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      Nephrotic syndrome due to minimal change disease secondary to spider bite: clinico-pathological case of a non-described complication of latrodectism

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          Abstract

          The patient was an 18-year-old man who developed nephrotic syndrome after a ‘wheat spider’ bite ( Latrodectus mactans). Due to this atypical manifestation of latrodectism, a renal biopsy was performed showing minimal change disease. The nephrotic syndrome subsided after 1 week without specific treatment. This self-limited evolution suggests that the mechanism of podocyte damage was temporary and potentially mediated by a secondary mechanism of hypersensitivity or direct effect of the α-latrotoxin. The patient did not show signs of relapse in subsequent checkup. This is the first reported case of nephrotic syndrome due to a minimal change lesion secondary to latrodectism.

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          Most cited references18

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          Clinical consequences of spider bites: recent advances in our understanding.

          Spider bite continues to be a controversial subject worldwide and attribution of clinical effects to different spiders is problematic because of poor case definition and paucity of clinical evidence. The effects of medically important spiders are sometimes underestimated and simultaneously there is misattribution of effects to harmless spider groups. The majority of suspected spider bites present as skin lesions or necrotic ulcers where the history of a spider bite must be confirmed. To be a definite spider bite, the patient must immediately observe the spider and there be evidence of the bite, such as pain. Important groups of spiders worldwide include the widow spiders (latrodectism), recluse spiders (loxoscelism) and some mygalomorph spiders including the Australian Funnel web spider. Most spiders only cause minor effects, including a large number of groups that have been implicated in necrotic arachnidism.
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            Unusual reactions to insect stings.

            A variety of unusual or unexpected reactions have occurred in a temporal relationship to insect stings. This review will summarize these case history reports in recent years. As these reactions are very infrequent, the review will also include prior reported unusual reactions attributed to insect stings. Acute encephalopathy occurred 8 days after yellow jacket stings, without any other obvious cause. There have been prior reports of other neurological reactions, myasthenia gravis, peripheral neuritis and Guillain-Barré syndrome related to insect stings. Acute renal failure with tubular necrosis has occurred following massive numbers of stings from Africanized honeybees. Nephrotic syndrome has been reported in the past following single stings. Silent myocardial infarction has occurred, probably related to acute anaphylactic symptoms immediately following a sting. There are recent reports of other pathology, diffuse alveolar hemorrhage and rhabdomyolysis and prior reports of thrombocytopenic purpura and vasculitis. As the result of ocular stings, local reactions have occurred with corneal pathology leading to cataracts. Other prior reported reactions to ocular stings include conjunctivitis, corneal infiltration, lens subluxation, and optic neuropathy. There is scarce information regarding the pathogenesis of the majority of the unusual reactions and the subsequent allergic status or risk for sting anaphylaxis of people who have had these unusual reactions. This review includes a variety of reactions, particularly involving neurological, renal and cardiovascular symptoms, related to insect stings. It is important that clinicians be aware of this relationship when assessing people with these reactions and address future prophylaxis.
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              Calcium regulates podocyte actin dynamics.

              Ca(2+)-mediated remodeling of the actin cytoskeleton is a dynamic process that regulates cell motility through the modulation of rho guanosine triphosphatase (GTPase) signaling. Kidney podocytes are unique, pericyte-like cells with a complex cellular organization consisting of a cell body, major processes, and foot processes (FPs). The FPs form a characteristic interdigitating pattern with FPs of neighboring podocytes, leaving in between filtration slits that are covered by the slit diaphragm (SD). The actin-based FP and the SD form the final barrier to proteinuria. Mutations affecting several podocyte proteins cause disruption of the filtration barrier and rearrangement of the highly dynamic podocyte actin cytoskeleton. Proteins regulating the plasticity of the podocyte actin cytoskeleton are therefore of critical importance for sustained kidney barrier function. Dynamic regulation of the actin-based contractile apparatus in podocyte FPs is essential for sustained kidney filter function. Thus, the podocyte represents an excellent model system to study calcium signaling and actin dynamics in a physiologic context. Here, we discuss the regulation of podocyte actin dynamics by angiotensin or bradykinin-mediated calcium influx and downstream Rho GTPase signaling pathways and how these pathways are operative in other cells including fibroblasts and cancer cells. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Clin Kidney J
                Clin Kidney J
                ckj
                Clinical Kidney Journal
                Oxford University Press
                2048-8505
                2048-8513
                April 2017
                26 December 2016
                26 December 2016
                : 10
                : 2
                : 229-232
                Affiliations
                [1 ]Department of Pathology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, RM, Chile
                [2 ]Nephrology Unit, Clínica Los Andes, Los Angeles, Provincia de Bío Bío, VIII [a ] Región, Chile
                [3 ]Nephrology Unit, Hospital Universitario Río Hortega, Valladolid, Spain
                Author notes
                Correspondence and offprint requests to: Gonzalo P. Méndez; E-mail: gmendez@ 123456med.puc.cl
                Article
                sfw110
                10.1093/ckj/sfw110
                5381243
                14f415a1-66c4-4ef8-ae07-82a492e0128d
                © The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA.

                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
                : 07 March 2016
                : 29 September 2016
                Page count
                Pages: 4
                Categories
                Glomerulopathies

                Nephrology
                latrodectism,minimal change disease,nephrotic syndrome,proteinuria,spider bite
                Nephrology
                latrodectism, minimal change disease, nephrotic syndrome, proteinuria, spider bite

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