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vascular ischaemia&#44; trauma&#44; drug use&#44; toxins&#44; sepsis&#44; electrocution&#44; etc&#46;&#41; having been reported&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The most significant complication of rhabdomyolysis is AKF that occurs in up to 33&#37; of patients present&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">3</span></a> The mechanism responsible for AKF lies in the release of myoglobin&#46; Three myoglobin-mediated nephrotoxic mechanisms have been described&#46; Renal vasoconstriction&#44; the formation of intratubular casts&#44; and direct damage to tubular cells&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">4&#44;5</span></a> The best treatment for rhabdomyolysis-associated AKF is prevention&#46; Increasing volume with crystalloid infusions to maintain good renal perfusion and high urinary flow&#44; along with initial alkalinisation&#44; are the bases for prevention&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">6</span></a> In the event that the aforementioned measures fail&#44; it will be necessary to start renal replacement therapy&#44; which is not indicated based on the levels of myoglobin or CK&#44; but based on the presence of life-threatening conditions such as hyperkalaemia&#44; hypercalcaemia&#44; anuria or volume overload&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">7</span></a> Once decided to conduct renal replacement therapy&#44; whether through intermittent haemodialysis or continuous techniques&#44; we must consider that the toxin responsible for AKF&#44; myoglobin&#44; has a Pm of 17<span class="elsevierStyleHsp" style=""></span>kD&#44; and is poorly removed by high-flux dialysers&#46;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">8&#44;9</span></a> We present a case of rhabdomyolysis with AKF in a kidney transplant patient who was treated with intermittent haemodialysis with an EMIC2 dialyser &#40;cut-off 40<span class="elsevierStyleHsp" style=""></span>kD&#41;&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">This is a 45-year-old patient with chronic kidney disease of unknown aetiology on peritoneal dialysis since 2009&#46; He received the first kidney transplant from a deceased donor in 2010&#44; with early vein thrombosis&#46; A thrombophilia test showed a state of hypercoagulability with hyperhomocysteinaemia and elevated factor <span class="elsevierStyleSmallCaps">viii</span>&#46; The second kidney transplant from a deceased donor was performed in 2013&#44; with an indefinite systemic anticoagulation prescription with sintrom<span class="elsevierStyleSup">&#174;</span>&#46; He had an episode of late acute rejection in January 2016 which was treated with steroids&#46; Later on&#44; he developed nephropathy due to BK virus with stage 4 CKD &#40;Cr 4&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46; In October 2016&#44; he had an episode of deep vein thrombosis in the left lower limb &#40;LLL&#41;&#46; Previously&#44; anticoagulant therapy was suspended due to lower gastrointestinal bleeding secondary to a colon polyp&#46; Treatment with sintrom was resumed and in December 2016 he was readmitted for acute LLL pain and sudden-onset oedema up to the root end of the limb&#44; again observing deep vein thrombosis in the femoral popliteal area&#46; At that time&#44; the patient was not adequately anticoagulated &#40;INR 1&#46;4&#41;&#44; and it was decided to treat him with sodium heparin&#46; Poor evolution with significant oedema of the LLL&#44; frailty&#44; and signs of poor distal infusion&#44; with the patient developing AKF in addition to CKD &#40;Cr 6&#46;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41; with dark urine and oliguria&#46; Ultrasound ruled out vascular involvement of the kidney graft and confirmed the existence of rhabdomyolysis &#40;CK 44&#44;915<span class="elsevierStyleHsp" style=""></span>mU&#47;ml&#44; lactate dehydrogenase 3100<span class="elsevierStyleHsp" style=""></span>U&#47;l&#44; GOT 392&#44; GPT 113&#41; and severe dyselectrolytaemia &#40;K 6&#46;6<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#44; bicarbonate 16<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#41;&#46; Despite the vigorous crystalloid infusion&#44; the patient&#39;s anuria continued&#44; with it becoming necessary to replace kidney function with emergency haemodialysis&#46; Two 6-h dialysis sessions were completed with a 1&#46;8<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span> EMIC2 dialyser &#40;Fresenius Polysulfone<span class="elsevierStyleSup">&#174;</span>&#41; and a cut-off of 40<span class="elsevierStyleHsp" style=""></span>kD with the goal of clearing myoglobin&#46; Pre- and post-dialysis myoglobin was measured at the first session&#44; showing a 50&#37; decrease &#40;pre-HD 47&#44;110<span class="elsevierStyleHsp" style=""></span>ng&#47;ml vs post-HD 23&#44;500<span class="elsevierStyleHsp" style=""></span>ng&#47;ml&#41;&#46; After the second session&#44; the patient resumed diuresis at a polyuria rate&#44; recovering the kidney function he had prior to rhabdomyolysis&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">We report this case to draw attention to the early start of replacement therapy&#44; with the use of dialysers with an intermediate cut-off &#40;40<span class="elsevierStyleHsp" style=""></span>kD&#41; probably being useful in that&#44; by increasing myoglobin clearance and decreasing serum levels&#44; they can contribute to an earlier recovery from AKF&#46;</p></span>"
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Letter to the Editor
Acute renal failure due to rhabdomyolysis. Renal replacement therapy with intermediate cut-off membranes (EMIC2)
Fracaso renal agudo por rabdomiólisis. Tratamiento con hemodiálisis y membranas de cut-off intermedio (EMIC2)
Rafael Díaz-Tejeiro
Corresponding author
rdtejeiro@ono.com

Corresponding author.
