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Acute Phosphate Nephropathy Alexander K View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector http://www.kidney-international.org the renal consult & 2009 International Society of Nephrology Acute phosphate nephropathy Alexander K. Rocuts1, Sushrut S. Waikar1, Mariam P. Alexander1,2, Helmut G. Rennke2 and Ajay K. Singh1 1Renal Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA and 2Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA minute. The rest of the examination was unremarkable. CASE PRESENTATION HerlaboratorydataissummarizedinTable1. A 60-year-old white Latino female with a clinical diagnosis A postoperative kidney ultrasound showed no of diabetes mellitus (diagnosed in 1993) and hypertension hydronephrosis. was referred to the chronic kidney disease clinic at The etiology of the acute kidney injury was unclear. Brigham and Women’s Hospital for the evaluation of acute Progressive diabetic nephropathy exacerbated by other kidney injury; serum creatinine had increased from a contributory factors, such as exposure to lisinopril, baseline of 0.9 to 1.5 mg/dl in a 11-week period. She was acetylsalicylic acid, or naproxen, was regarded as the most asymptomatic at the time of presentation. Her past plausible explanation. Despite discontinuation of these medical history included a total abdominal hysterectomy medications, kidney function did not improve; it worsened with bilateral salpingo oophorectomy and upper in a 4-week period after presentation. Hence, a kidney vaginectomy for high-grade squamous intraepithelial biopsy was performed. lesion of the cervix, 11 weeks prior to presentation. Three weeks prior to presentation (8 weeks after surgery) and within a week of each other, she was evaluated for two consecutive episodes of acute onset of chest pain with pulmonary edema in the setting of severe hypertension. KIDNEY BIOPSY Both episodes had blood pressures in excess of A total of nine glomeruli were in the core. The predominant 190–200 mm Hg systolic that resolved with intravenous feature observed on light microscopy was a multifocal diuretics. Cardiovascular workup revealed no evidence of deposition of calcium phosphate within the tubules ischemic heart disease. Additionally, renal evaluation (basophilic, rounded concretions), in the interstitium, and included magnetic resonance angiography with and focally along tubular basement membranes (Figure 1a). The without gadolinium, which did not reveal renal artery deposits of calcium were non-birefringent under polarized stenosis. However, serum creatinine peaked at 1.9 mg/dl light and were best visualized in the sections stained with immediately after surgical procedure and remained von Kossa stain (Figure 1b). Degenerative changes of the elevated at 1.5 mg/dl throughout the course of her current tubular epithelium were focally noted with flattening of presentation (corresponding to a glomerular filtration rate 2 the epithelium. Tubular necrosis was not seen. An associated of 33 ml/min per 1.73m , estimated by the modification in focally dense lymphocyte-rich mixed inflammatory infiltrate diet in renal disease III (MDRD 3) equation). At in the interstitium was also noted without interstitial presentation, medications included amlodipine, edema. Tubulitis was not present. Moderate tubular atrophy furosemide, metoprolol, lisinopril, atorvastatin, insulin and interstitial fibrosis affecting 30% of the parenchyma glargine, cyanocobalamin, acetylsalicylic acid, and were also observed. All of the glomeruli present in the naproxen. The patient had no prior exposure to sample were hypertrophic and showed marked mesangial radiocontrast agents. Physical examination revealed an sclerosis with the formation of distinctive acellular nodules overweight women weighing 207 lbs with a blood (Figure 1c). Globally sclerotic glomeruli were not observed. pressure of 142/60 mm Hg and a heart rate of 60 beats per On Periodic acid-Schiff and Jones’ methenamine silver stains, the peripheral capillary loops showed thickened walls and frequent double contours. Rare craters were also seen. There Correspondence: Ajay K. Singh, Renal Division, Department of Medicine, was mild arteriosclerosis. Arterioles exhibited moderate Brigham and Women’s Hospital, Harvard Medical School, Boston, sclerosis of the vessel walls with accumulation of hyaline Massachusetts, USA. E-mail: [email protected] material. On immunofluorescence microscopy, no significant Kidney International (2009) 75, 987–991; doi:10.1038/ki.2008.293; immune deposits were observed in the glomeruli. Electron published online 25 June 2008 microscopy examination yielded no additional diagnostic Received 18 October 2007; revised 4 February 2008; accepted 12 