Incidence of contrast-induced nephropathy after a computed tomography scan.

BACKGROUND AND AIMS: The term contrast-induced nephropathy is used to describe acute deterioration of renal function after the intravenous administration of iodinated contrast material. We aimed to estimate the incidence of contrast-induced nephropathy and to analyze the evolution of different biomarkers of renal function in patients who underwent computed tomography with intravenous contrast administration after premedication with oral hydration and N-acetylcysteine. MATERIAL AND METHODS: This prospective observational study included 112 patients with chronic renal failure (glomerular filtration rate (GFR) 30ml-60ml/min/1.73m2) scheduled for computed tomography with intravenous iodinated contrast material. We recorded demographic variables, dose of contrast material, diabetes mellitus, hypertension, and serum hemoglobin. We measured serum creatinine and GFR after premedication and after the CT examination. We summarized variables as means, standard deviations, and percentages. We used the Wilcoxon and Mann-Whitney tests to compare pre- and post-CT values and Pearson's r to analyze correlations. RESULTS: Incidence acute kidney injury: 0.9%; 95%CI: 0.36-1.4. Mean difference between pre- and post-CT creatinine: 0.04; 95%CI: 0.002-0.09, p<0.004. Mean difference between pre- and post-CT GFR: -3.06; 95%CI: -4.66 to -1.47), p<0.001. CONCLUSIONS: The incidence of contrast-induced nephropathy in patients with chronic renal failure and GFR 30ml-60ml/min/1.73m2 is low. The biomarkers of renal function analyzed improve in patients who receive premedication and the minimum dose of contrast material.

[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)