Myxoma Mimic in a Patient With Acute Myeloid Leukemia.

Cardiac masses are rare conditions that, depending on their size and location, can cause several cardiac and systemic symptoms. We describe a case of a 21-year-old male with a history of syphilis, pulmonary tuberculosis, and acute myeloid leukemia (AML), in whom a transthoracic echocardiogram assessment was solicited before the initiation of induction chemotherapy. The study revealed a pedunculated, highly mobile mass in the right atrium that protruded to the right ventricle. Surgical resection was performed. During surgery, tricuspid valve perforation was noted and was associated with severe tricuspid valve regurgitation. Histopathological analysis of the resected mass determined that the lesion was a cardiac thrombus.

From Karl Wurm and Guy Scadding's staging to 18F-FDG PET/CT scan phenotyping and far beyond: perspective in the evading history of phenotyping in sarcoidosis.

Sarcoidosis is an inflammatory granulomatous disease of unknown etiology involving any organ or tissue along with any combination of active sites, even the most silent ones clinically. The unpredictable nature of the sites involved in sarcoidosis dictates the highly variable natural history of the disease and the necessity to cluster cases at diagnosis based on clinical and/or imaging common characteristics in an attempt to classify patients based on their more homogeneous phenotypes, possibly with similar clinical behavior, prognosis, outcome, and therefore with therapeutic requirements. In the course of the disease's history, this attempt relates to the availability of a means of detection of the sites involved, from the Karl Wurm and Guy Scadding's chest x-ray staging through the ACCESS, the WASOG Sarcoidosis Organ Assessment Instruments, and the GenPhenReSa study to the 18F-FDG PET/CT scan phenotyping and far beyond to new technologies and/or the current "omics." The hybrid molecular imaging of the 18F-FDG PET/CT scan, by unveiling the glucose metabolism of inflammatory cells, can identify high sensitivity inflammatory active granulomas, the hallmark of sarcoidosis-even in clinically and physiologically silent sites-and, as recently shown, is successful in identifying an unexpected ordered stratification into four phenotypes: (I) hilar-mediastinal nodal, (II) lungs and hilar-mediastinal nodal, (III) an extended nodal supraclavicular, thoracic, abdominal, inguinal, and (IV) all the above in addition to systemic organs and tissues, which is therefore the ideal phenotyping instrument. During the "omics era," studies could provide significant, distinct, and exclusive insights into sarcoidosis phenotypes linking clinical, laboratory, imaging, and histologic characteristics with molecular signatures. In this context, the personalization of treatment for sarcoidosis patients might have reached its goal.

COVID-19, rinovirus y asma... ¿Una mala combinación? / COVID-19, rhinovirus and asthma... a bad conmbination?

La pandemia de COVID-19 enfrentó a la humanidad a un gran desafío y hemos ido aprendiendo a medida que avanzó. La aparición de este virus, su comportamiento por si solo y en conjunto con los otros virus nos mantuvo alerta.. Los pacientes pediátricos asmáticos, a pesar de lo que se pensó en un principio, son menos afectados y hacen un cuadro clínico más leve. Objetivo: presentar un caso clínico de un paciente asmático, con una evolución tortuosa por co-infección SARS-CoV-2 y Rinovirus (RV) y revisión de la litaratura. Se trata de un escolar de 6 años, asmático con mal control, con 2 dosis de vacuna anti SARS-CoV-2, que presento un estado asmático por rinovirus y posterior evolución con neumonía grave por SARS-CoV-2, requiriendo ventilación mecánica invasiva y estadía en UCI Pediátrica. Es probable que la gravedad del caso presentado se deba al mal control del asma antes de la infección, ya que se ha visto que los niños asmáticos alérgicos presentan un factor protector para infección grave por SARS-CoV-2, lo cual esta supeditado a un buen control de su enfermedad basal.

