Guía clínica para la atención de la persona con insuficiencia renal crónica / Clinical guide for the attention of people suffering from chronic renal insufficiency", "_i": "

En México la población con alteraciones renales va en aumento y la insuficiencia renal crónica (IRC) constituye una de las principales causas de atención hospitalaria para padecimientos crónico-degenerativos. Esta atención hospitalaria involucra directamente al personal de enfermería el cual realiza una serie de toma de decisiones con el objetivo de mejorar y/o mantener la salud de la persona con insuficiencia renal crónica; para lograrlo es necesario estandarizar los cuidados proporcionados a dicha población basándose en la evidencia científica y en las mejores prácticas. Lo anterior es posible con la aplicación de una guía clínica de cuidado enfermero dirigida a la persona con insuficiencia renal crónica, la cual a partir de la relación de los diagnósticos de enfermería con las intervenciones específicas de enfermería nos permita identificar los cuidados prioritarios, unificar criterios de atención y otorgar un cuidado de calidad. Esta guía de cuidado enfermero se basa en los conceptos metodológicos de Virginia Henderson, contemplando como punto de abordaje las necesidades alteradas ante la situación clínica pre-existente.

Kidney disease in the mexican population have increased, chronic renal failure (CRF) is the leading cause of hospital care. Nursing care aims to improve and maintain the health of the person with CRF; is necessary to achieve standardized care to such persons, based on scientific evidence and best practices of nursing, this is possible with the implementation of clinical guidelines or nursing care directed to the person with CRF, the relationship between nursing diagnoses and specific nursing care let us prioritize care, standardizing criteria of attention and providing high quality nursing care. This nursing care guideline is based on Virginia Henderson´s theoretical model, beginning with needs attention secondary to altered pre-existing medical condition.

Thrombin is present in the lungs of patients with primary extremity osteosarcoma and pulmonary metastases.

Osteosarcoma is a rare cancer, which metastasizes to the lung in up to 80% of cases. Thrombin is involved in metastasis and is present in the lungs of patients with pulmonary metastases (PM). To identify its role in PM and osteosarcoma, we measured thrombin levels in the bronchoalveolar lavage fluid (BALF) of 15 patients. BALF was collected at different stages of the disease and correlated with the diagnosis of PM. We also assessed fibrinogen overexpression in the tumors. We found that 11/15 (73%) patients with high thrombin levels in the lungs developed PM within the first 12 months from primary surgery. The median thrombin concentration in the BALF of these patients increased up to 8x10(-9) M (range, 3x10(-9)M-15x10(-9)M), which represents a more than 100-fold increase compared to patients without PM (p<0.0001). Eight of 15 (53%) primary and 11/15 (73%) metastatic samples showed fibrinogen overexpression. A significant difference between high thrombin levels, fibrinogen overexpression and PM was found compared to patients without PM (p=0.00073 and p=0.025). These results show that thrombin levels are increased in the lungs of patients with primary osteosarcoma and a high risk of developing PM. They suggest that thrombin may be involved in the development of PM.

Ki-67: a proliferative marker that may predict pulmonary metastases and mortality of primary osteosarcoma.

Alterations in Ki-67 activity have been associated with tumor progression and poor outcome in cancer patients. This study was undertaken to identify the potential of this proliferative marker as a predictor of pulmonary metastases (PM) and mortality in osteosarcoma patients. In 38 patients with tissue available for immunohistochemical analysis, overexpression of Ki-67 was assessed. Chi-square and log rank tests were used to determine differences between proportions of the marker with PM and mortality and survival distributions respectively. P values equal or less than .05 were considered statistically significant. The median follow up of this case series was 28 months. Eighteen (47.4%) of 38 patients developed PM, and 17 (44%) overexpressed Ki-67. We found a high frequency of PM (15 of 17) among those cases that overexpressed Ki-67. This relationship was significant (P = .000006) when compared to the rest of the group. We also found a statistically significant correlation between patients with positive and negative Ki-67 scores and higher and lower mortality (P = .000962). These findings suggest that Ki-67 overexpression could be used as a prognostic molecular marker for the development of PM in osteosarcoma patients.

Evidence that thrombin present in lungs of patients with pulmonary metastasis may contribute to the development of the disease.

