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Case Report
Who shot first? Three possible causes of a kidney infarction
¿Quién disparó primero? Infarto renal de tres posibles causas
Pablo González-Bustos, Ricardo Roa-Chamorro
Corresponding author
ricardoroa@gmail.com

Corresponding author.
, Fernando Jaén-Águila
Unidad de Riesgo Vascular, Medicina Interna, Hospital Universitario Virgen de las Nieves, Granada, Spain
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Acute renal infarction &#40;ARI&#41; is a rare pathology with a frequency of less than 1&#37;&#46; Classic clinical presentation consists of abdominal or renal fossa pain in up to half of the patients&#44; while other symptoms&#44; such as nausea&#44; vomiting&#44; or fever&#44; occur in fewer than 20&#37; of affected individuals&#46; ARF is often accompanied by high blood pressure &#40;HBP&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> It can be complicated to make a diagnosis&#44; given that the non-specific symptoms may cause the clinician to confuse ARF with other diseases&#44; such as nephrolithiasis or pyelonephritis&#46; As for its aetiology&#44; ARF can be caused by two major mechanisms&#58; thromboembolism and <span class="elsevierStyleItalic">in situ</span> thrombosis&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> What follows is a case report of a patient who presented with a multifactorial renal infarction&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Clinical case</span><p id="par0010" class="elsevierStylePara elsevierViewall">Forty-three year old male with a disease history of Poland syndrome affecting his right side&#44; non-smoker&#44; and non-drinker&#44; without any regular treatment&#46; He went to the emergency department for non-radiating pain in the left renal fossa of 48&#160;h of evolution&#59; no fever or other associated symptoms&#46; Physical examination revealed blood pressure &#40;BP&#41; 190&#47;110&#160;mmHg&#44; with no significant differences between both arms and lower extremities&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">In complementary testing&#44; the haemogram including erythrocyte sedimentation rate &#40;ESR&#41; and basic biochemistry &#40;including renal function&#44; transaminases&#44; creatine kinase&#44; and ions&#41; were normal&#46; Lactate dehydrogenase &#40;LDH&#41; was 338&#160;U&#47;L &#40;0&#8211;248&#41;&#46; Baseline coagulation was normal&#44; as were chest and abdominal X-rays&#46; The electrocardiogram revealed sinus rhythm at 74&#160;bpm with narrow QRS&#44; prominent R in V5&#8211;V6 without criteria of ventricular hypertrophy&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">An angioCT of the abdomen and pelvis was performed &#40;<a class="elsevierStyleCrossRefs" href="#fig0005">Figs&#46; 1 and 2</a>&#41;&#44; on which infarction of the left renal lower pole &#40;15&#37; of the renal parenchyma&#41; was evidenced&#44; with a decrease in the calibre of one of the segmental branches of the left renal artery&#46; This finding was suggestive of spontaneous dissection of an inferior branch of the left renal artery&#44; although as small scattered plaques of calcified atheromatosis were present at the level of the abdominal aorta&#44; an emboligenic aetiology or a lesion of the underlying renal artery could not be ruled out&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">For this reason&#44; the decision was made to extend the study with a transthoracic echocardiography&#44; which showed no evidence of structural heart disease&#46; In the acute phase&#44; aldosterone was 254&#160;pg&#47;mL &#40;38&#8211;150&#41; with normal renin&#46; TSH&#44; ACTH&#44; cortisol&#44; and metanephrines were normal&#46; Lipid profile exhibited total cholesterol 245&#160;mg&#47;dL&#44; HDL-C 49&#160;mg&#47;dL&#44; LDL-C 162&#160;mg&#47;dL&#44; TG 170&#160;mg&#47;dL&#44; apolipoprotein A 118&#160;mg&#47;dL&#44; apolipoprotein B 151&#160;mg&#47;dL&#44; and lipoprotein &#40;a&#41; 163&#160;mg&#47;dL &#40;5&#46;6&#8211;33&#46;8&#41;&#46; Additionally&#44; the special coagulation study conducted was positive in two independent samples &#40;with more than a 12-week interval between them&#41; for lupus anticoagulant&#44; as well as heterozygous Factor XII c4C&#62;T mutation&#46; The remaining special coagulation studies &#40;anticardiolipin and anti-beta2-glycoprotein I antibodies&#44; homocysteine&#44; factor V Leyden&#44; protein C and S deficiency&#44; antithrombin III deficiency&#41; and autoimmunity &#40;ANA&#44; ENAS&#41; were all negative&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">With these results&#44; the patient was diagnosed with renal infarction due to probable spontaneous renal artery dissection&#44; without being able to rule out that his procoagulant state&#44; with a confirmed antiphospholipid syndrome&#44; could be involved in the aetiology of this condition&#46; Furthermore&#44; the patient&#8217;s high cardiovascular risk due to hyperlipoproteinaemia &#40;a&#41; was considered to have played an important role in the aetiology of the &#91;clinical&#93; presentation&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">With respect to treatment&#44; the case was presented in a multidisciplinary session &#40;Internal Medicine&#44; Vascular Surgery&#44; and Interventional Radiology&#41;&#46; Given that the patient&#8217;s clinical symptoms had been present for more than 48&#160;h and 15&#37; of the parenchyma was affected&#44; the decision was made not to revascularise&#46; The patient was anticoagulated with acenocoumarol indefinitely&#44; in light of his antiphospholipid syndrome&#44; as well as strict control of