The COVID-19 pandemic presented a great challenge and we have been learning as it has progressed. The appearance of this virus, its behavior by itself and in conjunction with the other viruses kept us alert. Pediatric asthmatic patients, despite what was initially thought, are less affected and present a milder clinical picture. Objective: to present a clinical case of an asthmatic patient, with a tortuous evolution due to SARS-CoV-2 and Rhinovirus (RV) co-infection and a literature review. This is a 6-year-old schoolboy, asthmatic with poor control, with 2 doses of the SARS-CoV-2 vaccine, who presents asthmatic status due to rhinovirus and subsequent evolution with severe pneumonia due to SARS-CoV-2, requiring invasive mechanical ventilation and stay in Pediatric ICU. It is likely that the severity of the case presented is due to poor asthma control before infection, since it has been seen that allergic asthmatic children present a protective factor for severe infection by SARS-CoV-2, which is subject to good control of his basal disease.

Taquicardia ventricular asociada a mutación en el gen de ankirina B / Ventricular tachycardia associated to a mutation in the ankyrin B gen

Resumen Se presenta el caso de una mujer de 14 años, con taquicardiomiopatía secundaria a taquicardia ventricular. Se evidenció la presencia de una variante de significado incierto en el gen ANK2, por lo que se consideró un posible síndrome de ankirina B. La paciente fue tratada con éxito a través de ablación con radiofrecuencia. Tras dicho procedimiento, tuvo recuperación completa de su función ventricular izquierda y resolución de los complejos ventriculares prematuros y los episodios de taquicardia ventricular.

Abstract We report a case of a 14-year-old with tachycardiomyopathy due to ventricular tachycardia. A variant of uncertain significance of the ANK2 gene was identified, which is suggestive of a possible ankyrin-B syndrome. The patient underwent a successful radiofrequency ablation. After the procedure, the patient completely recovered her left ventricular function and there was resolution of the premature ventricular complexes and ventricular tachycardia.

Hipertensión arterial esencial: ¿cuál agente antihipertensivo elegir? / Essential hypertension: which antihypertensive agent to choose?

Resumen Introducción: La hipertensión arterial sistémica (HTA) constituye el principal factor de riesgo para morbilidad y mortalidad cardiovascular a nivel global, afecta a todas las edades, sin distinción de género y etnicidad. Su tratamiento continúa constituyendo un reto, dada la persistencia del pobre control, especialmente en países como Colombia. Objetivo: Mostrar la evidencia disponible respecto al tratamiento actualizado de la HTA y la elección certera de los agentes antihipertensivos acorde con la individualidad de cada paciente. Asimismo, consolidar y comparar el efecto hipotensor de cada agente antihipertensivo más usado. Metodología: Se realizó una búsqueda avanzada con los términos DeCS y MeSH: hipertensión, agentes antihipertensivos, hipertensión esencial y terapia combinada, en los motores de búsqueda PubMed, Clinical Key, Lilacs, Scielo. Un total de 109 artículos se seleccionaron para elaborar en la presente revisión de la literatura. Conclusiones: La individualización del manejo de la HTA lleva al reconocimiento de los distintos fenotipos, la presencia de complicaciones, el examen físico, el género y la raza como puntos fundamentales para elegir el agente antihipertensivo más adecuado que permita alcanzar las metas de control y propenda por la reducción y prevención de las complicaciones derivadas de un control no óptimo.

Abstract Introduction: Systemic arterial hypertension (HT) constitutes the main risk factor for cardiovascular morbidity and mortality at a global level, affecting all ages regardless of gender and ethnicity. Its treatment continues to be a challenge, given the persistence of poor control, especially in countries like Colombia. Objective: To show the available evidence regarding the updated treatments of HT and the correct choice of antihypertensive agents according to the individual needs of each patient. Likewise, to consolidate and compare the hypotensive effect of the most used antihypertensive agents. Methodology: An advanced search was carried out with the terms DeCS and MeSH: Hypertension, antihypertensive agents, Essential Hypertension and Combination Therapy through the search engines PubMed, Clinical Key, Lilacs, Scielo. A total of 109 articles were selected to prepare the present literature review. Conclusions: An individualized hypertension treatment plan leads to the recognition of the different phenotypes, the presence of complications, the gender, and race, which are fundamental aspects to consider when choosing the appropriate antihypertensive agents. These findings allow for the achievement of the desired blood pressure target and leads to reduction and prevention of complications derived from suboptimal control.