, Dabaiba Regidor, Jorge Morales, Mayte Padrón, Laura Cueto, Miguel Angel Muñoz, Marta Torres, Francisco Javier Ahijado, Jose Eugenio García Díaz
Servicio Nefrología, Hospital Virgen de la Salud, Toledo, Spain
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    "titulo" => "Acute renal failure due to rhabdomyolysis&#46; Renal replacement therapy with intermediate cut-off membranes &#40;EMIC2&#41;"
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        "titulo" => "Fracaso renal agudo por rabdomi&#243;lisis&#46; Tratamiento con hemodi&#225;lisis y membranas de cut-off intermedio &#40;EMIC2&#41;"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Rhabdomyolysis is a clinical syndrome caused by damaged skeletal muscle tissue and the release of its intracellular components&#44; including myoglobin&#44; lactate dehydrogenase&#44; creatine kinase &#40;CK&#41;&#44; and electrolytes into the blood stream and the interstitial space&#46; Its symptoms vary from a nearly asymptomatic condition&#44; with myalgia and elevated CK levels&#44; to an extremely serious condition with marked CK elevations&#44; severe electrolyte disorders d&#44; acute kidney failure &#40;AKF&#41;&#44; and disseminated intravascular coagulation &#40;DIC&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">1</span></a> The aetiology of the syndrome can be highly varied&#44; with both hereditary &#40;hereditary myopathies&#41;&#44; and acquired factors &#40;extreme physical activity&#44; exposure to extreme temperatures&#44; vascular ischaemia&#44; trauma&#44; drug use&#44; toxins&#44; sepsis&#44; electrocution&#44; etc&#46;&#41; having been reported&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The most significant complication of rhabdomyolysis is AKF that occurs in up to 33&#37; of patients present&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">3</span></a> The mechanism responsible for AKF lies in the release of myoglobin&#46; Three myoglobin-mediated nephrotoxic mechanisms have been described&#46; Renal vasoconstriction&#44; the formation of intratubular casts&#44; and direct damage to tubular cells&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">4&#44;5</span></a> The best treatment for rhabdomyolysis-associated AKF is prevention&#46; Increasing volume with crystalloid infusions to maintain good renal perfusion and high urinary flow&#44; along with initial alkalinisation&#44; are the bases for prevention&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">6</span></a> In the event that the aforementioned measures fail&#44; it will be necessary to start renal replacement therapy&#44; which is not indicated based on the levels of myoglobin or CK&#44; but based on the presence of life-threatening conditions such as hyperkalaemia&#44; hypercalcaemia&#44; anuria or volume overload&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">7</span></a> Once decided to conduct renal replacement therapy&#44; whether through intermittent haemodialysis or continuous techniques&#44; we must consider that the toxin responsible for AKF&#44; myoglobin&#44; has a Pm of 17<span class="elsevierStyleHsp" style=""></span>kD&#44; and is poorly removed by high-flux dialysers&#46;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">8&#44;9</span></a> We present a case of rhabdomyolysis with AKF in a kidney transplant patient who was treated with intermittent haemodialysis with an EMIC2 dialyser &#40;cut-off 40<span class="elsevierStyleHsp" style=""></span>kD&#41;&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">This is a 45-year-old patient with chronic kidney disease of unknown aetiology on peritoneal dialysis since 2009&#46; He received the first kidney transplant from a deceased donor in 2010&#44; with early vein thrombosis&#46; A thrombophilia test showed a state of hypercoagulability with hyperhomocysteinaemia and elevated factor <span class="elsevierStyleSmallCaps">viii</span>&#46; The second kidney transplant from a deceased donor was performed in 2013&#44; with an indefinite systemic anticoagulation prescription with sintrom<span