Dysregulation of ferroptosis may participate in the mitigating effect of CoCl2 on contrast-induced nephropathy.

BACKGROUND: Contrast agents can directly or indirectly induce renal tubular ischemia and hypoxic damage. Given that cobalt chloride (CoCl2) can protect renal tubules, the protective effect and potential mechanism of action of CoCl2 on contrast-induced nephropathy (CIN) warrant investigation. METHODS: A CIN mouse model was established to determine the protective effect of CoCl2 on renal injury in vivo. Then, TMT-based proteomics was performed to determine the differentially expressed proteins (DEPs), following which, enrichment analyses of gene ontology and the KEGG pathway were performed. In vitro, a CIN model was constructed with renal tubular epithelial cells (HK-2) to determine the effect of CoCl2 on potential targets and the role of the key protein identified from the in vivo experiments. RESULTS: CoCl2 treatment decreased the levels of BUN and serum creatinine (sCr), while increasing the levels of urea and creatinine (Cr) in the urine of mice after CIN injury. Damage to the renal tubules in the CoCl2 treatment group was significantly less than in the CIN model group. We identified 79 DEPs after treating the in vivo model with CoCl2, and frequently observed ferroptosis-related GO and KEGG pathway terms. Of these, Hp (haptoglobin) was selected and found to have a strong renoprotective effect, even though its expression level in kidney tissue decreased after CoCl2 treatment. In HK-2 cells, overexpression of Hp reduced the ferroptosis caused by erastin, while knocking down Hp negated the attenuation effect of CoCl2 on HK-2 cell ferroptosis. CONCLUSION: CoCl2 attenuated kidney damage in the CIN model, and this effect was associated with the decrease in ferroptosis mediated by Hp.

Dysregulation of ferroptosis may participate in the mitigating effect of CoCl2 on contrast-induced nephropathy / La desregulación de ferroptosis puede participar en el efecto mitigador de CoCl2 en la nefropatía inducida por contraste

Background: Contrast agents can directly or indirectly induce renal tubular ischemia and hypoxic damage. Given that cobalt chloride (CoCl2) can protect renal tubules, the protective effect and potential mechanism of action of CoCl2 on contrast-induced nephropathy (CIN) warrant investigation. Methods: A CIN mouse model was established to determine the protective effect of CoCl2 on renal injury in vivo. Then, TMT-based proteomics was performed to determine the differentially expressed proteins (DEPs), following which, enrichment analyses of gene ontology and the KEGG pathway were performed. In vitro, a CIN model was constructed with renal tubular epithelial cells (HK-2) to determine the effect of CoCl2 on potential targets and the role of the key protein identified from the in vivo experiments. Results: CoCl2 treatment decreased the levels of BUN and serum creatinine (sCr), while increasing the levels of urea and creatinine (Cr) in the urine of mice after CIN injury. Damage to the renal tubules in the CoCl2 treatment group was significantly less than in the CIN model group. We identified 79 DEPs after treating the in vivo model with CoCl2, and frequently observed ferroptosis-related GO and KEGG pathway terms. Of these, Hp (haptoglobin) was selected and found to have a strong renoprotective effect, even though its expression level in kidney tissue decreased after CoCl2 treatment. In HK-2 cells, overexpression of Hp reduced the ferroptosis caused by erastin, while knocking down Hp negated the attenuation effect of CoCl2 on HK-2 cell ferroptosis. Conclusion: CoCl2 attenuated kidney damage in the CIN model, and this effect was associated with the decrease in ferroptosis mediated by Hp.(AU)

