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The patient started haemodialysis for mesangiocapillary glomerulonephritis in 1976 when he was 24&#44; and received a kidney transplant from a live donor in 1983&#46; His immunosupressive treatment was azathioprine and steroids&#46; In 1989&#44; six years after the first transplant&#44; he suffered an acute myocardial infarction&#46; Two years later&#44; he began haemodialysis treatment once again due to chronic rejection of the allograft&#46;</p><p class="elsevierStylePara">In 1994&#44; when the patient was 42&#44; he received a second kidney transplant from a 44 year old female donor&#46; The donor and the recipient share three HLA alleles &#40;HLA A3&#44; B8 and DR3&#41;&#46; The panel reactive antibody &#40;PRA&#41; score was 29&#37;&#44; probably due to various blood transfusions during the course of the first transplant&#44; and to the transplanted organ itself&#46; Immunosuppressants initially administered following the second transplant consisted of steroids &#40;0&#46;5mg&#47;kg&#47;day&#41;&#44; azathioprine &#40;2mg&#47;kg&#47;day&#41; and cyclosporine A &#40;CyA&#41; &#40;10mg&#47;day&#41;&#46;</p><p class="elsevierStylePara">Following the transplant&#44; the patient developed postischaemic acute tubular necrosis&#44; which required two subsequent surgical procedures one month after the transplant to correct a urinary fistula&#46; At the time of the surgical procedure&#44; a kidney biopsy was performed which revealed acute stage 1 rejection&#59; steroids were administered as rescue treatment &#40;1g in four doses&#41;&#46; Two years later&#44; the azathioprine was substituted with mycophenolate &#40;tables 1 and 2&#41; because of decreased renal function with CyA&#46;</p><p class="elsevierStylePara">The patient&#191;s progress was satisfactory until June 2000&#44; when a routine analysis revealed significant leukocytosis &#40;34&#46;5 x 109&#47;l&#41; and thrombocytosis &#40;487 x 109&#47;l&#41; &#40;figure 1&#41;&#46; The patient experienced bilateral hip pain&#44; but had no other symptoms&#46; The examination was normal with no signs of spleen or liver enlargement&#46;</p><p class="elsevierStylePara">An MRI scan of the hip showed diffused bone marrow involvement in almost all bones&#46; The bone marrow aspiration and biopsy confirmed granulocytic and megakaryocytic hyperplasia compatible with CML&#46; No fibrosis was observed in the bone marrow and the patient was low-risk according to the Sokal index&#46;</p><p class="elsevierStylePara">The presence of the Philadelphia chromosome &#40;46XY t&#91;9&#59;22&#93;&#91;q34&#59;q11&#93;&#41; was detected by analysing the bone marrow karyotype&#46; Subsequent cytogenic molecular analyses with fluorescent in situ hybridation &#40;FISH&#41; revealed the presence of the BCR-ABL fusion gene in 90&#37; of the nuclei&#46; The RT-PCR confirmed the typical rearrangement of p210 BCR-ABL with the fusion transcript b2a2&#46; During two months&#44; the patient was treated with hydroxyurea&#44; with no results&#46; In September of this year&#44; the patient was placed in a clinical trial of Novartis STI571-0113 and received 400mg of Imatinib daily&#59; he showed a good tolerance of the drug with no adverse effects&#46; The patient went into complete&#44; sustained haematological remission&#44; complete cytogenetic remission&#44; and molecular remission at two&#44; six and nine months respectively&#44; and this continues to be the case today &#40;figure 2&#41;&#46; Fourteen years after his second transplant&#44; the patient maintains an acceptable level of renal function &#40;stage III chronic renal disease&#41; and has not experienced acute rejection&#44; decreased hepatic function or new cardiovascular events &#40;table 1&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">This case shows that Imatinib is a safe&#44; effective drug for the treatment of CML in kidney transplant patients&#46; Our patient responded rapidly to the treatment&#58; peripheral blood and bone marrow became normal in the first two months&#44; and cytogenetic and molecular remission occurred during the first year of treatment&#46; These results are in line with IRIS1 study&#44; which showed a complete cytogenetic response in 89&#37; of patients with a low Sokal index&#44; and a survival rate of 83&#37;&#46; Lastly&#44; that study and our patient&#191;s case both show that an early cytogenetic and molecular response is associated with better long-term evolution and a lower risk of progression to the accelerated phase or blast crisis&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">The use of Imatinib in this patient may also have had a beneficial immunosuppressant effect for the transplanted kidney&#44; as suggested by recent in-vitro and animal studies showing that this drug may have immunomodulating effects&#46; Appel et al&#46; showed that Imatinib can inhibit the differentiation of CD34&#43; stem cells into dendritic cells &#40;DC&#41;&#46; Furthermore&#44; T-cell activation may be inhibited&#44; since DC cells&#191; secretion of cytokines and chemokines decreases&#46;<span class="elsevierStyleSup">7</span> Imatinib also inhibits the development of monocytes and macrophages in