Guía clínica española del acceso vascular para hemodiálisis / Spanish clinical guidelines on vascular access for haemodialysis

El acceso vascular para hemodiálisis es esencial para el enfermo renal tanto por su morbimortalidad asociada como por su repercusión en la calidad de vida. El proceso que va desde la creación y mantenimiento del acceso vascular hasta el tratamiento de sus complicaciones constituye un reto para la toma de decisiones debido a la complejidad de la patología existente y a la diversidad de especialidades involucradas. Con el fin de conseguir un abordaje consensuado, el Grupo Español Multidisciplinar del Acceso Vascular (GEMAV), que incluye expertos de las cinco sociedades científicas implicadas (nefrología [S.E.N.], cirugía vascular [SEACV], radiología vascular e intervencionista [SERAM-SERVEI], enfermedades infecciosas [SEIMC] y enfermería nefrológica [SEDEN]), con el soporte metodológico del Centro Cochrane Iberoamericano, ha realizado una actualización de la Guía del Acceso Vascular para Hemodiálisis publicada en 2005. Esta guía mantiene una estructura similar, revisando la evidencia sin renunciar a la vertiente docente, pero se aportan como novedades, por un lado, la metodología en su elaboración, siguiendo las directrices del sistema GRADE con el objetivo de traducir esta revisión sistemática de la evidencia en recomendaciones que faciliten la toma de decisiones en la práctica clínica habitual y, por otro, el establecimiento de indicadores de calidad que permitan monitorizar la calidad asistencial.

Vascular access for haemodialysis is key in renal patients both due to its associated morbidity and mortality and due to its impact on quality of life. The process, from the creation and maintenance of vascular access to the treatment of its complications, represents a challenge when it comes to decision-making, due to the complexity of the existing disease and the diversity of the specialities involved. With a view to finding a common approach, the Spanish Multidisciplinary Group on Vascular Access (GEMAV), which includes experts from the five scientific societies involved (nephrology [S.E.N.], vascular surgery [SEACV], vascular and interventional radiology [SERAM-SERVEI], infectious diseases [SEIMC] and nephrology nursing [SEDEN]), along with the methodological support.

Riñón «en herradura», adenocarcinoma renal / No disponible

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[Coeliac disease and membranous nephropathy]. / Enfermedad celíaca y nefropatía membranosa.

Celiac disease results from the interaction between gluten and immune, genetic, and environmental factors. Although the main clinical manifestations are derived from gastrointestinal system, it has been described some renal diseases, especially chronic glomerulonephritis. We describe a young female patient with celiac disease that it appears after delivery. Moreover, she develops simultaneously nephrotic proteinuria and microhematuria as a result of membranous nephropathy. The treatment with gluten-free diet and other conservative measures (ACEI and statin) is followed by clinical improvement and simultaneous decrease of tissue antitransglutaminase IgA-antibodies and complete remission of proteinuria. We review the relationship between celiac disease and membranous nephropathy and the role of diet in the management of both diseases.

Enfermedad celíaca y nefropatía membranosa / No disponible

La enfermedad celíaca se produce por la interacción entre el gluten contenido en los cereales y varios factores genéticos y autoinmunes. Aunque las manifestaciones clínicas predominantes son digestivas, se han descrito varias manifestaciones sistémicas. También se ha asociado con varias enfermedades renales, entre las que predominan las glomerulonefritis. Describimos el caso de una paciente con una enfermedad celíaca aparecida tras su primera gestación que de forma simultánea presenta proteinuria nefrótica y microhematuria, con sustrato morfológico de nefropatía membranosa. Tras recibir tratamiento con medidas conservadoras (IECA, estatina) y dieta sin gluten, se aprecia mejoría de la clínica digestiva, y desaparición de los anticuerpos antitransglutaminasa tisular tipo IgA y de la proteinuria. Revisamos la relación entre enfermedad celíaca y nefropatía membranosa y el papel de la dieta libre de gluten en el control de las mismas (AU)

Celiac disease results from the interaction between gluten and immune, genetic, and environmental factors. Although the main clinical manifestations are derived from gastrointestinal system, it has been described some renal diseases, especially chronic glomerulonephritis. We describe a young female patient with celiac disease which appears after delivery. Moreover, she develops simultaneously nephrotic proteinuria and microhematuria as a result of membranous nephropathy. The treatment with glutenfree diet and other conservative measures (ACEI and statin) is followed by clinical improvement and simultaneous decrease of tissue antitransglutaminase IgA-antibodies and complete remission of proteinuria. We review the relationship between celiac disease and membranous nephropathy and the role of diet in the management of both diseases (AU)

[Comorbidity, anemia and response to erythropoiesis stimulating agents in chronic hemodialysis]. / Relación entre comorbilidad, anemia y respuesta a derivados eritropoyéticos en pacientes incluidos en programa de hemodiálisis periódicas.