Antecedentes: Los agentes de contraste pueden inducir isquemia tubular renal y daño hipóxico de manera directa o indirecta. Dado que el cloruro de cobalto (CoCl2) puede proteger los túbulos renales, el efecto protector y el mecanismo de acción potencial de CoCl2 en la nefropatía inducida por contraste (NIC) merecen ser investigados. Métodos: Se estableció un modelo de NIC en ratones para determinar el efecto protector de CoCl2 en la nefropatía in vivo. Seguidamente, se realizó un análisis proteómico por TMT para determinar las proteínas diferencialmente expresadas (DEP) y, a continuación, un análisis de enriquecimiento de ontología genética y vía KEGG. In vitro, se construyó un modelo NIC en células epiteliales de túbulos renales (HK-2) para determinar el efecto de CoCl2 en los objetivos potenciales y el rol de la proteína clave identificada en los experimentos in vivo. Resultados: El tratamiento con CoCl2 redujo los niveles de BUN y de creatinina sérica e incrementó, a la vez, los de urea y creatinina en la orina de los ratones, tras la lesión NIC. El daño a los túbulos renales en el grupo de tratamiento con CoCl2 fue significativamente menor que en el grupo de modelo NIC. Identificamos 79 DEP tras el tratamiento en el modelo in vivo con CoCl2 y observamos con frecuencia ontología genética relacionada con ferroptosis y términos de vías KEGG. De ellos, se seleccionó la haptoglobina (Hp) y se encontró que tenía un fuerte efecto renoprotector, aun cuando su nivel de expresión en el tejido renal se redujo tras el tratamiento con CoCl2. En las células HK-2, la sobreexpresión de Hp redujo la ferroptosis causada por erastina, a pesar de que el descenso de Hp negó el efecto atenuador de CoCl2 en la ferroptosis de las células HK-2. Conclusión: El CoCl2 atenuó el daño renal en el modelo NIC y se asoció este efecto al descenso de ferroptosis mediada por Hp.(AU)

Estudio prospectivo aleatorizado sobre el impacto del preacondicionamiento isquémico remoto sobre la nefropatía por contraste en pacientes intervenidos de reparación aórtica endovascular / Prospective randomized study on the impact of remote ischemic preconditioning on contrast induced nephropathy in endovascular aortic repair patients

Introducción: el mayor inconveniente del uso de contrastes yodados en la práctica clínica es la nefropatía por contraste, que aumenta la morbimortalidad y los costes hospitalarios. El preacondicionamiento isquémico remoto (PCIR) es una técnica de protección tisular no invasiva que ha demostrado ser capaz de disminuir la afectación renal tras la administración de contraste intravascular. Objetivo: el objetivo principal del estudio es valorar el impacto del PCIR en la incidencia de la nefropatía inducida por contraste en pacientes intervenidos de reparación aórtica endovascular (EVAR). Material y métodos: se incluyeron pacientes intervenidos de EVAR electivo asignados de manera secuencial en grupo control y de preacondicionamiento (C y P, respectivamente). Se analizaron parámetros bioquímicos pre- y posoperatorios (a las 24 y a las 72 horas y a los 30 días). Resultados: el 98,3 % de los pacientes incluidos en el estudio fueron varones, sobre una muestra total de 120 pacientes. La media de edad fue de 73 años (rango: 56-87). La diabetes y la insuficiencia renal crónica preoperatoria (entendida como filtrado glomerular < 60 ml/min) estuvieron presentes en el 29,16 % y en el 38,33 % de los pacientes, respectivamente. La mitad de la muestra recibió preacondicionamiento en el preoperatorio. Un total de 24,17 % pacientes desarrollaron nefropatía a pesar de sueroterapia con o sin preacondicionamiento. En el posoperatorio (24-72 h) el preacondicionamiento no modificó la incidencia de nefropatía, creatinina y urea sérica o tasa de filtrado glomerular (eFG). Sin embargo, a los 30 días el grupo preacondicionado mostró una mejoría significativa de las cifras de creatinina y de ureas séricas (1,46 ± 0,3 frente a 1,03 ± 0,5; p < 0,001; 61,06 ± 27,5 mg/dl frente a 43,78 ± 12,9 mg/dl; p = 0,003) y aumento de eFG (56,37 ± 23,4 ml/min /1,73 m2 frente a 72,85 ± 17,7ml/min/ 1,73 m2; p = 0,004)...(AU)

