Avances clínicos en calcificación vascular / No disponible

Se han seleccionado los artículos que aportan respuestas alas preguntas de más interés desde el punto de vista clínicoen cuanto a la calcificación vascular.1. ¿Cómo se mide?: Se analizan estudios que ponen demanifiesto la utilidad de diferentes herramientas paracuantificarla.2. ¿Qué mide?: En pacientes en diálisis como en la poblacióngeneral la calcificación vascular y la rigidez arterialson factores pronósticos de morbi-mortalidad. Otrosmarcadores como la fetuína A, se asocian a mortalidaden pacientes en hemodiálisis pero no en pacientes enestadios precoces de enfermedad renal crónica.3. ¿Qué la provoca?: En dos estudios seleccionados vuelvea demostrarse que el bajo recambio óseo y la diabetescondicionan enfermedad cardiovascular y calcificaciónvascular respectivamente.4. ¿Cómo se trata?: Aún no existe evidencia clínica de regresiónde la calcificación vascular. Sin embargo, enun estudio prospectivo en pacientes incidentes en hemodiálisisse demuestra que el sevelamer comparadocon los compuestos de calcio atenúa la progresión dela calcificación vascular y confiere mayor supervivencia.En un estudio en pacientes prevalentes, comparandoambos compuestos, el sevelamer sólo beneficiaen supervivencia a pacientes mayores de 65 años.Queda por demostrar en estudios clínicos prospectivossi el paricalcitol y el cinacalcet confirman los buenosresultados experimentales (AU)

The articles providing answers to the questions on vascular calcificationof most interest from a clinical point of view were selected.1. How is it measured?: Studies showing the clinical utility ofdifferent tools to quantify it were analyzed.2. What does it measure?: Both in dialysis patients and the generalpopulation, vascular calcification and arterial stiffnessare prognostic factors for morbidity and mortality. Other markerssuch as fetuin-A are associated with mortality in patientson hemodialysis but not in patients in early stages of chronickidney disease.3. What causes it?: In two selected studies, it was demonstratedagain that low bone turnover and diabetes cause cardiovasculardisease and vascular calcification, respectively.4. How is it treated?: There is still no clinical evidence of regressionof vascular calcification. However, a prospective study innew hemodialysis patients showed that sevelamer comparedto calcium compounds slows the progression of vascular calcificationand confers greater survival. A study comparingboth compounds in chronic hemodialysis patients showedthat sevelamer only had a benefit on survival in patients olderthan 65 years. It remains to be demonstrated whether thegood experimental results of paricalcitol and cinacalcet areconfirmed in prospective clinical studies (AU)

Control del fósforo y tratamiento con vitamina D enEnfermedad Renal Crónica antes del inicio de diálisis / No disponible

La hiperfosfatemia es una complicación que aparece ya enestadios tempranos de la enfermedad renal crónica (ERC) yque ha demostrado tener graves consecuencias en los pa-cientes con nefropatía. En la actualidad se están estudiadonuevos reguladores del fósforo como son el FGF-23, unahormona fosfatúrica y contra-reguladora de la vitamina D,y kloto, co-factor necesario para la activación del FGF-23.Las principales consecuencias de la hiperfosfatemia descri-tas en pacientes con ERC no en diálisis son la calcificaciónectópica, el incremento de la mortalidad y la más rápidaprogresión de la ERC. Todo ello indica la necesidad de bus-car un control estricto del Pi. Para ello, destacan en la ac-tualidad dos fármacos como son el carbonato de lantano yel sevelamer. Aunque no existen estudios diseñados espe-cíficamente para esta población aún no en diálisis, parecenser fármacos eficaces y seguros. Otra complicación de laERC es el defecto en la síntesis de vitamina D que segúnlos estudios publicados recientemente, ha resultado sermás prevalente y aparecer en estadios más tempranos dela enfermedad de lo que se creía inicialmente. Existe unamplio debate respecto a la necesidad de administrar su-plementos de vitamina D de forma sistemática por losefectos pleiotrópicos de dicha hormona, ajenos al desarro-llo de la enfermedad ósea renal. Por esas dudas, si bien nohay acuerdo en la administración rutinaria, sí hay consen-so en la necesidad de medir los valores de 1,25-dihidroxivi-tamina D y 25-hidroxivitamina D, así como esperar el re-sultado de los numerosos estudios que se están llevandoacabo acerca del impacto de la vitamina D en la progresiónde factores de riesgo cardiovascular, en la ERC y las posi-bles consecuencias de su administración indiscriminada (AU)