bone marrow progenitor cells&#46;<span class="elsevierStyleSup">8 </span>Lastly&#44; Dietz et al&#46; showed that Imatinib can inhibit T-cell proliferation by arresting the proliferation of lymphocytes in G<span class="elsevierStyleInf">0</span> phase&#46;</p><p class="elsevierStylePara">Some studies suggest that imatinib in the presence of cyclosporine can cause renal failure due to acute tubular necrosis&#46;<span class="elsevierStyleSup">10&#44;11</span> Despite receiving both drugs&#44; our patient&#191;s renal function remained stable from the moment when treatment with Imatinib was started&#46; Creatinine levels oscillated between 1&#46;75 and 2&#46;4mg&#47;dl with low levels of proteinuria &#40;the maximum proteinuria level was 0&#46;56g&#47;dl&#41;&#44; &#40;table 1&#41;&#46;</p><p class="elsevierStylePara">Serious hepatic side effects have also been described&#44; including fulminant liver failure associated with imatinib treatment&#46;<span class="elsevierStyleSup">12-15</span> Our patient&#44; who was positive for HCV&#44; experienced no changes in liver function during treatment&#46; Liver function remained within the normal range at all times&#44; despite having detectable HCV RNA in blood plasma&#44; which tends to be the case for most HCV patients following a transplant&#46;<span class="elsevierStyleSup">16</span> &#40;Table 3&#41;&#46;</p><p class="elsevierStylePara">Imatinib&#44; according to the manufacturer&#44; may have adverse effects in cardiac patients due to the risk of heart failure&#46; Our patient&#44; who suffered a myocardial infarction at the age of 37&#44; has experienced no adverse effects and his cardiac stress test this year was normal&#46;</p><p class="elsevierStylePara">We conclude that imatinib is a safe and effective treatment for kidney transplant patients with CML&#46; Furthermore&#44; in vitro and animal studies suggest that the drug may have immunomodulating effects that could be beneficial for a transplant&#46; <br></br></p><p class="elsevierStylePara"><a href="grande&#47;45118078&#95;f1&#95;p605&#46;jpg" class="elsevierStyleCrossRefs"><img src="45118078_f1_p605.jpg"></img></a></p><p class="elsevierStylePara">Figure 1&#46; </p><p class="elsevierStylePara"><a href="grande&#47;45118078&#95;t1&#95;p606&#46;jpg" class="elsevierStyleCrossRefs"><img src="45118078_t1_p606.jpg" alt="Patient&#39;s renal function over the last 13 years"></img></a></p><p class="elsevierStylePara">Table 1&#46; Patient&#39;s renal function over the last 13 years</p><p class="elsevierStylePara"><a href="grande&#47;45118078&#95;t2&#95;606&#46;jpg" class="elsevierStyleCrossRefs"><img src="45118078_t2_606.jpg" alt="Creatinine&#44; cyclosporin &#40;CyA&#41; and mycophenolate &#40;MMF&#41; levels during treatment with imatinib"></img></a></p><p class="elsevierStylePara">Table 2&#46; Creatinine&#44; cyclosporin &#40;CyA&#41; and mycophenolate &#40;MMF&#41; levels during treatment with imatinib</p><p class="elsevierStylePara"><a href="grande&#47;45118078&#95;t3&#95;p606&#46;jpg" class="elsevierStyleCrossRefs"><img src="45118078_t3_p606.jpg" alt="Liver function and hep C status from one month after starting treatment"></img></a></p><p class="elsevierStylePara">Table 3&#46; Liver function and hep C status from one month after starting treatment</p><p class="elsevierStylePara"><a href="grande&#47;45118078&#95;f2&#95;p607&#46;jpg" class="elsevierStyleCrossRefs"><img src="45118078_f2_p607.jpg"></img></a></p><p class="elsevierStylePara">Figure 2&#46; </p>"
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        "resumen" => "Abstract Chronic myeloid leukemia &#40;CML&#41; is a myeloproliferative disorder characterized by clonal expansion of cells in the myeloid line&#44; expressing the BCRABL fusion protein responsible for the oncogenic effect of CML&#46; The current frontline therapy in CML is the BCR-ABL tyrosine kinase inhibitor&#44; Imatinib&#46; Although this drug has been shown to improve survival in CML patients&#44; its role in the context of a transplant setting has not been widely described in the literature&#46; We report on the long term molecular remission of CML in a 55 year old man with a second renal transplant who is hepatitis C virus positive&#44; and has associated cardiovascular and immunological risk factors&#46;"
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        "resumen" => "<p class="elsevierStylePara">La leucemia mieloide cr&#243;nica &#40;LMC&#41; es una enfermedad mieloproliferativa caracterizada por la expansi&#243;n clonal de c&#233;lulas mieloides que expresan la prote&#237;na de fusi&#243;n BCR-ABL&#44; responsable de los efectos oncog&#233;nicos de la LMC&#46; La terapia actual en el tratamiento de LMC es el inhibidor de la BCR-ABL tiros&#237;n-kinasa&#44; imatinib&#46; Aunque este f&#225;rmaco ha demostrado mejorar la supervivencia en pacientes con LMC&#44; su papel en el contexto del trasplante renal no ha sido ampliamente descrito en la literatura&#46; Presentamos un caso de remisi&#243;n molecular de LMC en un var&#243;n de 55 a&#241;os con un segundo trasplante renal&#44; hepatitis C y con riesgos cardiovasculares e inmunol&#243;gicos asociados&#46;</p>"
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