialysis in neonatal enema-induced hyperphosphatemia

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.

Sodium Phosphate Tablets and Acute Phosphate Nephropathy: How Much Hydration Is “Adequate”?

Sodium Phosphate Tablets and Acute Phosphate Nephropathy: How Much Hydration Is “Adequate”?

Acute phosphate nephropathy after bowel cleansing: still a menace

Acute phosphate nephropathy after bowel cleansing: still a menace

Acute phosphate nephropathy

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. 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. 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.

Acute phosphate nephropathy

Acute phosphate nephropathy (APhN) is a clinical pathological entity characterized by acute and subsequent chronic renal failure following exposure to oral sodium phosphate (OSP) bowel purgatives. Renal biopsy findings include acute and chronic tubular injury with prominent tubular and interstitial calcium phosphate deposits. Risk factors for APhN include older age, female gender, hypertension, chronic kidney disease (CKD), and treatment with angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and diuretics. The pathomechanism of APhN involves hypovolemia-induced avid proximal salt and water reabsorption, delivery of a large phosphate load to the distal nephron, and precipitation of calcium phosphate in the distal tubule and collecting duct. To date, 37 cases of biopsy-proven APhN have been reported, and epidemiologic studies have produced inconsistent results regarding the incidence of acute kidney injury (AKI) following the use of OSP purgatives. OSP solution was withdrawn from the market in December of 2008, but OSP tablets, offered by prescription only, remain available. Prevention of APhN is best achieved by avoiding OSP in high-risk patients, aggressive hydration before, during, and after OSP administration, minimizing the dose of OSP, and maintaining a minimum of a 12 h interval between OSP administrations.

Crystalluric and tubular epithelial parameters during the onset of intratubular nephrocalcinosis: illustration of the 'fixed particle' theory in vivo

The 'fixed particle' theory states that, besides crystal formation in the tubular fluid, crystal adhesion to the tubular epithelium is a prerequisite for the development of intratubular nephrocalcinosis. It has been hypothesized that the tubular epithelium, in order to bind crystals, needs to be phenotypically altered. Whereas most evidence hereto is provided by in vitro experiments, we set out to illustrate this theory in vivo. We simultaneously investigated the temporal changes of nephrocalcinosis-associated parameters during and shortly after a 4-day ethylene glycol (EG)-administration period in rats. We measured oxaluria, crystal formation, crystalluria, apoptosis, epithelial injury/ regeneration and luminal membrane expression of several crystal-binding molecules [hyaluronan (HA), osteopontin (OPN) and for the first time in vivo, annexin-2 (ANX2) and nucleolin-related-protein (NRP) and one of their receptors (CD44, HA/OPN-receptor]. Clinically, renal biopsies of preterm infants, transplant patients and acute phosphate nephropathy patients were stained for ANX2, NRP, HA and OPN. In the presence of a rather constant and persistent intratubular crystal formation, crystal retention gradually increased during EG-administration and markedly increased after arrest thereof, indicating that the development of crystal adhesion requires more than just the presence of crystals in the tubular fluid. All luminal membrane markers and a regenerating/dedifferentiated epithelium, unlike apoptosis, to various extents were upregulated concurrently and in association with crystal adhesion. However, both in humans and rats, expression of luminal molecules was not confined to crystal-containing tubules. Altogether, these findings allow better insight into the mechanisms underlying the 'fixed particle' theory in vivo and indicate that an altered epithelial phenotype with crystal-binding properties precedes crystal adhesion, thereby corroborating the requirement of tubular epithelial phenotypical changes in the development of intratubular nephrocalcinosis.

Sodium Phosphate Tablets and Acute Phosphate Nephropathy

Mackey, Ann Corken RPh, MPH1; Green, Lanh PharmD, MPH1; Amand, Keith St MD1; Avigan, Mark MD, CM1 Author Information

Acute Phosphate Nephropathy

Corridor Consult Antoine Abcar, MD; Aviv Hever, MD; Jasminder S Momi, MD; John J Sim, MD Summer 2009 - Volume 13 Number 3 Introduction Acute phosphate nephropathy (APN) is an underrecognized cause of both acute and chronic renal failure.1 Individ

Acute phosphate nephropathy

Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USACASE PRESENTATIONA 60-year-old white Latino female with a clinical diagnosisof diabetes mellitus (diagnosed in 1993) and hypertensionwas referred to the chronic kidney disease clinic atBrigham and Women’s Hospital for the evaluation of acutekidney injury; serum creatinine had increased from abaseline of 0.9 to 1.5mg/dl in a 11-week period. She wasasymptomatic at the time of presentation. Her pastmedical history included a total abdominal hysterectomywith bilateral salpingo oophorectomy and uppervaginectomy for high-grade squamous intraepitheliallesion of the cervix, 11 weeks prior to presentation. Threeweeks prior to presentation (8 weeks after surgery) andwithin a week of each other, she was evaluated for twoconsecutive episodes of acute onset of chest pain withpulmonary edema in the setting of severe hypertension.Both episodes had blood pressures in excess of190–200mmHg systolic that resolved with intravenousdiuretics. Cardiovascular workup revealed no evidence ofischemic heart disease. Additionally, renal evaluationincluded magnetic resonance angiography with andwithout gadolinium, which did not reveal renal arterystenosis. However, serum creatinine peaked at 1.9 mg/dlimmediately after surgical procedure and remainedelevated at 1.5mg/dl throughout the course of her currentpresentation (corresponding to a glomerular filtration rateof 33ml/min per 1.73m

Biochemical and Physiologic Changes Following Sodium Phosphate Preparation for Colonoscopy

Background and Objectives: Sodium phosphate (NaP) is a widely used bowel preparation regimen. Acute phosphate nephropathy accompanied by nephrocalcinosis and a reduced glomerular filtration has been increasingly reported after NaP preparation. We aimed to evaluate biochemical and physiologic changes following NaP preparation. Methods: Patients with normal renal function (creatinine level ≤ 1.5 mg/dl) scheduled for colonoscopy were enrolled. Two doses of 45 ml. NaP (phosphate 373.5 mEq/45 ml) followed by 2 liters of water were taken with 12 hours interval. Clinical data and blood chemistry were collected at baseline, 24 hours after NaP taking and 3 days later. 12-hour urine was collected prior to NaP taking, and after each dose of NaP. For patients with acute rising of creatinine ≥ 0.3 mg/dl was defined as having acute kidney injury (AKI), and their data were compared with those of the whole group. Results: There were 30 patients with mean (SD) age of 58.9 (12.6) years. Data are showed in Table. Twenty-four hours after NaP taking, serum phosphate increased sharply, contrasting with reducing serum calcium, sodium, potassium, chloride and magnesium. Urine acidosis and increased urine excretion of phosphate occurred together. Elevated serum phosphate returned to baseline 3 days later. There was no change in serum creatinine and parathyroid hormone levels. Two patients developed transient AKI without other biochemical difference from the whole group. Conclusions: After NaP taking, transient hyperphosphatemia, hypocalcemia, phosphaturia with urine acidosis occurred. Urine acid excretion may be the physiologic response to acute phosphate loading in order to enhance renal phosphate excretion and prevent phosphate nephropathy. No significantly different parameters were identified in patients with AKI. Further study is essential to confirm our study.