Early cellular events in the lung which may lead to the development of pulmonary metastases (PM) are still poorly understood. Thrombin, a key component of the coagulation cascade, may be involved in the development of PM as it has been shown to be an enhancer of platelet-tumor interaction in vitro and metastasis in vivo, and because it has been found in high levels in lungs from patients with PM. In this study, we assessed the potential role of thrombin in promoting PM by inducing an enhancement of tumor cell adhesion to platelets and tumor cell chemoinvasion and proliferation. We used bronchoalveolar lavage fluid (BALF) from 20 patients with PM. Results were compared with those from healthy controls. We found an enhancement of adhesion of PM-BALF-treated tumor cells to untreated platelets. BALF from patients with PM significantly increased chemoinvasion and proliferation in three human tumor cell lines. These activities were attenuated significantly by a thrombin inhibitor: hirudin. These results indicate that the thrombin present in the lungs of patients with PM is, at least in part, responsible for their adhesive, invasive and mitogenic activity on three different tumor cell lines. They also suggest that thrombin may be involved in the development of PM.

Frecuencia y distribución de metástasis pulmonar por sarcoma óseo en el Instituto Nacional de Cancerología: periodo 1986-1996 / Frequency and distribution of pulmonary metastases induced by bone sarcoma in the Instituto Nacional de Cancerologia: period 1986-1996

Antecedentes. Los sarcomas óseos son poco frecuentes, pero inducen hasta 80 por ciento de metástasis pulmonar. En población mexicana esta información se desconoce, por lo que describimos su frecuencia en el Instituto Nacional de Cancerología. Métodos. Se revisaron los expedientes de pacientes con sarcoma, registrados entre 1986-1996. Se recabo información demográfica, la histología del tumor y el tiempo de desarrollo de la metástasis. Resultados. Se incluyeron en el estudio 173 casos. De éstos, 74 (43 por ciento) desarrollaron metástasis pulmonar; 102 (60 por ciento) fueron hombres y 71 (40 por ciento) mujeres. Se observó una mediana de edad de 21 años. Se registraron 120 (70 por ciento) casos con diagnóstico de osteosarcoma, 54 (45 por ciento) de los cuales presentaron metástasis; 35 (20 por ciento) casos de condrosarcoma, en 10 (29 por ciento) de los cuales se confirmó metástasis a pulmón y 18 (10 por ciento) casos con sarcoma de Ewing, 10 (56 por ciento) de éstos con metástasis. Considerando la fecha de ingreso, se observaron medianas de tiempo de desarrollo de metástasis pulmonar de hasta 15 meses. A 50 meses, en los pacientes con sarcoma de Ewing, se calculó una supervivencia del 60 por ciento, significativamente menor a la observada en los otros grupos (p=0.0368). Los pacientes con osteosarcoma y metástasis presentaron una supervivencia del 70 por ciento a 50 meses, significativamente menor a la registrada de los osteosarcomas sin metástasis (p=0.0319). Conclusiones. Se encontró una frecuencia del 43 por ciento de metástasis pulmonar. El osteosarcoma y el sarcoma de Ewing fueron los principales inductores de este tipo de metástasis y los grupos en los que se registraron los menores tiempos de supervivencia en presencia o no de metástasis, respectivamente

Maximal PDGF-induced lung fibroblast chemotaxis requires PDGF receptor-alpha.

Alteration of the platelet-derived growth factor (PDGF) receptor system could be important in enhancing the mitogenic and chemotactic potential of lung fibroblasts during pulmonary fibrogenesis. We previously reported that interleukin-1 beta (IL-1 beta) upregulates the PDGF receptor-alpha (PDGFR-alpha) gene, and in this study we sought to establish the importance of the PDGFR-alpha relative to the PDGFR-beta in mediating a chemotactic response to PDGF-AA, -AB, and -BB. Pretreatment of fibroblasts for 24 h with IL-1 beta increased chemotaxis to all three PDGF isoforms. IL-1 beta pretreatment markedly increased the maximal number of 125I-labeled PDGF-AA binding sites but did not change the number of 125I-PDGF-AB or PDGF-BB sites. However, IL-1 beta increased 125I-PDGFR-AB affinity twofold. Neomycin (5 mM) was used as a PDGFR-alpha antagonist and completely blocked 125I-PDGF-AA binding and PDGF-AA-induced chemotaxis. The binding affinity of 125I-PDGF-AB and 125I-PDGF-BB was increased two-to threefold by neomycin, and chemotaxis to PDGF-AB and PDGF-BB was enhanced. These results define a role for the PDGFR-alpha as a regulatory receptor subtype that is necessary for PDGF isoforms to exert maximal chemotaxis.