Definición de displasia broncopulmonar propuesta por la Comisión Neo SOCHINEP / Definition of bronchopulmonary dysplasia proposed by the Neo SOCHINEP Commission

La displasia broncopulmonar (DBP) es la enfermedad crónica más frecuente del recién nacido prematuro. Los avances en su prevención y tratamiento han permitido una mayor sobrevida de prematuros más pequeños, pero su incidencia se ha mantenido estable en el tiempo, con una fisiopatología y presentación clínica que abarca un amplio espectro y que difiere de la DBP descrita originalmente hace más de 50 años. Aún existen controversias en su definición, la que se ha establecido en base al tratamiento, específicamente al requerimiento de soporte respiratorio. Las definiciones más utilizadas son el requerimiento de oxígeno por 28 días y a las 36 semanas de edad gestacional corregida (EGC). Recientemente se ha propuesto definirla en base al requerimiento de ventilación mecánica a las 36 semanas de EGC, lo que identificaría a los prematuros con DBP más grave y mayor probabilidad de complicaciones respiratorias y neurológicas en los 2 primeros años de vida. Nuestro objetivo en la comisión de Neo-SOCHINEP es el de recomendar la definición y clasificación que nos parece más adecuada para identificar a los prematuros portadores de DBP, considerando los aspectos fisiopatológicos, del compromiso de la función pulmonar y consecuencias prácticas de la definición en nuestro medio. También proponemos la definición del requerimiento de oxígeno en el prematuro cuando esta en neonatología, las condiciones e interpretación de la saturometría contínua cuando está pronto al alta y el seguimiento de la oxigenoterapia posterior al alta.

Bronchopulmonary dysplasia (BPD) is the most frequent chronic disease of the premature newborn. Advances in its prevention and treatment have allowed a greater survival of smaller preterm infants, but its incidence has remained stable over time, with a pathophysiology and clinical presentation that covers a wide spectrum and differs from the BPD originally described more than 50 years ago. There are still controversies in its definition, which has been established based on the treatment, specifically the requirement of respiratory support. The most used definitions are the oxygen requirement for 28 days and at 36 weeks of postmenstrual age (PMA). It has recently been proposed a definition based on the requirement of mechanical ventilation at 36 weeks of PMA, which would identify premature infants with more severe BPD and a greater probability of respiratory and neurological complications in the first 2 years of life. Our objective in the Neo-SOCHINEP commission is to recommend the definition and classification that we believe is most appropriate to identify premature infants with BPD, considering the pathophysiological aspects, the compromised lung function, and practical consequences of the definition in our medium. We also propose the definition of the oxygen requirement in premature infants when they are in neonatology, the conditions and interpretation of continuous saturation when they are soon discharged, and the follow-up of post-discharge oxygen therapy.

Angioplastia con balón de venas pulmonares por estenosis tras ablación percutánea de fibrilación auricular / Balloon angioplasty of pulmonary vein stenosis after percutaneous ablation of atrial fibrillation

Resumen Se presenta el caso de un hombre de 31 años, con historia de fibrilación auricular paroxística, a quien se realizó exitosamente una ablación por radiofrecuencia de venas pulmonares guiada por un sistema de mapeo tridimensional EnSite™. Tres meses después del procedimiento presentó hemoptisis y dolor torácico de características pleuríticas, motivo por el cual se le realizó una angiotomografía computarizada coronaria que evidenció una estenosis grave de la vena pulmonar superior izquierda y una estenosis moderada de la vena inferior izquierda. El paciente fue sometido a angioplastia con balón, con la cual se normalizó la perfusión pulmonar.

