Encefalopatía hipóxica y necrosis laminar cortical / Hipoxic encephalopathy and cortical laminar necrosis

Introducción. La necrosis laminar cortical se caracteriza por la destrucción de la corteza cerebral, fundamentalmente de la tercera capa, ante situaciones de disminución de aporte energético al cerebro. Las lesiones cerebrales producidas se conocen gracias a estudios procedentes de autopsias, pero se han publicado pocas descripciones sobre los cambios apreciados en la neuroimagen. Presentamos el caso de una paciente que sufrió encefalopatía hipóxica secundaria a un estado epiléptico prolongado y en la que la resonancia magnética (RM) cerebral mostraba cambios compatibles con necrosis laminar cortical. Caso clínico. Se trata de una mujer de 16 años, epiléptica desde la infancia, que padeció un estado de crisis tonicoclónicas generalizadas tras el cual quedó en coma. A las tres semanas presentaba una situación de mutismo, existía reflejo de parpadeo a la amenaza y movimientos de persecución ocular ante estímulos visuales, pero sin respuesta motora o verbal intencionada. Mostraba hipertonía generalizada y temblor fino en las extremidades superiores, y movilizaba de forma espontánea las mismas, sin asimetrías. A los dos meses la situación clínica estaba estabilizada. Una RM cerebral realizada entonces mostró hiperseñal difusa en la corteza y los ganglios basales en secuencias potenciadas en T2 y FLAIR (Fluid-Attenuated Inversion Recovery), e hiposeñal en la sustancia blanca subcortical acompañada de una marcada hiperseñal que delimitaba los surcos de la convexidad en secuencias potenciadas en T1. Conclusiones. Las situaciones de hipoxia prolongada, como el estado epiléptico, dan lugar a la necrosis del manto cortical. Ello se traduce clínicamente en la aparición de encefalopatía hipóxica y, radiológicamente, en características alteraciones de señal conocidas como necrosis laminar cortical (AU)

A prospective randomised European multicentre study of medium-long run mortality and morbidity comparing acetate-free biofiltration and bicarbonate dialysis.

In recent years, the progressive increase in the mean age of the population entering chronic dialysis treatment has been responsible, on the one hand, for the growing number of patients undergoing regular dialysis, and on the other, for the high number of "critical" patients, both as a result of their age and the presence of concomitant morbidity. Thus, dialysis treatment today is not only aimed at waste removal and water-electrolyte homeostasis, but also at a reduction in morbidity and mortality, and at improving the patients' quality of life, thanks to the use of biocompatible materials and the achievement of good cardiovascular tolerance to treatment. Consequently, diffusive-convective dialysis procedures have been on the increase, since they combine better depuration with the use of biocompatible high-flux membranes. Acetate-free biofiltration (AFB) is a diffusive-convective dialysis procedure which utilises a high-flux membrane, AN69, post-dilution infusion of a sodium bicarbonate solution (NaHCO3), and a dialysate which is completely free of any buffer, and thus also free of acetate, which may have various negative effects on the patient. A number of studies have already shown the better hemodynamic stability and the reduction of intradialytic side-effects during AFB. All these, however, were short-term studies. To verify the beneficial effects of AFB in the long run, a three year multicentre randomised European trial has been proposed to compare bicarbonate hemodialysis (BD), a technique used in nearly 80% of the world's dialysis population, and AFB. The specific aim of the investigation is to verify, in a large number of patients, the results of hemodialysis treatment in terms of morbidity, mortality and quality of life. The study involves 80 hemodialysis units across Italy, France, Germany, Spain, Slovenia and Croatia, with enrollment of about 400 patients considered "critical" for at least one of the following reasons: age, diabetes, dialysis cardiovascular instability. Fifty percent of the patients are to undergo AFB with the AN69 membrane and bicarbonate solution infusion (NaHCO3 145 or 167 mEq/lt), and the other fifty percent are to be treated by BD, with any membrane except the nonmodified cellulosic one. Biochemical, cardiological, and nutritional parameters will be considered throughout the study. Mortality, morbidity both in terms of intra- and interdialysis symptoms - and hospitalisation rate, as well as the patients' quality of life, evaluated by the SF36 questionnaire, will be analysed.

Membranous glomerulonephritis in rheumatoid arthritis unrelated to gold, D-penicillamine or other connective tissue disease.

We report a 58-year-old woman with classical rheumatoid arthritis (RA) who developed a membranous glomerulonephritis (MGN). She had never been treated with gold or D-penicillamine; other connective tissue diseases as well as hepatitis B were excluded. We suggest that the responsible cause of MGN is RA.

Monoclonal gammopathy associated with crescentic glomerulonephritis and antimyeloperoxidase antibodies.

A 68-year-old male patient suffering from dizziness, gait instability, deafness, and visual loss showed proteinuria, hematuria, reduced creatinine clearance, and a monoclonal IgA lambda component. Renal biopsy revealed crescentic glomerulonephritis. Serum antibodies against myeloperoxidase were identified. These antibodies were IgG, not related to the IgA monoclonal component. This clinical description adds new information to the spectrum of diseases associated with glomerulonephritis and antimyeloperoxidase antibodies and illustrates that a monoclonal component cannot be directly implicated in the pathogenesis of a vasculitic process associated with antineutrophil cytoplasm antibodies.