Introduction: the biggest drawback of using iodinated contrasts in clinical practice is contrast nephropathy, which increases morbidity and mortality and hospital costs. Remote ischemic preconditioning (RIPC) is a non-invasive tissue protection technique that has proven to be able to reduce renal involvement after intravascular contrast administration. Objective: the main goal of this study was to assess the impact of RIPC on the incidence of contrast-inducednephropathy in patients undergoing endovascular aortic repair (EVAR).Material and methods: patients who underwent elective EVAR were included, and then sequentially assigned to the control and preconditioning groups (groups C and p, respectively). Pre- and postoperative hematocrit (at 24, 72 hours, and 30 days) was analyzed. Results: total of 98.3 % of the patients included in the study were men out of a total sample of 120 patients. The mean age was 73 years (range, 56-87). Diabetes and preoperative chronic kidney disease (understood as glomerular filtration rates < 60 mL/min) were present in 29.16 % and 38.33 % of the patients, respectively. Half of the sample received preconditioning in the preoperative period. A total of 24.17 % of the patients developed nephropathy despite fluid therapy with or without preconditioning. At the postoperative period (24 h-72 h), preconditioning did not modify the incidence rate of nephropathy, serum creatinine and urea, or even the estimated glomerular filtration rate (eGFR). However, at the 30-day follow-up the preconditioned group showed a significant improvement in serum creatinine and urea levels (1.46 ± 0.3 vs 1.03 ± 0.5; p < 0.001; 61.06 ± 27.5 mg/dL vs 43 .78 ± 12.9 mg/dL; p = 0.003) and eGFR increase (56.37 ± 23.4 mL/min/1.73 m2 vs 72.85 ± 17.7mL/min/1.73 m2; p = 0.004).Conclusions: RIPC seems effective in alleviating the effects of iodinated contrast on the kidneys of patients...(AU)

Diuresis inducida frente a hidratación combinada en pacientes sometidos a procedimientos cardiovasculares percutáneos: metanálisis de ensayos clínicos aleatorizados / Diuresis-matched versus standard hydration in patients undergoing percutaneous cardiovascular procedures: meta-analysis of randomized clinical trials

Introducción y objetivos: La nefropatía inducida por contraste (NIC) es una potencial complicación de los procedimientos que requieren la administración de medio de contraste yodado. El RenalGuard, que suministra una adecuada hidratación combinada con diuresis inducida por furosemida, es una alternativa a las estrategias convencionales de hidratación. Según la literatura disponible, la evidencia sobre el RenalGuard no es concluyente, por lo que hemos realizado un metanálisis utilizando una construcción bayesiana. Métodos Se realizaron búsquedas en Medline, Cochrane Library y Web of Science de ensayos aleatorizados de RenalGuard frente a estrategias estándar de hidratación periprocedimiento. El objetivo primario fue el desarrollo de NIC. Los objetivos secundarios fueron muerte por cualquier causa, shock cardiogénico, edema agudo de pulmón (EAP) e insuficiencia renal que requería terapia de reemplazo renal. Para cada resultado se calculó un riesgo relativo (RR) con el correspondiente intervalo de credibilidad del 95% (ICr95%). Registro número CRD42022378489 en PROSPERO database. Resultados Se incluyeron 6 estudios. El RenalGuard se asoció con una reducción relativa significativa de NIC (mediana de RR=0,54; ICr95%, 0,31-0,86) y EAP (mediana de RR=0,35; 95%ICr, 0,12-0,87). No se observaron diferencias significativas para los otros parámetros secundarios [muerte por cualquier causa (RR=0,49; ICr95%, 0,13-1,08), shock cardiogénico (RR=0,06; ICr95%, 0,00-1,91), terapia de reemplazo renal (RR=0,52; ICr95%, 0,18-1,18)]. El análisis Bayesiano también mostró que el RenalGuard obtuvo una alta probabilidad de posicionarse primero con respecto a todos los objetivos secundarios. Estos resultados fueron consistentes en múltiples análisis de sensibilidad. Conclusiones En los pacientes sometidos a procedimientos cardiovasculares percutáneos, el RenalGuard se asoció con un menor riesgo de NIC y EAP. (AU)