Abstract We report the case of a 31-year-old male patient with a history of paroxysmal atrial fibrillation, who underwent a successful radiofrequency pulmonary vein ablation using EnSite™ three-dimensional mapping system. Three months after the procedure, patient presented with hemoptysis and pleuritic chest pain. A coronary computed tomography angiography was performed, which showed a severe left superior pulmonary vein stenosis and a moderate left inferior pulmonary vein stenosis. A balloon angioplasty was performed with subsequent restoration of pulmonary perfusion.

Effects of infliximab on lung and circulating natural killer cells, CD56+ T cells and B cells in sarcoidosis.

BACKGROUND: Tumour necrosis factor α (TNF-α) is pivotal in sarcoid granuloma formation, and inhibitors of TNF-α offer an attractive third-line treatment option in sarcoidosis. The sarcoid inflammation is characterised by an exaggerated T helper 1 response, and evidence indicates a contribution of dysregulated and/or deficient NK (natural killer) cells, CD56+ T cells and B cells. OBJECTIVES: Insight into how TNF-α inhibitors influence these cells may provide more information on inflammatory mechanisms in sarcoidosis and improve understanding of such treatment. We therefore evaluated treatment effects of the TNF-α inhibitor infliximab on lung and peripheral blood (PB) NK, CD56+ T cells and B cells. METHODS: Fifteen patients were assessed with PB samples, spirometry and CT scan, and 11 of them also underwent bronchoalveolar lavage (BAL) close to start of infliximab treatment. These investigations were repeated after 6 months of treatment. RESULTS: Twelve out of 15 patients disclosed a clinical improvement at follow-up. Median percentage of BAL fluid (BALF) CD56+ T cells increased while a decrease was seen in PB (p<0.05 and 0.005, respectively). No significant changes were observed for NK cells. There was a trend towards increased median percentage of PB B cells (p=0.07), and a negative correlation was observed between PB and BALF B cells after treatment (p<0.05). CONCLUSION: In conclusion, 6 months of infliximab treatment in patients with sarcoidosis, of whom the majority benefited from the treatment, influenced immune cells in the lung and circulation differently, highlighting the importance of investigating several compartments concomitantly when evaluating treatment effects on the inflammatory activity.

Diaphragmatic Paraganglioma in an Adolescent Male.

Paragangliomas are an infrequent type of neuroendocrine tumor that commonly produces catecholamines. We describe a case of a 14-year-old male with a history of uncontrolled hypertension who presented to the emergency department with a headache, palpitations, and profuse sweating. Symptoms were explained by the presence of a catecholamine-producing paraganglioma located at the right diaphragm. One year after radical surgical resection, the patient remains normotensive and does not require hypertensive medications.

Recent advances in sarcoidosis genomics: epigenetics, gene expression, and gene by environment (G × E) interaction studies.

PURPOSE OF REVIEW: We aim to review the most recent findings in genomics of sarcoidosis and highlight the gaps in the field. RECENT FINDINGS: Original explorations of sarcoidosis subphenotypes, including cases associated with the World Trade Center and ocular sarcoidosis, have identified novel risk loci. Innovative gene--environment interaction studies utilizing modern analytical techniques have discovered risk loci associated with smoking and insecticide exposure. The application of whole-exome sequencing has identified genetic variants associated with persistent sarcoidosis and rare functional variations. A single epigenomics study has provided background knowledge of DNA methylation mechanisms in comparison with gene expression data. The application of machine-learning techniques has suggested new drug repositioning for the treatment of sarcoidosis. Several gene expression studies have identified prominent inflammatory pathways enriched in the affected tissue. SUMMARY: Certainly, sarcoidosis research has recently advanced in the exploration of disease subphenotypes, utilizing novel analytical techniques, and including measures of clinical variation. Nevertheless, large-scale and diverse cohorts investigated with advanced sequencing methods, such as whole-genome and single-cell RNA sequencing, epigenomics, and meta-analysis coupled with cutting-edge analytic approaches, when employed, will broaden and translate genomics findings into clinical applications, and ultimately open venues for personalized medicine.

