Journal Information
Vol. 29. Issue. S1.March 2009
Pages 1-77
Vol. 29. Issue. S1.March 2009
Pages 1-77
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PROGRESSION FACTORS IN CHRONIC KIDNEY DISEASE. IMMUNOLOGICAL MECHANISMS
Factores de progresión de la enfermedad renal crónica. Mecanismos no inmunológicos
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4469
Luis Capdevila Plazaa, Juan José Cuberob, Enrique Lunab, Román Hernández-Gallegob
a Servicio de Nefrología, Hospital Vall d¿Hebron, Barcelona, Barcelona, España,
b Servicio de Nefrología, Complejo Hospitalario Universitario Infanta Cristina, Badajoz, Badajoz, España,
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Los factores no inmunológicos que parecen contribuir a la progresión del daño renal y, por consiguiente, a la pérdida de función son, entre otros: la hipertensión arterial (HTA), la proteinuria, la dislipemia, etc. 1. Tratamiento de la HTA: la presión arterial (PA) debe medirse periódicamente en todos los pacientes trasplantados. Igual que se ha descrito en los riñones propios, en los pacientes con trasplante renal, la HTA se muestra como factor de riesgo de progresión del deterioro de la función del injerto. La HTA representa un marcador clínico de la nefropatía crónica del injerto y contribuye a la pérdida del injerto y a la morbimortalidad de estos pacientes (grado de evidencia C). En los pacientes trasplantados renales, las cifras de PA recomendadas son <130/80 mmHg, bajando a niveles de la PA <125/75 mmHg si existe proteinuria >1 g/d. Dado que la HTA y la proteinuria se asocian frecuentemente en el curso de la nefropatía crónica, un abordaje terapéutico conjunto parece más racional cuando ambas situaciones concurren simultáneamente (grado de recomendación C). Para el control de la PA en el receptor de un trasplante renal, es muy importante iniciar medidas higiénicodietéticas junto con el tratamiento médico. Todos los agentes antihipertensivos son efectivos y aún no existe una preferencia clara en ninguna guía, y la mayoría de los pacientes necesitará dos o más fármacos antihipertensivos. Los IECA o ARA II son de elección en los pacientes con proteinuria. Al iniciar tratamiento con IECA o ARA II, o al aumentar dosis, es preciso monitorizar función renal y caliemia a las 1-2 semanas. Además, en los pacientes trasplantados con ERC estadio 4-5 y en tratamiento con IECA o ARA II se debe monitorizar periódicamente la caliemia. 2. Tratamiento de la proteinuria: conocido marcador de daño renal que contribuye a la progresión de la insuficiencia renal. La reducción a cifras <0,5 g/24 horas es el objetivo terapéutico. Tanto los IECA como los ARA II son los fármacos de elección en este tipo de paciente, pero con monitorización cuidadosa de función renal y del potasio, especialmente en el paciente trasplantado con ERC estadio 4-5. 3. Tratamiento de la dislipemia: en todo paciente trasplantado debe realizarse una evaluación periódica del perfil lipídico (colesterol total, HDL-c, LDL-c y triglicéridos). Además del impacto negativo en la enfermedad cardiovascular, la hiperlipemia también se ha relacionado con la nefropatía crónica del injerto. Los pacientes trasplantados deben considerarse de alto riesgo cardiovascular, considerándose el objetivo terapéutico un LDL-c <100 mg/dl (grado de recomendación C). 4. Otras medidas: control de la diabetes mellitus, manteniendo niveles de hemoglobina glucosilada <7%, cese del hábito tabaquico, evitar el sobrepeso, antiagregación individualizada, medidas especialmente destinadas a la protección cardiovascular y, por tanto, también a la protección del injerto renal.

In kidney transplantation patient and graft survival are excellent in short-term and mid-term, although they remain stable in the long-term. The incidence of acute rejection has decreased to 8%-15%. Despite marked progress in understanding immunologic mechanisms involved in transplantation, new tools are required to detect early changes that could affect allograft function allowing us to anticipate histological lesions and providing a more accurate use of immunosuppressive drugs. From an immunologic point of view, efforts should be directed to avoid interstitial fibrosis and tubular atrophy (IF/TA) and to prevent antibody-mediated rejection. The most frequent cause of late graft loss is IF/TA. Improvement in kidney transplant results have been achieved with calcineurin inhibitors -CNI- (cyclosporin and tacrolimus), antiproliferative agents (mycophenolate mofetil and enteric-coated mycophenolic acid) and T-celldepleting antibodies. The combination of tacrolimus + mycophenolate mofetil + steroids has been the gold standard in kidney transplant immunosuppression. An adequate balance in order to maintain the appropiate immune response is essential to the patient to avoid infections or neoplasias as well to prevent rejection. In renal transplant recipients with chronic kidney disease stage 4T in which renal function remains stable, immuno-suppressive drugs can be continued at the usual maintenance doses. As GFR declines, CNI and antiproliferative drugs should be reduced.

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