INTRODUCTION: Patients treated with haemodialysis have a high prevalence of co-morbidity that induces a elevate mortality risk. On the other hand, these patients have anaemia whose treatment is based in erythropoiesis stimulating agents. To date there are not enough studies to determine if co-morbidity alters erythropoietin response and the relationship between co-morbidity, response to treatment of anaemia and resistance to erythropoiesis-stimulating agents. OBJECTIVES: We have the following objectives: i) to study the prevalence of associated diseases in patients treated with haemodialysis in our Hospital Unit and to evaluate the co-morbidity Charlson Index, ii) to know the degree of anaemia control, dose and response to erythropoiesis-stimulating agents, and iii) to determine the relationship with co-morbidity and anaemia treatment. PATIENTS AND METHODS: We designed a retrospective study in stable haemodialysis treated patients. We calculated the Charlson co-morbidity index adjusted to age and we analysed levels of haemoglobin in the 6 months before study, dose of erythropoiesis-stimulating agents and its resistance index defined as doses of erythropoiesis-stimulating agents/weight (kg)/week/haemoglobin (g/dL). The different variables included in Charlson index were considered as independent variables and the index to repose to erythropoiesis-stimulating agents as a dependent variable, using bivariant and multivariate statistical analysis. RESULTS: We included 58 patients (31 males and 27 females), median age of 69.5 years (range 24-88), mean haemodialysis 83.7 months. Mean Charlson index was 7.4 +/- 2.8 (range 2-13). Comorbidity-age Charlson index was 2 in 3.4% of patients; 10.3% had 3 or 4 points; 43.2% between 5 and 7 and 43,1% 8 or more. Mean haemoglobin levels was 11,7+/-1,2 g/dL. Mean erythropoiesis-stimulating agents dose was 163.7+/-114.5 IU/kg/week and resistance index 14.1+/-9.7. Most of patients (57%) had a IRE value higher than 10. Fourteen patients (24%) had haemoglobin less than 11 g/dL, and 3 of them (5.1%) received erythropoiesis-stimulating agents more than 300 IU/kg/week. Nine subjects (15.5%) was treated with high dose of erythropoiesis-stimulating agents (>300 IU/kg/week): 3 of them had Hb>or=11 g/dL and 6 had Hb<11 g/dL. We did not found that the intensity of Charlson index is related with the degree of anaemia control or response to erythropoiesis-stimulating agents. CONCLUSIONS: Although the co-morbidity index is high and the response to erythropoiesis-stimulating agents is inadequate. In our study there is not relationship between these conditions.

[Lupus nephritis and hypothyroidism]. / Nefritis lúpica e hipotiroidismo.

Thyroid diseases could be associated with several renal alterations. In the present report we describe a patient with SLE with inactive renal involvement and symptomatic hypothyroidism that developed a clinical picture similar to lupus flare.

[CA-P control in haemodialysis and K/DOQI guidelines]. / Control del metabolismo calcio-fósforo en hemodiálisis y su adecuación a las guías K/DOQI 2003.

BACKGROUND: The publication in 2003 of the K/DOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease recommended targets levels for serum iPTH, Ca, P, and CaxP product. However, many patients do not achieved these target ranges. It is necessary to known the percentage of patients out of range in order to prevent the development of bone disease and to reduce mortality and morbidity. OBJECTIVES: To know the degree of control of Ca-P metabolism in haemodialysis patients in our haemodilalysis facilities and the achievement of target levels recommended by K/DOQI Guidelines. PATIENTS AND METHODS: We have retrospectively investigated in 190 prevalent haemodialysis patients (males 58.2%, ratio M/F 1.4, mean age 70 years, range 17-87 years, at least 3 months in haemodialysis) the serum levels of Ca, albumin-corrected serum Ca, P, CaxP product and iPTH in all analitycal determinations performed in 2004. In each patient we have obtained the average (and median) of these serum markers. Cut-off levels were carried out following the recommendations of the K/DOQI Guidelines. RESULTS: The average of serum Ca and albumin-corrected serum Ca is normal (means +/- SD = 8.9 +/- 0.6 mg/dL and 9.2 +/- 0.7 mg/dL, respectively); however, 53.7% has normal values, 9.1% hypocalcemia and 37.1% hypercalcemia. The average of serum P is also normal (mean +/- SD = 5.0 +/- 1.3 mg/dL); however, only 57.2% has normal values, and 11.7% has hypophosphoremia and the remaining 31, 1% hyperphosphoremia. The CaxP product is normal (mean +/- SD = 46.3 +/- 13.3 mg2/mL2), 4.9% with low values and 23.4% with high values. The median of serum iPTH is 253 pg/mL, but only 31.1% of them have normal values, 25.1% low range values and 43.7% has hyperparathyroidism; 9.3% with iPTH higher than 800 pg/mL. The percentage of patients with hyperphosphoremia is higher in the group with iPTH higher than 300 pg/mL (23.3% vs. 40%, chi2, p= 0.006). In patients with PTHi in normal range, 3.6% have low CaxP product and the remaining 17.8% high CaxP product. Overall, only 25% of patients falls within recommended ranges for all indicators of mineral metabolism and 17% has all serum markers outside these recommendations. CONCLUSIONS: The degree of control of mineral metabolism in haemodyalisis patients if clearly insufficient and a large percentage of them do not achieved the recommended serum targets recommended by K/DOQI Guidelines. This groups of patients are exposed to a increased risk for oseous and cardiovascular morbimortality. The analysis of adequacy must be performed with percentage of patients out of range in order to apply new therapeutical strategies.

