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      Renal cortical necrosis complicating laundry detergent ingestion

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          Abstract

          Accidental oral detergent ingestion usually causes mild gastrointestinal manifestations including nausea, vomiting and diarrhea as well as upper airway irritation. There are a limited number of reported oral detergent ingestions leading to acute kidney injury, mainly due to rhabdomyolysis. We present an ultimately fatal case of laundry detergent ingestion leading to biopsy proven severe cortical necrosis and irreversible renal damage. Detergent ingestion was associated with widespread endothelial injury leading to a picture of thrombotic microangiopathy. Among the detergent ingredients ingested by the patient, sodium borate raised the highest concern as a potential toxin exacerbated further by severe hypovolaemia and consequent decrease in renal toxin excretion. As sodium borate is dialyzable, haemodialysis should be a consideration early after laundry detergent ingestion.

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          Clinical manifestations of toxicity in a series of 784 boric acid ingestions.

          A retrospective chart review was conducted at two regional poison centers to determine the clinical outcome of boric acid ingestions and to assess the relationship between serum boric acid levels and clinical presentation. A total of 784 cases were studied; all but 2 were acute ingestions. No patients developed severe manifestations of toxicity, and 88.3% were entirely asymptomatic. The most common symptoms were vomiting, abdominal pain, and diarrhea. Lethargy, headache, lightheadedness, and atypical rash were seen less frequently. Boric acid levels were obtained in 51 patients and ranged from 0 to 340 micrograms/mL. Blood levels were 70 micrograms/mL or more in 7 patients; 4 remained asymptomatic, whereas the other 3 had nausea or vomiting. Dialysis was performed in 4 of these 7 patients, only 1 of whom had symptoms (vomiting). On the basis of data from 9 patients, the mean half-life of boric acid was determined to be 13.4 hours (range, 4.0 to 27.8). Hemodialysis in 3 patients significantly shortened the half-life compared with pre- and postdialysis half-lives. Our results suggest that acute boric acid ingestions produce minimal or no toxicity and that aggressive treatment is not necessary in most patients.
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            Does hemolytic uremic syndrome differ from thrombotic thrombocytopenic purpura?

            Both hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are characterized by thrombotic microangiopathy (TMA), affecting mainly the kidney and brain, respectively. Diagnosis of HUS or TTP has been complicated by the fact that these disorders share several clinical characteristics, and by the dearth of knowledge regarding the pathogenesis of TMA. Advances in the identification of pathogenic features--deficiency of the metalloprotease ADAMTS13 in TTP and association of mutated complement proteins with atypical HUS--have gone some way towards improving clinicians' ability to distinguish between the two diseases. Here, we pose the following question: is it important to patient management that HUS be distinguished from TTP? By discussing what is known about the pathogenesis, clinical features and treatment of these two conditions we address this question, and propose a new nomenclature for TMA.
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              Acute ingestions of boric acid

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                Author and article information

                Journal
                NDT Plus
                NDT Plus
                ckj
                ndtplus
                NDT Plus
                Oxford University Press
                1753-0784
                1753-0792
                February 2009
                26 November 2008
                26 November 2008
                : 2
                : 1
                : 40-42
                Affiliations
                [1 ]Renal Division
                [2 ]Renal Division
                [3 ]Pathology Division, Brigham and Women's Hospital, Boston, MA, USA
                [4 ]Department of Medicine, MetroWest Medical Center
                [5 ]Department of Nephrology, University of Medicine and Pharmacy, Targu Mures, Romania
                Author notes
                Correspondence and offprint requests to: Leonardo Vidal Riella, Medical Research Building 4th floor, Renal Division, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. Tel: +00-1-617-732-5252; Fax: +1-617-732-6392; E-mail: lriella@ 123456rics.bwh.harvard.edu
                Article
                sfn178
                10.1093/ndtplus/sfn178
                4421478
                25949283
                1db82b82-b1b4-4c38-a12e-6b0ebc26c2dc
                © The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 29 September 2008
                : 24 October 2008
                Categories
                Case Report

                Nephrology
                acute kidney injury,cortical necrosis,detergent
                Nephrology
                acute kidney injury, cortical necrosis, detergent

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