Introduction and objectives: Contrast-associated acute kidney injury (CA-AKI) is a potential complication of procedures requiring administration of iodinated contrast medium. RenalGuard, which provides real-time matching of intravenous hydration with furosemide-induced diuresis, is an alternative to standard periprocedural hydration strategies. The evidence on RenalGuard in patients undergoing percutaneous cardiovascular procedures is sparse. We used a Bayesian framework to perform a meta-analysis of RenalGuard as a CA-AKI preventive strategy. Methods We searched Medline, Cochrane Library and Web of Science for randomized trials of RenalGuard vs standard periprocedural hydration strategies. The primary outcome was CA-AKI. Secondary outcomes were all-cause death, cardiogenic shock, acute pulmonary edema, and renal failure requiring renal replacement therapy. A Bayesian random-effect risk ratio (RR) with corresponding 95% credibility interval (95%CrI) was calculated for each outcome. PROSPERO database number CRD42022378489. Results Six studies were included. RenalGuard was associated with a significant relative reduction in CA-AKI (median RR, 0.54; 95%CrI, 0.31-0.86) and acute pulmonary edema (median RR, 0.35; 95%CrI, 0.12-0.87). No significant differences were observed for the other secondary endpoints [all-cause death (RR, 0.49; 95%CrI, 0.13-1.08), cardiogenic shock (RR, 0.06; 95%CrI, 0.00-1.91), and renal replacement therapy (RR, 0.52; 95%CrI, 0.18-1.18)]. The Bayesian analysis also showed that RenalGuard had a high probability of ranking first for all the secondary outcomes. These results were consistent in multiple sensitivity analyses. Conclusions In patients undergoing percutaneous cardiovascular procedures, RenalGuard was associated with a reduced risk of CA-AKI and acute pulmonary edema compared with standard periprocedural hydration strategies. (AU)

Diuresis-matched versus standard hydration in patients undergoing percutaneous cardiovascular procedures: meta-analysis of randomized clinical trials.

INTRODUCTION AND OBJECTIVES: Contrast-associated acute kidney injury (CA-AKI) is a potential complication of procedures requiring administration of iodinated contrast medium. RenalGuard, which provides real-time matching of intravenous hydration with furosemide-induced diuresis, is an alternative to standard periprocedural hydration strategies. The evidence on RenalGuard in patients undergoing percutaneous cardiovascular procedures is sparse. We used a Bayesian framework to perform a meta-analysis of RenalGuard as a CA-AKI preventive strategy. METHODS: We searched Medline, Cochrane Library and Web of Science for randomized trials of RenalGuard vs standard periprocedural hydration strategies. The primary outcome was CA-AKI. Secondary outcomes were all-cause death, cardiogenic shock, acute pulmonary edema, and renal failure requiring renal replacement therapy. A Bayesian random-effect risk ratio (RR) with corresponding 95% credibility interval (95%CrI) was calculated for each outcome. PROSPERO database number CRD42022378489. RESULTS: Six studies were included. RenalGuard was associated with a significant relative reduction in CA-AKI (median RR, 0.54; 95%CrI, 0.31-0.86) and acute pulmonary edema (median RR, 0.35; 95%CrI, 0.12-0.87). No significant differences were observed for the other secondary endpoints [all-cause death (RR, 0.49; 95%CrI, 0.13-1.08), cardiogenic shock (RR, 0.06; 95%CrI, 0.00-1.91), and renal replacement therapy (RR, 0.52; 95%CrI, 0.18-1.18)]. The Bayesian analysis also showed that RenalGuard had a high probability of ranking first for all the secondary outcomes. These results were consistent in multiple sensitivity analyses. CONCLUSIONS: In patients undergoing percutaneous cardiovascular procedures, RenalGuard was associated with a reduced risk of CA-AKI and acute pulmonary edema compared with standard periprocedural hydration strategies.