class="elsevierStyleSup">&#174;</span>&#46; He had an episode of late acute rejection in January 2016 which was treated with steroids&#46; Later on&#44; he developed nephropathy due to BK virus with stage 4 CKD &#40;Cr 4&#46;1<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41;&#46; In October 2016&#44; he had an episode of deep vein thrombosis in the left lower limb &#40;LLL&#41;&#46; Previously&#44; anticoagulant therapy was suspended due to lower gastrointestinal bleeding secondary to a colon polyp&#46; Treatment with sintrom was resumed and in December 2016 he was readmitted for acute LLL pain and sudden-onset oedema up to the root end of the limb&#44; again observing deep vein thrombosis in the femoral popliteal area&#46; At that time&#44; the patient was not adequately anticoagulated &#40;INR 1&#46;4&#41;&#44; and it was decided to treat him with sodium heparin&#46; Poor evolution with significant oedema of the LLL&#44; frailty&#44; and signs of poor distal infusion&#44; with the patient developing AKF in addition to CKD &#40;Cr 6&#46;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#41; with dark urine and oliguria&#46; Ultrasound ruled out vascular involvement of the kidney graft and confirmed the existence of rhabdomyolysis &#40;CK 44&#44;915<span class="elsevierStyleHsp" style=""></span>mU&#47;ml&#44; lactate dehydrogenase 3100<span class="elsevierStyleHsp" style=""></span>U&#47;l&#44; GOT 392&#44; GPT 113&#41; and severe dyselectrolytaemia &#40;K 6&#46;6<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#44; bicarbonate 16<span class="elsevierStyleHsp" style=""></span>mEq&#47;l&#41;&#46; Despite the vigorous crystalloid infusion&#44; the patient&#39;s anuria continued&#44; with it becoming necessary to replace kidney function with emergency haemodialysis&#46; Two 6-h dialysis sessions were completed with a 1&#46;8<span class="elsevierStyleHsp" style=""></span>m<span class="elsevierStyleSup">2</span> EMIC2 dialyser &#40;Fresenius Polysulfone<span class="elsevierStyleSup">&#174;</span>&#41; and a cut-off of 40<span class="elsevierStyleHsp" style=""></span>kD with the goal of clearing myoglobin&#46; Pre- and post-dialysis myoglobin was measured at the first session&#44; showing a 50&#37; decrease &#40;pre-HD 47&#44;110<span class="elsevierStyleHsp" style=""></span>ng&#47;ml vs post-HD 23&#44;500<span class="elsevierStyleHsp" style=""></span>ng&#47;ml&#41;&#46; After the second session&#44; the patient resumed diuresis at a polyuria rate&#44; recovering the kidney function he had prior to rhabdomyolysis&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">We report this case to draw attention to the early start of replacement therapy&#44; with the use of dialysers with an intermediate cut-off &#40;40<span class="elsevierStyleHsp" style=""></span>kD&#41; probably being useful in that&#44; by increasing myoglobin clearance and decreasing serum levels&#44; they can contribute to an earlier recovery from AKF&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; D&#237;az-Tejeiro R&#44; Regidor D&#44; Morales J&#44; Padr&#243;n M&#44; Cueto L&#44; Mu&#241;oz MA&#44; et al&#46; Fracaso renal agudo por rabdomi&#243;lisis&#46; Tratamiento con hemodi&#225;lisis y membranas de cut-off intermedio &#40;EMIC2&#41;&#46; Nefrolog&#237;a&#46; 2018&#59;38&#58;664&#8211;665&#46;</p>"
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Article information
ISSN: 20132514
Original language: English
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2020 January 214 34 248
2019 December 159 50 209
2019 November 150 50 200
2019 October 157 28 185
2019 September 245 33 278
2019 August 188 47 235
2019 July 129 43 172
2019 June 133 55 188
2019 May 110 46 156
2019 April 102 68 170
2019 March 69 41 110
2019 February 23 29 52
2019 January 46 42 88
2018 December 124 55 179
2018 November 192 20 212
2018 October 159 18 177
2018 September 125 17 142
2018 August 80 13 93
2018 July 43 10 53
2018 June 51 12 63
2018 May 43 14 57
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¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?