Renal allograft loss due to proximal extension of ileofemoral deep venous thrombosis.

Renal allograft recipients with thrombophilic (hypercoagulable) states are at higher risk for early allograft loss. Presumably, the combination of endothelial injury at surgery and thrombophilia predisposes to arterial or venous thrombosis. Of 270 consecutive renal transplants at our center one allograft failed secondary to renovascular thrombosis. At exploration the iliac and renal veins were thrombosed. Thrombectomy and re-implantation were attempted, but unsuccessful. Also noted at surgery was extensive clot in the femoral vein that could not be removed by embolectomy catheters. Post-operatively, a Doppler ultrasound confirmed the presence of extensive deep venous thrombosis (DVT) in the femoral and popliteal veins. The adherent nature of this clot, the extent of clot found less than 12 h after renal transplantation and the absence of leg edema suggested that the DVT existed prior to surgery. This case demonstrates that a pre-existing, asymptomatic DVT can precipitate allograft thrombosis and highlights the importance of diagnosing thrombophilia in patients undergoing renal transplantation. Current practices in our unit have evolved to include screening for thrombophilia in all patients with a suggestive history. As thrombophilic states are increasingly appreciated in the end-stage renal disease population, effective management of these patients while on hemodialysis and at the time of renal transplantation presents an ongoing challenge.

Evaluation of the antimeningococcal immunoglobin activity against five strains of Neisseria meningitidis group B from Latin America using mice as model.

To know the activity of antimeningococcal immunoglobulin, Balb/c mice of 18-22 g of body weight were challenged with 5 serotype B strains of Neisseria meningitidis (Nm) isolated from patients of different Latin American countries. The specific antimeningococcal Ig was extracted from the serum of volunteers previously vaccinated with the antimeningococcal BC vaccine VA-MENGOC-BC (Finlay Institute, Havana, Cuba). The Ig was intraperitoneally (IP) administered in a unique dose of 10 mg/mouse. The strains A, B, C, CH and D were inoculated IP in the following charges: strain A, 20 LD50; B, 25 LD50; C, 44.5 LD50; CH, 36 LD50, and D, 200, 20 and 2 LD50. For each strain, a control group received living bacteria and virulent stimulating factor (VSF). The Ig was injected 30 min before or 30 min after the challenge dose had been given, except for strain D, which only received the Ig 30 min after the challenge. As VSF, 0.5 mg of iron in the form of iron dextran was used. The experiment was analyzed considering the survival time after the challenge for each strain compared to the corresponding control group (C). When the Ig was used 30 min before the challenge, the protection period for the A strain was (C:18.1h) more than 72h (P<0.001) and 100% survival; for the B strain, (C:29.5h) 42h (P<0.05) and almost 20% survival; for the C strain (C:16.5h) 35h (P<0.01) with a 40% survival, and the CH strain (C:18.1h) 26.5h (P<0.02), with a 20% survival. When the Ig was injected 30 min after the challenge, the average survival time and the survival for the A strain was 28h (P<0.05) with 62.5%; for the B strain it was 42 h (P<0.005) and 0.0%; for the C strain 27.3 h (P<0.05) and 30%; for the CH strain 25.8h (P<0.05) and 0.0%, and for the D strain 19.1h, 26h, and more than 72h with a 0.0%, 60% and 100%, depending on the challenging dose. In general, the specific Ig used showed a protective effect in mice against the different Latin American strains tested. Additionally, the experimental model proved to be useful for the study of the antimeningococcal human Ig.