Nefropatía inducida por contraste posterior a la angioplastia coronariatransluminal percutánea / Induced nephropathy for contrast posterior to coronary trans-luminal percutaneous angioplasty

Introducción: La nefropatía inducida por contraste, constituye una complicación de la angioplastia coronaria transluminal percutánea. Objetivo: Contribuir a la preparación de las especialidades que intervienen en la prevención de la nefropatía inducida por contraste en la angioplastia coronaria transluminal percutánea. Métodos: Se realizaron búsquedas electrónicas y en bibliotecas, en SciELO, IMBIOMED, PubMed, Latindex, Google Académico, DOAJ, Dialnet, Medline y Scopus; en idioma español e inglés, así como revisiones de libros de textos con la información sobre la nefropatía inducida por contraste secundario a la realización de una angioplastia coronaria transluminal percutánea. Se revisaron un total de 63 artículos, se seleccionaron 34 por su aporte bibliográfico a la investigación. Conclusiones: Las especialidades afines que se relacionan con pacientes sometidos a angioplastia coronaria transluminal percutánea deben intensificar sus esfuerzos por prevenir la nefropatía inducida por contraste (AU)

Introduction: Induced nephropathy for contrast, constitutes a complication of the coronary trans-luminal percutaneous angioplasty. Objective: To contribute to the preparation os specialties that take part in the prevention of induced nephropathy for contrast in the coronary trans-luminal percutaneous angioplasty. Methods: Electronic and library searches were performed in SciELO, IMBIOMED, PubMed, Latindex, Google Academic, DOAJ, Dialnet, Medline and Scopus; in English and Spanish as well as revisione in text books with the information about Induced nephropathy for contrast secondary to the performance of coronary trans-luminal percutaneous angioplasty. A total of 63 articles, 34 were selected because of their bibliographic contribution to the research. Conclusions: Specialties which are related to patients submitted to coronary trans-luminal percutaneous angioplasty should intensify their efforts for preventing induced nephropathy for contrast(AU)

Radiological iodinated contrast-induced nephropathy. / Nefropatía inducida por contrastes iodados radiológicos.

The use of iodinated contrast media can cause renal toxicity. Whether contrast media are exclusively responsible for kidney damage is currently the subject of debate, given that in most cases, other potential causes of the renal failure are present. With current low-osmolar and iso-osmolar contrast media, the incidence rate of contrast-induced nephropathy is estimated to be <1% in the low-risk population but can increase to 37% in patients who are administered contrast by an intra-arterial administration and/or who have renal failure with an estimated glomerular filtration rate (eGFR) <30mL/min/1.73m2. To minimize the risk of renal toxicity, the recommendation is to administer the least amount of contrast possible and ensure appropriate volume expansion by infusing 0.9% saline solution.

Contrast induced nephropathy in patients with primary percutaneous coronary intervention with or without metabolic syndrome / Nefropatía inducida por contraste en pacientes con intervención coronaria percutánea primaria con o sin síndrome metabólico

Abstract: Contrast induced nephropathy (CIN) is defined as the absolute increment of serum creatinine ≥ 0.5 mg/dL or an increment more than 25% of basal creatinine, without any other identified cause, within 48 hours after contrast media administration. Objective: Determine the CIN risk in patients with Acute Coronary Syndrome (ACS) with or without metabolic syndrome (MetS) treated with primary percutaneous coronary intervention (PCI). Material and methods: A prospective, observational, longitudinal and comparative study, in patients with ACS admitted to the Coronary Care Unit or Intensive Care Unit. PCI was performed with a serum creatinine (sCr) of ≤ 1.2 mg/dL prior intervention. Serum creatinine determinations were conducted 24-48 hours post PCI. The statistical test for analysis of free distribution quantitative variables was performed with Mann Whitney U test, and for qualitative variables Chi square test (χ2). Likelihood-ratio and confidence interval of 95% with p = 0.05. Results: 420 patients with infarction code were studied, 323 men (76.9%), 97 women (23.1%), with ages between 56-70 years. They were divided into 2 groups: group A 176 (41.9%) with MetS and group B 244 (58%) without MetS. CIN was present in 43 patients (10.2%) group A and in 29 (6.9%) group B. RR: 2.05, CI 95% 1.33-3.15, p = 0.0012. Conclusions: MetS is a risk factor (RF) for the development of CIN in patients with ACS who undergo PCI. Therefore, this syndrome should be kept in mind for an early detection and prevention of the development of CIN.