A Gene-Environment Interaction Between Smoking and Gene polymorphisms Provides a High Risk of Two Subgroups of Sarcoidosis.

The influence and effect of cigarette smoking in sarcoidosis is unclear. Here, we evaluated gene-environment interaction between multiple genetic variants including HLA genes and smoking in sarcoidosis defined by two clinical phenotypes, Löfgren's syndrome (LS) and patients without Löfgren's syndrome (non-LS). To quantify smoking effects in sarcoidosis, we performed a gene-environment interaction study in a Swedish population-based case-control study consisting of 3,713 individuals. Cases and controls were classified according to their cigarette smoking status and genotypes by Immunochip platform. Gene-smoking interactions were quantified by an additive interaction model using a logistic regression adjusted by sex, age and first two principal components. The estimated attributable proportion (AP) was used to quantify the interaction effect. Assessment of smoking effects with inclusion of genetic information revealed 53 (in LS) and 34 (in non-LS) SNP-smoking additive interactions at false discovery rate (FDR) below 5%. The lead signals interacting with smoking were rs12132140 (AP = 0.56, 95% CI = 0.22-0.90), p = 1.28e-03) in FCRL1 for LS and rs61780312 (AP = 0.62, 95% CI = 0.28-0.90), p = 3e-04) in IL23R for non-LS. We further identified 16 genomic loci (in LS) and 13 (in non-LS) that interact with cigarette smoking. These findings suggest that sarcoidosis risk is modulated by smoking due to genetic susceptibility. Therefore, patients having certain gene variants, are at a higher risk for the disease. Consideration of individual's genetic predisposition is crucial to quantify effects of smoking in sarcoidosis.

Evolución clínica de las pacientes con amenaza de parto prematuro, en el Hospital Primero de Mayo, de enero a diciembre de 2015 / Clinical evolution of patients with threatened premature birth, at "Hospital Primero de Mayo", from January to December 2015

La evolución clínica de las pacientes con diagnóstico de parto pretérmino depende de una valoración clínica oportuna como la importancia de los antecedentes de parto prematuro previo en la historia clínica, la medición de la longitud cervical y una evaluación acertada en el inicio de un trabajo de parto verdadero. El presente estudio es un estudio descriptivo retrospectivo que trata sobre la evolución clínica de las pacientes con diagnóstico de parto prematuro las mediadas diagnosticas al momento del ingreso. Se realizó la revisión de 148 expedientes clínicos de pacientes a quienes se les ingreso con diagnóstico de Amenaza de Parto Prematuro en el periodo comprendido de enero a diciembre de 2015. La muestra se calculó a partir de un universo de 482 pacientes quienes ingresaron durante el año 2015. A los expedientes revisados se le aplicó un instrumento de elaboración propia de los investigadores basado en los objetivos del estudio y en las variables a estudiar. La información obtenida se tabuló mediante cuadros de salida usado Microsoft Excel y se graficó mediante el uso de dicho software. Los resultados obtenidos arrojaron un porcentaje de 54% en antecedentes de pacientes con parto prematuro versus un 46% de las pacientes sin dicho antecedente que es el resultado esperado según la literatura. De igual manera al 90% de las pacientes en el estudio no se les realizo medición de longitud cervical y que se considera un predictor de suma importancia para parto prematuro, pues si se encuentra relacionado directamente con el parto prematuro. Se pudo evidenciar que en el 76% de las pacientes el criterio con el cual se realizó el diagnóstico fue la actividad uterina sin presentarse cambios cervicales, realizando medidas innecesarias como el uso de tocolisis, antibióticos, y maduración pulmonar verificando el 90% de estos casos parto arriba de las 37 semanas, incluso en el ingreso posterior tuvieron necesidad de conducir con oxitocina o inducir en trabajo de parto

Approach for Identifying Human Leukocyte Antigen (HLA)-DR Bound Peptides from Scarce Clinical Samples.