information, but confirmed the tubular degenerative changes February 2008; published online 25 June 2008 observed on light microscopy. Kidney International (2009) 75, 987–991 987 the renal consult AK Rocuts et al.: Acute phosphate nephropathy CLINICAL DIAGNOSIS (OSPS), also known as Fleet Phospho-soda (C.B. Fleet, Acute kidney injury from acute phosphate nephropathy and Lynchburg, VA, USA), 1 day before gynecological surgery diabetic nodular glomerulosclerosis. (11 weeks prior to presentation). Blood pressure was last noted as 127/50 mm Hg. Kidney function has not returned to CLINICAL FOLLOW-UP baseline (serum creatinine of 1.9 mg per 100 ml with an On subsequent visits, a more detailed evaluation of the patient’s estimated glomerular filtration rate of 30 ml/min per 1.73m2 history revealed exposure to oral sodium phospho-soda by MDRD 3 equation) 5 months after sodium phospho-soda exposure. The most recent albumin-to-creatinine ratio is Table 1 | Laboratory parameters at presentation 513 mg albumin per gram of creatinine. Laboratory data of Investigation Value Reference value the patient at the baseline and after OSPS exposure are summarized in Figure 2. Complete blood count White blood cells 4.27 k/ml4–10k/ml Hemoglobin 9.6 g/dl 11.5–16.4g/dl DISCUSSION Platelets 260 k/ml 150–450k/ml Acute phosphate nephropathy is an unusual cause of acute kidney injury. It is most frequently reported in elderly Serum chemistry Sodium 139 mmol/l 136–142mmol/l patients, particularly among women, following exposure to Potassium 4.5 mmol/l 3.5–5mmol/l the bowel-cleansing preparation, OSPS. Acute phosphate Chloride 103 mmol/l 98–108mmol/l nephropathy is a diagnosis that tends to be overlooked, as Calcium 9.1 mg/dl 8.8–10.5mg/dl Phosphate 3.8 mg/dl 2.4–5.0mg/dl OSPS is not widely recognized as a precipitating cause of Creatinine 1.5 mg/dl 0.7–1.3mg/dl acute kidney injury. We present a patient with an underlying Total CO2 27 mmol/l 23–32mmol/l history of diabetes and hypertension with acute kidney injury Other chemistry that was initially attributed to the progression of diabetic PTH 108.1 pg/ml 11–80pg/ml nephropathy, but on kidney biopsy was diagnosed as acute Glucose 178 mg/dl 54–118mg/dl phosphate nephropathy secondary to OSPS exposure. OSPS preparations are used as part of a bowel-cleansing Urinalysis pH 6 4.5–8.0 regimen; they prepare the colon for X-ray or endoscopic 1–4 Specific gravity 1.011 1.003–1.035 examination as well as for surgery. OSPS preparations Blood 1+ 0 emerged in 1990 as better alternatives to standard bowel Protein 2+ 0 preparations and were regarded as very safe and effective 1 Serum electrophoresis No abnormal solutions for adequate mucosal visualization. However, as electrophoretic their use continued to grow, case reports of serious electrolyte pattern noted disturbances (including some fatal outcomes) appeared in ab c Figure 1 | Renal biopsy findings in acute phospho-nephropathy. (a) Coarse basophilic, rounded deposits of calcium phosphate are present within the lumina of tubules (hematoxylin–eosin, high-power field, original magnification  40). (b) The widespread multifocal nature of the intratubular calcium–phosphate deposits is best illustrated with the von Kossa stain (von Kossa stain, high-power field, original magnification  60). (c) Glomeruli displaying mesangial sclerosis with the formation of distinctive acellular nodules (periodic acid-Schiff stain, high-power field, original magnification  40). 988 Kidney International (2009) 75, 987–991 AK Rocuts et al.: Acute phosphate nephropathy the renal consult 80 10 9.2 9.5 9.5 9.2 9 70 9 68 8 60 8.2 ) 2 7 50 6 38 4.8 40 5 33 4.1 4.1 4 30 26 26 3.7 2.7 3 Estimated GFR (ml/min/1.73m 27 20 2.6 Total urine protein-to-creatinine ratio 1.47 2 (g/g), calcium (mg/dl) and phosphate (mg/dl) 10 0.96 1 0.91 0 0 Baseline Postop 2 3 4 5 Time from SPS Exposure (months) Estimated GFR (ml/min/1.73m2) Calcium (mg/dl) Phosphate (mg/dl) Proteinuria (g/g) Figure 2 | Acute phosphate nephropathy progression after OSPS exposure. Graph shows the trends of estimated glomerular filtration rate, serum calcium and phosphate, and total urine protein-to-creatinine ratio at baseline and up to 5 months after exposure to OSPS. The arrow marks the time when the patient was exposed to OSPS. the literature; they are associated with severe electrolyte published a scientific background paper advising against the abnormalities (hyperphosphatemia, hypernatremia, hypoka- use of these preparations in patients with kidney disease, lemia, hypocalcemia, and hypomagnesemia), metabolic impaired renal function, dehydration, or uncorrected elec- acidosis, acute kidney injury, and death when higher than trolyte abnormalities.12 Multiple media
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