RESUMO
Resumen Gran parte de los pacientes con mieloma múltiple inician con signos y síntomas relacionados con la infiltración de células plasmáticas o el exceso de cadenas ligeras kappa. La enfermedad renal es común con enfermedad heterogénea que puede involucrar diferentes mecanismos. Se comunica el caso de un paciente con sospecha de mieloma múltiple debido a la existencia de lumbalgia, insuficiencia renal, anemia e hipercalcemia; con electroforesis de proteínas séricas negativa para hipergammaglobulinemia, en quien se confirmó el diagnóstico al demostrar la existencia de cadenas ligeras kappa en tejido renal; se realiza una revisión de la bibliografía actual.
Abstract Much of the patients with multiple myeloma present with signs and symptoms related to plasma cells infiltration or by the excess of kappa light chains. Kidney disease is common and has a heterogeneous pathophysiology that may involve different mechanisms. We present the case of a patient with suspected multiple myeloma because of low back pain, renal failure, anemia and hypercalcemia; without hipergammaglobulinemia in the electrophoresis, in whom the diagnosis was confirmed by the presence of kappa chains light in renal tissue; a review of current literature is made.
RESUMO
We evaluated 249 patients (pts) with first acute myocardial infarction: 1. Pts without thrombolysis, n = 119, 2. Pts treated with thrombolysis within 6 hours following MI, n = 80 and 3. Pts treated with thrombolysis between 6-12 hours after MI. Arrhythmic events were evaluated during follow up. All underwent heart rate variability studies and coronary angiogram where anterograde flow (TIMI) and collateral flow (Rentrop scale 0-2 = poor collateral flow and 3 = good collateral flow) were determined. Pts in group 2 and 3 showed a better anterograde and collateral flow than group 1 (p < 0.001). A lower spectral power in the high frequency band and a higher ratio low/high frequency band were observed in group 1 (p < 0.05). Conjunctive consolidation analysis showed more malignant arrhythmias in TIMI 0-2 with poor collateral flow than TIMI 0-2 with good collateral flow (17/138-12.3% vs 0/14-0%). Kaplan Meier analysis was able to demonstrate more cardiac sudden death events in TIMI 0-2 with poor collateral flow than TIMI 0-2 with good collateral flow or TIMI 3 (x2 = 7.22, p = 0.028), independently of thrombolytic treatment.