Platelet-derived growth factor (PDGF)-AA, -AB, and -BB induce differential chemotaxis of early-passage rat lung fibroblasts in vitro.

Platelet-derived growth factor (PDGF) isoforms are chemoattractants and mitogens for cells of mesenchymal origin that could be important mediators of pulmonary fibrogenesis. We have previously reported that particle-activated alveolar macrophages secrete homologues of PDGF that are composed of all three PDGF isoforms (PDGF-AA, -AB, and -BB). This mixture of macrophage-derived PDGF, once dissociated from the PDGF-alpha-macroglobulin complex, induces chemotaxis of rat lung fibroblasts (RLF) in the nanomolar range. In addition, we have reported that PDGF isoforms induce differential proliferation of RLF (PDGF-BB > PDGF-AB > PDGF-AA). In the present study, we sought to determine the relative chemotactic potency of the three PDGF isoforms and correlate these responses to the relative abundance of the two types of PDGF cell-surface receptors: PDGF-alpha receptor (PDGF-R alpha) and PDGF-beta receptor (PDGF-R beta). We also investigated the chemotactic activity of combinations of two PDGF isoforms simultaneously. Isolates of early-passage RLF were assayed for chemotaxis in 48-microwell chambers. Swiss mouse 3T3 cells were assayed in parallel as a positive control cell line for PDGF-R alpha and PDGF-R beta expression. RLF responded differentially to the PDGF isoforms: PDGF-AB and PDGF-BB were potent chemoattractants and stimulated maximal chemotactic responses between 4 and 8 ng/ml PDGF, whereas PDGF-AA elicited a weak chemotactic response that was maximally 15% of that obtained with either B-chain isoform. PDGF-AB and PDGF-BB were also the most potent chemoattractants for Swiss 3T3 cells, and their response to these B-chain isoforms was approximately 40% greater than that obtained for RLF.(ABSTRACT TRUNCATED AT 250 WORDS)

[Antifoaming agent microembolism in patients undergoing extracorporeal circulation. Its frequency in post mortem material and its pathogenic potential in vitro]. / Microembolias de antiespumante en pacientes sometidos a circulación extracorpórea. Frecuencia en material post mortem y su potencial patógeno in vitro.

Antifoam microembolisms in patients that undergo open heart surgery, represent a risk for postoperative complications. We decided to study its frequency in an autopsy population of patients who died after heart surgery. Forty-five patients were selected and histological sections from the kidneys were studied under light microscopy, scanning electron microscopy and X-ray microanalysis. Thirty-six cases (80%) showed microemboli in the glomerular capillaries lumens. There was a positive correlation between the number of particles found and the length of the surgery. Microemboli were composed of an amorphous fraction and a particulated one composed of silicon. In vitro experimentation demonstrated that the particles are capable to induce cell lysis in a dose related manner. They also are susceptible of been phagocitated by macrophages. We conclude that bubble oxygenator are capable to induce microembolisms in a high percentage of the cases studied. Components of the microemboli are cytotoxic. Therefore microembolisms could be participating in the morbidity of patients subjects to cardiopulmonary bypass.

Lung cell toxicity experimentally induced by a mixed dust from Mexicali, Baja California, Mexico.

Lung disease caused by nonoccupational exposures to inorganic particles from the soil has been reported in several areas of the world. We tested the toxic potential of dust samples from a Mexican city (Mexicali) that is frequently affected by dust storms and is geographically related to the area of San Diego, CA, where constituents of the soil have been reported to be fibrogenic. We found that samples of Mexicali dust are a mixture of approximately 75% potassium aluminum silicates (illite) and approximately 20% silica. Respirable size particles were highly hemolytic and induced lactic dehydrogenase release from alveolar macrophages exposed in vitro. Animals instilled intratracheally with the dust developed a multifocal interstitial lung disease associated with deposits of the aluminum silicates, which were identified by X-ray microanalysis. Inhalation studies in rats demonstrated that the majority of particles were deposited preferentially at the first alveolar duct bifurcations. Twenty-four hours later, numerous particles had been ingested by alveolar macrophages that had migrated to those sites of deposition. It is proposed that alveolar macrophages are attracted to the deposited particles by complement fragments since Mexicali dust is capable of activating complement proteins from both serum and bronchoalveolar lavage. Activation resulted in alveolar macrophage chemotaxis. Mexicali dust induced biological activities and lung changes similar to those of asbestos and silica, suggesting that this material could be an etiologic agent of pulmonary fibrosis in exposed individuals.