Resumen: La nefropatía inducida por contraste (NIC) se define como el incremento absoluto de creatinina sérica ≥ 0.5 mg/dL o un incremento del 25% de la creatinina basal, sin otra causa identificada, en un periodo de 48 horas posterior a la exposición al medio de contraste. Objetivo: Determinar el riesgo de NIC en pacientes con síndrome coronario agudo (SCA) con y sin síndrome metabólico (SM) tratados con intervencionismo coronario percutáneo (ICP). Material y métodos: Estudio prospectivo, observacional, longitudinal, comparativo, en pacientes con SCA admitidos a la Unidad de Cuidados Coronarios o a la Unidad de Cuidados Intensivos. La ICP fue realizada con creatinina sérica (Crs) previa ≤ 1.2 mg/dL. Las determinaciones de creatinina sérica se efectuaron 24-48 horas postICP. Para el análisis de las variables cuantitativas se utilizó la prueba de U de Mann-Whitney y para variables cualitativas, prueba de Chi cuadrada (χ2) con nivel de significancia e intervalos de confianza del 95% con p = 0.05. Resultados: 420 pacientes de código infarto fueron estudiados, 323 hombres (76.9%), 97 mujeres (23.1%) con edades de 56 a 70 años. Se dividieron en dos grupos: grupo A 176 (41.9%) con SM, grupo B, 244 (58%) sin SM. Se presentó NIC en 43 pacientes (10.2%) del grupo A y en 29 (6.9%) del grupo B. RR: 2.05, IC 95% 1.33-3.15, p = 0.0012. Conclusiones: El SM es un factor de riesgo (FR) para desarrollar NIC en pacientes con SCA sometidos a ICP. Por lo tanto, debe tenerse en cuenta para la detección temprana y prevención de NIC.

Prospective evaluation of the development of contrast-induced nephropathy in patients with acute coronary syndrome undergoing rotational coronary angiography vs. conventional coronary angiography: CINERAMA study. / Evaluación prospectiva del desarrollo de nefropatía inducida por contraste en pacientes con síndrome coronario agudo tratados con angiografía coronaria rotacional vs. angiografía coronaria convencional: Estudio CINERAMA.

INTRODUCTION AND OBJECTIVES: Rotational coronary angiography (RCA) requires less contrast to be administered and can prevent the onset of contrast-induced nephropathy (CIN) during invasive coronary procedures. The aim of the study is to evaluate the impact of RCA on CIN (increase in serum creatinine ≥0.5mg/dl or ≥25%) after an acute coronary syndrome. METHODS: From April to September 2016, patients suffering acute coronary syndromes who underwent diagnostic coronary angiography, with the possibility of ad hoc coronary angioplasty, were prospectively enrolled. At the operator's discretion, patients underwent RCA or conventional coronary angiography (CCA). CIN (primary endpoint), as well as analytical, angiographic and clinical endpoints, were compared between groups. RESULTS: Of the 235 patients enrolled, 116 patients received RCA and 119 patients received CCA. The RCA group was composed of older patients (64.0±11.8 years vs. 59.7±12.1 years; p=0.006), a higher proportion of women (44.8 vs. 17.6%; p<0.001), patients with a lower estimated glomerular filtration rate (76±25 vs. 86±27ml/min/1.73 m2; p=0.001), and patients who underwent fewer coronary angioplasties (p<0.001) compared with the CCA group. Furthermore, the RCA group, received less contrast (113±92 vs. 169±103ml; p<0.001), including in diagnostic procedures (54±24 vs. 85±56ml; p<0.001) and diagnostic-therapeutic procedures (174±64 vs. 205±98ml; p=0.049) compared with the CCA group. The RCA group presented less CIN (4.3 vs. 22.7%; p<0.001) compared to the CCA group, and this finding was maintained in the regression analysis (Adjusted relative risk: 0.868; 95% CI: 0.794-0.949; p=0.002). There were no differences in clinical endpoints between the groups. CONCLUSIONS: RCA was associated with lower administration of contrast during invasive coronary procedures in acute coronary syndrome patients, resulting in lower incidence of CIN, in comparison with CCA.

