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Acute phosphate nephropathy

Oral sodium phosphate bowel purgatives and acute phosphate nephropathy... [Pg.579]

Acute phosphate nephropathy pathophysiology risk factors ... [Pg.579]

In 2003, Desmeules et al. described a new pattern of renal failure resulting from the use of OSPS [29]. A 71-year-old female with a baseline creatinine of 1.0 mg/ dl presented with acute kidney injury and a creatinine of 4.5 mg/ dl two weeks following the use of OSPS. Renal biopsy revealed numerous tubular calcium phosphate deposits. Scanning electron microscopy and energy-dispersive x-ray microanalysis revealed that the calcium phosphate deposits formed crystals of hydroxyapatite. The patient s creatinine declined to 1.7 mg/dl at one year of follow-up. The authors described the process as "phosphosoda-induced nephrocalcinosis" and proposed the term "acute phosphate nephropathy". [Pg.582]

There have been additional recent reports of acute phosphate nephropathy following the use of OSPS (Table 2) [19, 31-33]. Similar to the majority of cases previously described, these patients appear to have taken OSPS at the correct dose and in the absence of clear contra-indications. Also similar to the previous reports, none of the patients have returned to normal renal function and no patient presented in the initial 24 hours with symptoms of hyperphosphatemia such as tetany or cardiac arrest. One case is of particular interest in that the pahent underwent renal biopsy both before and after exposure to OSPS [32]. The patient initially presented with nephrotic syndrome and normal renal function. Renal biopsy revealed membranous nephropathy (MN). In an effort to exclude a second-... [Pg.584]

Table 2 Biopsy-documented reports of acute phosphate nephropathy. [Pg.585]

Acute phosphate nephropathy is commonly accompanied by mild to moderate interstitial inflammation composed of mainly lymphocytes. The interstitial inflammation is not associated with significant tubulitis and likely represents a response to the tubular injury and calcium phosphate deposition. Glomeruli typically appear unremarkable. Vascular disease is commonly encountered but is an expected finding given the mean age and high incidence of hypertension in patients with APhN. [Pg.586]

Oral phosphate administration leading to renal calcium phosphate precipitation has been described in children with X-linked hypophosphatemic rickets. Children with this condition are treated with oral phosphate and vitamin D and frequently developed ultrasonographic evidence of nephrocalcinosis, and the grade of nephrocalcinosis correlates with cumulative phosphate intake [46]. Renal biopsy findings are similar to those seen in acute phosphate nephropathy, with calcifications confined to tubules and the peritubular interstitium [47]. [Pg.588]

Age is an important risk factor for fhe development of acute phosphate nephropathy. Gumurdulu et al. examined electrolyte levels in 70 patients who received two 45-ml doses of OSPS separated by 12 hours and found that the mean increase in serum phosphorus was 3.6 mg/dl in patients between the age of 25-35 years, compared to an increment of 5.5 mg/ dl in individuals over the age of 56 [61]. The mean change in phosphate correlated strongly with patient age (Pearson s r =... [Pg.589]

Multiple studies have attempted to address the issue of incidence of acute phosphate nephropathy. During calender year 2005, C.B. Fleet, a large producer of OSPS, reported 10 serious adverse events (SAE) for every 1,000,000 doses sold, but did not specify how many of these involved the kidney [66]. Clearly, the overwhelming majority of SAE s are unreported. The relatively small number of enrolled patients significantly flaws prospective studies of APhN, and ethical considerations may limit the ability to perform prospective stiidies.Retrospective studies may be flawed if they are underpowered, do not take into account biases in selection of bowel preparation, and do not appropriately define renal failure [67, 68]. [Pg.590]

Desmeules S. Gergeron MJ, Isenring P Acute phosphate nephropathy and renal failure. N Engl J Med 2003 349 1006-7. 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 3389-3396. [Pg.593]

Beyea A, Block C, Schned A. Acute phosphate nephropathy following oral sodium phosphate solution to cleanse the bowel for colonoscopy. Am J Kidn Dis 2007 50 151-4,2007. [Pg.593]

Urinary tract Acute phosphate nephropathy has been described as a possible complication after the use of oral sodium phosphate or phosphorus-containing medications. [Pg.755]

From July 2006 to September 2008, 10 cases of acute phosphate nephropathy, associated with sodium phosphate tablets for bowel cleansing, were reported to the FDA s Adverse Event Reporting System database [85 ]. Renal biopsy in these patients showed nephrocalcinosis (calcium phosphate crystal deposition in the distal tubules and collecting ducts). All these patients had at least one underlying susceptibility factor for acute renal insufficiency, such as pre-existing renal impairment, hypertension, diabetes mellitus, advanced age, underlying electrolyte imbalance, and... [Pg.755]

Connor A, Sykes L, Roberts IS, Weston CE. Acute phosphate nephropathy after sodium phosphate preparations. Br Med J 2009 338 47-9. [Pg.766]

Corken Mackey A, Green L, St. Amand K, Avigan M. Sodium phosphate tablets and acute phosphate nephropathy. Am J Gastroenterol 2009 104 1903-6. [Pg.766]


See other pages where Acute phosphate nephropathy is mentioned: [Pg.579]    [Pg.584]    [Pg.584]    [Pg.586]    [Pg.586]    [Pg.586]    [Pg.590]    [Pg.590]    [Pg.590]    [Pg.590]    [Pg.591]    [Pg.591]    [Pg.123]    [Pg.129]    [Pg.756]   
See also in sourсe #XX -- [ Pg.579 , Pg.580 , Pg.581 , Pg.582 , Pg.583 , Pg.584 , Pg.585 , Pg.586 , Pg.587 , Pg.588 , Pg.589 , Pg.590 , Pg.591 , Pg.592 , Pg.593 ]

See also in sourсe #XX -- [ Pg.123 ]




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