Hyperphosphatemia is a complication that appears in the earlystages of chronic kidney disease (CKD) and that has been shownto have serious consequences in kidney disease patients. Newphosphate regulators are currently being studied such as FGF-23, a counter-regulatory phosphaturic hormone for vitamin D,and klotho, a cofactor necessary for activation of FGF-23. Themain consequences of hyperphosphatemia described in CKD patientsnot on dialysis are ectopic calcification, increased mortalityand more rapid progression of CKD. All this indicates the needfor strict control of Pi. The two most currently used drugs for thispurpose are lanthanum carbonate and sevelamer. Althoughthere are no studies specifically designed for this predialysis population,these drugs appear to be effective and safe. Anothercomplication of CKD is vitamin D deficiency which, according torecently published studies, is more prevalent and appears in earlierstages of the disease than was initially thought. There is widedebate on the need to administer vitamin D supplements systematicallydue to the pleiotropic effects of this hormone andwhich are unrelated to development of renal bone disease. Becauseof these doubts, there is no agreement on routine administration,although there is consensus on the need to measure1,25-dihydroxyvitamin D and 25-hydroxyvitamin D values and towait for the result of numerous studies that are being carriedout on the impact of vitamin D on progression of cardiovascularrisk factors in CKD and the possible consequences of its indiscriminateadministration (AU)

[Clinical advances in vascular calcification]. / Avances clínicos en calcificación vascular.

The articles providing answers to the questions on vascular calcification of most interest from a clinical point of view were selected. 1. How is it measured?: Studies showing the clinical utility of different tools to quantify it were analyzed. 2. What does it measure?: Both in dialysis patients and the general population, vascular calcification and arterial stiffness are prognostic factors for morbidity and mortality. Other markers such as fetuin-A are associated with mortality in patients on hemodialysis but not in patients in early stages of chronic kidney disease. 3. What causes it?: In two selected studies, it was demonstrated again that low bone turnover and diabetes cause cardiovascular disease and vascular calcification, respectively. 4. How is it treated?: There is still no clinical evidence of regression of vascular calcification. However, a prospective study in new hemodialysis patients showed that sevelamer compared to calcium compounds slows the progression of vascular calcification and confers greater survival. A study comparing both compounds in chronic hemodialysis patients showed that sevelamer only had a benefit on survival in patients older than 65 years. It remains to be demonstrated whether the good experimental results of paricalcitol and cinacalcet are confirmed in prospective clinical studies.

[Control of phosphorus and treatment with vitamin D in chronic kidney disease prior to the start of dialysis]. / Control del fósforo y tratamiento con vitamina D en Enfermedad Renal Crónica antes del inicio de diálisis.

Hyperphosphatemia is a complication that appears in the early stages of chronic kidney disease (CKD) and that has been shown to have serious consequences in kidney disease patients. New phosphate regulators are currently being studied such as FGF- 23, a counter-regulatory phosphaturic hormone for vitamin D, and klotho, a cofactor necessary for activation of FGF-23. The main consequences of hyperphosphatemia described in CKD patients not on dialysis are ectopic calcification, increased mortality and more rapid progression of CKD. All this indicates the need for strict control of Pi. The two most currently used drugs for this purpose are lanthanum carbonate and sevelamer. Although there are no studies specifically designed for this predialysis population, these drugs appear to be effective and safe. Another complication of CKD is vitamin D deficiency which, according to recently published studies, is more prevalent and appears in earlier stages of the disease than was initially thought. There is wide debate on the need to administer vitamin D supplements systematically due to the pleiotropic effects of this hormone and which are unrelated to development of renal bone disease. Because of these doubts, there is no agreement on routine administration, although there is consensus on the need to measure 1,25-dihydroxyvitamin D and 25-hydroxyvitamin D values and to wait for the result of numerous studies that are being carried out on the impact of vitamin D on progression of cardiovascular risk factors in CKD and the possible consequences of its indiscriminate administration.

[Postpartum hemolytic uremic syndrome: a rare entity and a treatment challenge]. / Síndrome hemolítico-urémico post-parto: entidad rara de manejo complejo.