Contrast-induced nephropathy in patients undergoing percutaneous coronary intervention / Nefropatía inducida por medio de contraste en angiografías coronarias

Abstract: Introduction: Contrast-induced nephropathy (CIN) is defined as the impairment of renal function and is measured as either a 25% increase in serum creatinine (SCr) from baseline or 0.5 mg/dL increase in absolute value, within 48-72 hours of intravenous contrast administration. Objectives: Objectives were to calculate incidence of CIN and to describe the clinical and periprocedural risk factors for patients receiving contrast media. Secondary objective was to compare mortality between group 1 and group 2. Material and methods: In a retrospective, observational, descriptive cohort study, patients who were admitted to the hospital for diagnostic and/or therapeutic coronary angiography between January 2014 to September 2015, the serum creatinine and glomerular filtration rate (GFR) prior to angiography and 72 hours later was measured. Results: 70 patients were included, of which 14.2% developed CIN. The leading risk factors for developing AKI were: age > 65 years (OR 12.6, CI95 1.6-105.9, p = 0.03); the presence of anemia (OR 7.5, CI95 1.8-31.2, p = 0.006); and procedural time more than 90 minutes (OR 16, CI95 3.1-85.3, p = 0.001). Higher mortality was observed in the NIC group (30% vs. 1.6%, p = 0.004). Conclusions: The incidence is higher than in the literature review. The leading associated risk factors were age > 65, anemia and procedural time > 90 minutes. The development of CIN carries a higher mortality.

Resumen: Introducción: Se define como nefropatía inducida por medio de contraste (NIC) a un aumento absoluto de la creatinina sérica mayor a 0.5 mg/dL o un aumento relativo de la creatinina sérica mayor al 25%, 48-72 horas posteriores a la exposición al medio de contraste en comparación con los niveles previos después de haber excluido otras causas de lesión renal aguda (LRA). Objetivo: Determinar la incidencia de NIC y analizar los factores de riesgo asociados en los pacientes que desarrollaron LRA posterior a un procedimiento de angiografía coronaria. Se determinó mortalidad entre ambos grupos como objetivo secundario. Material y métodos: Se realizó un estudio de cohortes, observacional, descriptivo y retroelectivo. Se analizaron los pacientes que ingresaron en enero de 2014 a septiembre de 2015, para angiografía coronaria diagnostica y/o terapéutica. Se determinó la creatinina sérica y tasa de filtración glomerular (TFG) previa a la angiografía y 72 horas; además se identificaron los factores de riesgo asociados al desarrollo de NIC. Resultados: Se incluyeron 70 pacientes, de los cuales 14.2% desarrollaron NIC. Los factores de riesgo predictores más importantes para desarrollar FRA fueron la edad > 65 años (OR 12.6; IC95 1.6-105.9, p = 0.03); la presencia de anemia (OR 7.5; IC95 1.8-31.2, p = 0.006); y una duración de procedimiento mayor a 90 minutos (OR 16; IC95 3.1-85.3, p = 0.001). Se observó mayor mortalidad en el grupo NIC (30 versus 1.6%, p = 0.004). Conclusiones: La incidencia reportada es mayor que la literatura. Los factores de riesgo asociados más importantes fueron la edad > 65, anemia y procedimiento > 90 minutos. El desarrollo de NIC conlleva una mayor mortalidad.