Immune-mediated diseases strongly associating with human leukocyte antigen (HLA) alleles are likely linked to specific antigens. These antigens are presented to T cells in the form of peptides bound to HLA molecules on antigen presenting cells, e.g. dendritic cells, macrophages or B cells. The identification of HLA-DR-bound peptides presents a valuable tool to investigate the human immunopeptidome. The lung is likely a key player in the activation of potentially auto-aggressive T cells prior to entering target tissues and inducing autoimmune disease. This makes the lung of exceptional interest and presents an ideal paradigm to study the human immunopeptidome and to identify antigenic peptides.Our previous investigation of HLA-DR peptide presentation in the lung required high numbers of cells (800 × 10(6) bronchoalveolar lavage (BAL) cells). Because BAL from healthy nonsmokers typically contains 10-15 × 10(6) cells, there is a need for a highly sensitive approach to study immunopeptides in the lungs of individual patients and controls.In this work, we analyzed the HLA-DR immunopeptidome in the lung by an optimized methodology to identify HLA-DR-bound peptides from low cell numbers. We used an Epstein-Barr Virus (EBV) immortalized B cell line and bronchoalveolar lavage (BAL) cells obtained from patients with sarcoidosis, an inflammatory T cell driven disease mainly occurring in the lung. Specifically, membrane complexes were isolated prior to immunoprecipitation, eluted peptides were identified by nanoLC-MS/MS and processed using the in-house developed ClusterMHCII software. With the optimized procedure we were able to identify peptides from 10 × 10(6) cells, which on average correspond to 10.9 peptides/million cells in EBV-B cells and 9.4 peptides/million cells in BAL cells. This work presents an optimized approach designed to identify HLA-DR-bound peptides from low numbers of cells, enabling the investigation of the BAL immunopeptidome from individual patients and healthy controls in order to identify disease-associated peptides.

T-cell receptor-HLA-DRB1 associations suggest specific antigens in pulmonary sarcoidosis.

In pulmonary sarcoidosis, CD4(+) T-cells expressing T-cell receptor Vα2.3 accumulate in the lungs of HLA-DRB1*03(+) patients. To investigate T-cell receptor-HLA-DRB1*03 interactions underlying recognition of hitherto unknown antigens, we performed detailed analyses of T-cell receptor expression on bronchoalveolar lavage fluid CD4(+) T-cells from sarcoidosis patients.Pulmonary sarcoidosis patients (n=43) underwent bronchoscopy with bronchoalveolar lavage. T-cell receptor α and ß chains of CD4(+) T-cells were analysed by flow cytometry, DNA-sequenced, and three-dimensional molecular models of T-cell receptor-HLA-DRB1*03 complexes generated.Simultaneous expression of Vα2.3 with the Vß22 chain was identified in the lungs of all HLA-DRB1*03(+) patients. Accumulated Vα2.3/Vß22-expressing T-cells were highly clonal, with identical or near-identical Vα2.3 chain sequences and inter-patient similarities in Vß22 chain amino acid distribution. Molecular modelling revealed specific T-cell receptor-HLA-DRB1*03-peptide interactions, with a previously identified, sarcoidosis-associated vimentin peptide, (Vim)429-443 DSLPLVDTHSKRTLL, matching both the HLA peptide-binding cleft and distinct T-cell receptor features perfectly.We demonstrate, for the first time, the accumulation of large clonal populations of specific Vα2.3/Vß22 T-cell receptor-expressing CD4(+) T-cells in the lungs of HLA-DRB1*03(+) sarcoidosis patients. Several distinct contact points between Vα2.3/Vß22 receptors and HLA-DRB1*03 molecules suggest presentation of prototypic vimentin-derived peptides.