cardiovascular risk factors&#46; Treatment was initiated with rosuvastatin 20&#47;ezetimine 10&#160;mg daily&#46; After a few hours during which the patient was hypertensive&#44; he did not require antihypertensive treatment&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0040" class="elsevierStylePara elsevierViewall">Renal infarction is a rare pathology&#44; with a frequency of less than 1&#37;&#46; It is suspected to be underdiagnosed&#44; given that its clinical presentation is non-specific and can be confused with other more common diseases &#40;nephrolithiasis&#44; pyelonephritis&#44; <span class="elsevierStyleItalic">etc&#46;</span>&#41;&#46;The finding of renal infarction is often incidental when performing an imaging test&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The causes of ARI can be divided into two main groups&#58; thromboembolism and <span class="elsevierStyleItalic">in situ</span> thrombosis&#46; The first group includes atrial fibrillation &#40;inasmuch as it is the most frequent aetiology&#44; performing a Holter-ECG may be of interest in these patients&#41;&#44; septic thrombi in the context of endocarditis&#44; or thrombi formed as a result of the rupture of an atheroma plaque of the suprarenal aorta&#46; Less common are direct thromboses in the renal artery&#46; They can arise from spontaneous dissection&#44; trauma&#44; fibromuscular dysplasia&#44; polyarteritis nodosa&#44; or Marfan syndrome&#46; Less than 10&#37; of all ARI are caused by hypercoagulable states&#46; In up to one third of the cases&#44; the cause of renal infarction is never determined&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;3</span></a> A higher incidence of renal infarct dissection in Poland syndrome has not been reported&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">The diagnosis of ARI is primarily based on a high degree of clinical suspicion&#44; supported by elevated LDH concentrations in the analysis and confirmed by angio-CT&#44; where a wedge-shaped parenchymal perfusion defect is typically observed&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">In our case&#44; there were several possible explanations for ARI&#46; The angioCT lesion initially suggested a spontaneous dissection of the segmental branch of the left renal artery&#46; In addition&#44; the patient had an antiphospholipid syndrome and atheroma plaques in the aorta with very high lipoprotein &#40;a&#41; values&#44; with the high risk of cardiovascular disease this entailed&#44; making it impossible to be sure that the AKI was attributable to any one of these causes alone&#59; the three factors therefore had to be treated individually&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">As for ARI treatment&#44; the first step should be to assess the possiblility of reperfusion of the artery&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;6</span></a> The patients seen to benefit most are those with an evolution time of less than 24&#160;h&#59; those having an ARI of more than 24&#160;h and with new-onset AHT or worsening of the usual figures&#44; renal failure&#44; haematuria&#44; or fever&#44; and those patients in whom ARI is caused by a dissection of the renal artery&#46; Individuals with atrophic kidneys do not benefit from treatment with arterial reperfusion&#46; In all patients&#44; the need for anticoagulation should be evaluated&#44; as well as strict control of cardiovascular risk factors&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In many cases&#44; patients can develop hypertension during the first week&#44; due to renin release&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">In conclusion&#44; ARI is difficult to diagnose and requires a complex aetiological study for adequate treatment&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Funding</span><p id="par0070" class="elsevierStylePara elsevierViewall">The authors state that they have not received any funding for this article&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflict of interests</span><p id="par0075" class="elsevierStylePara elsevierViewall">The authors have no conflict of interests to declare&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Renal infarction is a rare disease whose incidence is less than 1&#37;&#46; The symptoms can be abdominal or flank pain&#44; nausea&#44; vomiting&#44; fever or hypertension&#46; The diagnosis is complex&#44; and it is based on symptoms&#44; blood analysis with an elevated level of lactate dehydrogenase and computed tomography angiography&#46; The two major causes of renal infarction are thromboembolism and <span class="elsevierStyleItalic">in situ</span> thrombosis&#46; The treatment depends on an adequate etiological diagnosis&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">El infarto renal agudo &#40;IRA&#41; es una patolog&#237;a con frecuencia inferior al 1&#37; y diagn&#243;stico complejo&#46; Puede manifestarse como dolor abdominal o en fosa renal&#44; asociando n&#225;useas&#44; v&#243;mitos&#44; fiebre o incluso hipertensi&#243;n&#44; entre otros&#46; El diagn&#243;stico est&#225; basado en una alta sospecha cl&#237;nica&#44; con elevaci&#243;n de lactato deshidrogenasa &#40;LDH&#41; en los an&#225;lisis y angio-TC con defecto de perfusi&#243;n renal parenquimatosa en cu&#241;a&#46; En cuanto a la etiolog&#237;a del IRA&#44; podemos distinguir dos grupos etiol&#243;gicos&#58; tromboemb&#243;licos y trombosis <span class="elsevierStyleItalic">in situ</span>&#46; Es importante realizar un adecuado diagn&#243;stico causal para realizar un tratamiento correcto&#46;</p></span>"
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