Nefritis lúpica, micofenolato e infección por citomegalovirus / No disponible

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[Acute renal failure and hypertension]. / Fracaso renal agudo en paciente hipertenso.

Ischemic nephropathy could be complicated with hypertension and acute worsening of chronic renal failure secondary to ACE inhibitors or AT receptor antagonist treatments and arterial occlusion. We describe a patient with bilateral renal artery stenosis and hypertension treated with ATI receptor antagonist (valsartan) that developed rapid worsening of renal function that required dialysis. Percutaneous transluminal renal artery angioplasty and stenting, complemented with hydratation and valsartan suppression achieves rapid and sustained recovery of renal function.

Higher graft salvage rate in renal allograft rupture associated with acute tubular necrosis.

BACKGROUND: Renal allograft rupture is an early postoperative complication threatening graft and patient survival. We reviewed the etiology and prognostic factors for renal allograft rupture. MATERIAL AND METHODS: Among 657 renal transplants performed between 1990 and 2001, renal allograft rupture was diagnosed in 10 cases. Statistical analysis by Student t test, ANOVA, and chi-square was performed to assess donor and recipient characteristics. Multivariate logistic regression to predict renal allograft rupture used variables with P <.15 in the univariate analysis. RESULTS: Patients with renal allograft rupture were mainly men and young. Renal allograft rupture incidence was higher among allografts from non-heart-beating donors, kidneys with delayed graft function, or patients with a high antibody titer. Histopathological findings revealed that six renal allograft ruptures were secondary to acute rejection, three to acute tubular rejection and one to allograft infarction. Only one of six renal allograft ruptures (17.7%) secondary to rejection was resolved by surgery; two of the three patients (66.7%) with acute tubular necrosis were successfully operated and a nephrectomy was performed for the patient with allograft infarction. By multivariate logistic regression analysis, factors shown to be predictive for renal allograft rupture were: delayed graft function, age of recipient, peak panel-reactive antibody >25%, and initial immunosuppressive treatment without antithymocyte globulin. CONCLUSIONS: Higher graft salvage rates are possible in cases of graft rupture associated with acute tubular necrosis.

Calcificación coronaria en paciente en hemodiálisis / No disponible

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[Familial focal and segmentary hyalinosis]. / Hialinosis focal y segmentaria familiar.

Focal segmental glomerulosclerosis represents a finding in several renal disorders, characterized by proteinuria and sometimes by arterial hypertension and progressive decline in renal function. There are primary (idiopathic and familial) and secundary forms. In the last 20 years several familial cases has been reported, with a great genetic heterogeneity (dominant and recessive forms) and with multiple associations with particular MHC class-I and class-II gene loci, being Al, DR3 o DR7 the most frequently reported. We described three members of same family with focal segmental hyalinosis that shared the HLA haplotype A31 B61 DR13. This association has not been described previously. We highlight that genetic and acquired factors (obesity, hypertension...) could have importance in the development of progressive renal failure in these patients.

Hialinosis focal y segmentaria familiar / A family with focal segmental glomerulosclerosis

Las glomerulonefritis con hialinosis focal y segmentaria son la expresión morfológica de varias entidades clínicas de diversa etiología. Sus manifestaciones clínicas son también muy inespecíficas: proteinuria con o sin síndrome nefrótico y en algunos casos hipertensión arterial e insuficiencia renal progresiva. Existen formas primarias (idiopáticas o familiares) y secundarias. En los últimos 20 años se han comunicado varios casos familiares, con una gran heterogeneidad genética (formas dominantes y recesivas) habiéndose postulado asociaciones con determinados antígenos del complejo de histocompatibilidad mayor (MHC) clase I y II, siendo Al, DR3 o DR7 los más frecuentes. Describimos la aparición de hialinosis focal y segmentaria en tres miembros de una familia que comparten A31 B61 DR13, asociación no descrita. Resaltamos que la combinación de factores genéticos y adquiridos (obesidad, hipertensión) pueden ser importantes en el desarrollo de insuficiencia renal progresiva en estos enfermos

Focal segmental glomerulosclerosis represents a finding in several renal disorders, characterized by proteinuria and sometimes by arterial hypertension and progressive decline in renal function. There are primary (idiophatic and familial) and secundary forms. In the last 20 years several familial cases has been reported, with a great genetic heterogeneity (dominant and recessive forms) and with multiple associations with particular MHC class-I and class-II gene loci, being Al, DR3 o DR7 the most frecuently reported. We described three members of same family with focal segmental hyalinosis that shared the HLA haplotype A31 B61 DR13. This association has not been described previously. We highlight that genetic and acquired factors (obesity, hypertension…) could have importance in the development of progressive renal failure in these patients

Insuficiencia renal aguda por dihidroergotamina

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