[Prevalence of genetic prothrombotic factors (factor V Leiden and II20210 prothrombin mutation) in glomerular nephropathies with or without thrombosis]. / Prevalencia de factores protrombóticos de base genética (factor V Leiden y mutación II20210 de la protrombina) en nefropatías glomerulares con o sin trombosis.

The presence of genetic prothrombotic factors (factor V Leiden and the prothrombin II20210 mutation) was investigated in 38 patients with glomerulonephritis with or without a history of thrombotic events and/or nephrotic syndrome. We found an increased prevalence (36%) of heterozygous factor V Leiden in those patients with a history of thrombotic events. This is ten times the prevalence in the normal Spanish population. Carrier status for this mutation may be a determining factor in the development of thrombotic events along with the acquired disorders of coagulation to which these patients are prone. We found only one patient who was a carrier of the G-A II20210 mutation of the prothrombin gene; this patient had no history of venous thrombosis or embolism. Our findings suggest the need to measure activated protein C resistance and to look for the most frequent genotype causing it, Factor V Leiden, in patients with glomerulonephritis to identify those at risk who may benefit from prophylaxis against thrombosis.

Prevalencia de factores protrombóticos de base genética (factor V Leiden y mutación II20210 de la protrombina) en nefropatías glomerulares con o sin trombosis / Prevalence of genetic protrombotic factors (factor V Leiden and protrombin II20210 mutation) in glomerular nephropathies with or without thrombosis

Se investigó de forma prospectiva en 38 pacientes portadores de nefropatías glomerulares, con o sin antecedentes de síndrome nefrótico y/o manifestaciones tromboembólicas, la presencia de factores protrombóticos de base genética (factor V Leiden y mutación 1120210 de la protrombina), comprobando una elevada prevalencia de factor V Leiden (36 por ciento) en aquellos que tenían antecedentes de manifestaciones trombóticas, 10 veces superior a la de la población normal en nuestra Área de Salud (4 por ciento), y similar a la de pacientes no nefrológicos con enfermedad tromboembólica venosa. La situación de portador de esta mutación podría ser un factor determinante en la aparición de trombosis, en asociación con otros trastornos adquiridos de la coagulación que tienen lugar en estos pacientes. Por lo que respecta a la mutación 11202,0 de la protrombina estuvo presente sólo en un caso aunque en ausencia de manifestaciones de enfermedad tromboembólica venosa. Creemos aconsejable, por tanto, la determinación de la resistencia a la proteína C activada y su genotipo más frecuente, el factor V Leiden, en enfermos con glomerulonefritis con vistas a posibles actuaciones de profilaxis tromboembólica (AU)

Effects of recombinant human erythropoietin on functional and injury endothelial markers in peritoneal dialysis patients.

Clinical effects of recombinant human erythropoietin (rHuEPO) such as thrombosis, convulsions, hyperviscosity, hypertension, and angiogenic effect in culture cells have been described. We studied the rHuEPO effect on endothelial damage markers and endothelial function markers: tissue-type plasminogen activator (t-PA), nitrate (NO3), thrombomodulin (TM), and von Willebrand factor (vWF). Twenty-six peritoneal dialysis patients treated with rHuEPO and 19 controls were included. The study design for rHuEPO patients consisted of four periods: long-term treatment (rHuEPO-1); 2 months of withdrawal (rHuEPO-2); and 4 months on 5000 IU/week rHuEPO subcutaneously, with markers being measured after 2 months (rHuEPO-3) and after 4 months (rHuEPO-4). After 2 months of rHuEPO withdrawal, a decrease in hemoglobin level appeared (11+/-1.8 g/dL to 9.2+/-1.5 g/dL, p < 0.01). After rHuEPO reintroduction, this value reached 10.6+/-1.5 g/dL at two months, and 11.1+/-1.4 g/dL at four months. A significant increase in t-PA ratio was observed from two months without rHuEPO to two months on rHuEPO, returning to previous values after four months. Similarly, TM increased for patients with creatinine clearances (CrC) < 5 mL/min. No changes in the higher-than-normal plasma vWF levels were found during the various periods. A statistically significant lower value was found in controls compared with rHuEPO-4 patients. A statistically significant increase in NO3 levels was observed in the pre-venous occlusion (VO) test immediately after the re-introduction of rHuEPO. This increment returned to prior values four months after rHuEPO was reintroduced. Our results show that rHuEPO treatment causes an increase in some endothelial damage markers (TM, t-PA) and modifies endothelial function markers (t-PA ratio, NO3). These changes might favor thrombosis and atherosclerosis.

Fibrinolytic activity in laparoscopic cholecystectomy.

The aim of this study was to examine the fibrinolytic activity in laparoscopic cholecystectomy (LC) to determine whether changes occur that might indicate a greater risk of thrombosis. The study was carried out in 20 patients who had undergone laparoscopic surgery for cholelithiasis without complications. The average age was 59.4 years (34-77 years). Seventy-five percent were women. The mean operating time was 70 minutes (35-120 minutes). Pneumoperitoneum at 14 mm Hg was maintained in all patients, and they were in 30 degrees reverse Trendelenburg position. Postoperative mobilization was obtained before 24 hours, and patients were discharged 48 hours after surgery. The control group was composed of 12 patients, evenly distributed by age, sex, and length of surgery, who had undergone Bassini herniorrhaphy without complications or relapses. The following hemostatic parameters were studied: plasma fibrinolytic activity (PFA), euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator (t-PA), fast-acting plasminogen activator inhibitor-1 (PAI-1), and D-dimer (D-D). Samples were obtained at the following times: (1) under basal conditions the day before surgery, (2) preoperatively, (3) at the end of surgery, (4) 24 hours after surgery, and (5) on the seventh day following surgery. No patient had clinical manifestations of thromboembolic disease immediately after surgery or during an average follow-up period of 16 months (range 15-18 months). Analysis of the results of global fibrinolysis showed that fibrinolytic activity was enhanced only in the postoperative period (third sample) of the LC patients. The fraction of euglobulins enhances fibrinolytic activity in both groups in the third sample with regard to the other determinations; the LC patients showed a higher degree of significance (p<0.005). A significant increase of postoperative t-PA in both groups was found, being more significant in the LC group (p<0.005). In the PAI-1 values, no significant differences existed between either determinations or groups. A significant increase in D-dimer (p<0.05) occurred in the immediate postoperative period (third sample) and 24 hours later (fourth sample), returning to normal basal values on the seventh day. No significant differences were found between the two groups. These results seem to indicate that LC produces an increase in the fibrinolytic activity in plasma as a result of the liberation of tissue plasminogen activator from the venous endothelium, which could indicate hypocoagulability during the immediate postoperative period and, therefore, signify less thrombotic risk for patients undergoing this procedure.