TET2 and CSMD1 genes affect SBP response to hydrochlorothiazide in never-treated essential hypertensives.

BACKGROUND: Thiazide diuretics have been recommended as a first-line antihypertensive treatment, although the choice of 'the right drug in the individual essential hypertensive patient' remains still empirical. Essential hypertension is a complex, polygenic disease derived from the interaction of patient's genetic background with the environment. Pharmacogenomics could be a useful tool to pinpoint gene variants involved in antihypertensive drug response, thus optimizing therapeutic advantages and minimizing side effects. METHODS AND RESULTS: We looked for variants associated with blood pressure response to hydrochlorothiazide over an 8-week follow-up by means of a genome-wide association analysis in two Italian cohorts of never-treated essential hypertensive patients: 343 samples from Sardinia and 142 from Milan. TET2 and CSMD1 as plausible candidate genes to affect SBP response to hydrochlorothiazide were identified. The specificity of our findings for hydrochlorothiazide was confirmed in an independent cohort of essential hypertensive patients treated with losartan. Our best findings were also tested for replication in four independent hypertensive samples of European Ancestry, such as GENetics of drug RESponsiveness in essential hypertension, Genetic Epidemiology of Responses to Antihypertensives, NORdic DILtiazem intervention, Pharmacogenomics Evaluation of Antihypertensive Responses, and Campania Salute Network-StayOnDiur. We validated a polymorphism in CSMD1 and UGGT2. CONCLUSION: This exploratory study reports two plausible loci associated with SBP response to hydrochlorothiazide: TET2, an aldosterone-responsive mediator of αENaC gene transcription; and CSMD1, previously described as associated with hypertension in a case-control study.

Cystatin C and contrast-induced acute kidney injury.

BACKGROUND: Cystatin C (CyC) is more sensitive than serum creatinine (sCr) to rapidly detect acute changes in renal function. METHODS AND RESULTS: We measured CyC together with sCr in 410 consecutive patients with chronic kidney disease undergoing either coronary and/or peripheral angiography and/or angioplasty. sCr was assessed at baseline and 24 and 48 hours after contrast media exposure. CyC was assessed at baseline and at 24 hours. Major adverse events (including death of any cause and dialysis) at 12 months were assessed. At 48 hours after contrast media exposure, contrast-induced acute kidney injury (defined as a sCr increase > or =0.3 mg/dL) occurred in 34 patients (8.2%). A CyC increase concentration > or =10% at 24 hours after contrast media exposure was detected in 87 patients (21.2%). This was the best CyC cutoff for the early identification of patients at risk for contrast-induced acute kidney injury (negative predictive value=100%; positive predictive value=39.1%). According to the defined cutoffs (that is, increase in CyC > or =10% and sCr > or =0.3 mg/dL), major adverse events occurred in 16 of 297 patients (5.4%) without any cutoffs satisfied (group 1), in 9 of 49 patients (18.4%) with only a CyC increase > or =10% (group 2), and in 9 of 31 patients (29%) with both cutoffs satisfied (group 3). By logistic regression analysis, the independent predictors of major adverse events at 1 year were group 2 (odds ratio=2.52; 95% confidence interval, 1.17 to 5.41; P=0.02), group 3 (odds ratio=4.45; 95% confidence interval, 1.72 to 11.54; P=0.002), and baseline glomerular filtration rate (odds ratio=0.91; 95% confidence interval, 0.88 to 0.95; P<0.001). CONCLUSIONS: In patients with chronic kidney disease, CyC seems to be a reliable marker for the early diagnosis and prognosis of contrast-induced acute kidney injury.