Hemolytic uremic syndrome (HUS) is a rare entity that in 7% of cases has been related to oral contraceptives, pregnancy and puerperium, In this clinical setting prognosis is worse and renal replacement therapy is usually needed. Different authors agree that plamapheresis is the treatment of choice, and has improved patient survival to 80-90%. We describe a case of a young woman that 10 days postpartum developed thrombocytopenia, microangiopathic hemolytic anemia and acute renal failure with nephrotic range proteinuria. With the suspicion of HUS she was started on plasmapheresis initially stopped due to an anaphylactic reaction to plasma and finally due to hyperhidratation with acute pulmonary edema needing mechanical ventilation. Renal biopsy confirmed the diagnosis. Clinical course was complicated with refractory hypertension and infectious complications In conclusion postpartum HUS is a rare clinical entity , that forces a differential diagnosis with hypertensive complications of pregnancy. It is associated to multiple complications difficult to handle during follow-up. Plasmapheresis treatment adds complexity to clinical care but is the only treatment of proven efficacy in order to improve survival and renal prognosis.

Síndrome hemolítico-urémicopost-parto: entidad rara de manejo complejo / No disponible

El síndrome hemolítico urémico (SHU) es una entidad de escasa incidencia, donde un 7% de casos se asocia a la toma de anticonceptivos orales, al embarazo y al puerperio, siendo tales casos de peor pronóstico, pues frecuentemente necesitan tratamiento renal sustitutivo1. Distintos autores coinciden en que la plasmaféresis es la terapia de elección, que ha mejorado la supervivencia a 80-90%2,3. Describimos el caso de una joven que en el décimo día del puerperio presenta plaquetopenia, anemia hemolíticamicroangiopática (AHM), e insuficiencia renal con proteinuria nefrótica. Con la orientación de SHU se pauta plasmaféresis, que se suspende inicialmente por alergia al plasma infundido, y definitivamente por hiperhidratación con edema agudo de pulmón (EAP) que precisa ventilación mecánica. La biopsia renal confirma el diagnóstico de presunción. La evolución resulta tórpida, marcada por la hipertensión arterial (HTA) refractaria y complicaciones infecciosas. En conclusión, el SHU post-parto es una patología poco frecuente, que asocia muchas complicaciones de difícil manejo a lo largo de su evolución y que obliga al diagnóstico diferencial con los estados hipertensivos del embarazo4. A su vez, el tratamiento con plasmaféresis añade complejidad al cuadro, pero es el único procedimiento que ha demostrado mejorar la supervivencia y el pronóstico renal (AU)

Hemolytic uremic syndrome (HUS) is a rare entity that in 7% of cases has been related to oral contraceptives, pregnancy and puerperium, In this clinical setting prognosis is worse and renal replacement therapy is usually needed. Different authors agree that plamapheresis is the treatment of choice, and has improved patient survival to 80-90%. We describe a case of a young woman that 10 days postpartum developed thrombocytopenia, microangiopathic hemolytic anemia and acute renal failure with nephritic range proteinuria. With the suspiction of HUS she was started on plasmapheresis initially stopped due to an anaphylactic reaction to plasma and finally due to hyperhidratation with acute pulmonary edema needing mechanical ventilation. Renal biopsy confirmed the diagnosis. Clinical course was complicated with refractory hypertension and infectious complications In conclusion postpartum HUS is a rare clinical entity , that forces a differential diagnosis with hypertensive complications of pregnancy. It is associated to multiple complications difficult to handle during follow-up. Plasmapheresis treatment adds complexity to clinical care but is the only treatment of proven efficacy in order to improve survival and renal prognosis (AU)

Situación clínica del paciente en el momento de iniciar diálisis. Estudio INESIR / Clinical status of the patient at the time of dialysis onset: INESIR study

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Eficiencia de implantar en atención primaria un programa dirigido a conseguir la referencia precoz al nefrólogo de los pacientes con insuficiencia renal crónica / Efficiency of implementing a program aimed at achieving early referral to the nephrologist of patients with chronic renal failure in primary care

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El "asesino silencioso" actúa temprano / "Silent murder kills at dawn

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Dilemas del presente y perspectivas de futuro en el tratamiento de la osteodistrofia renal / No disponible

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