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Copyright of Argentinian Journal of Respiratory & Physical Therapy (AJRPT) is the property of Asociacion Civil Cientifica de Difusion y Promocion de la Kinesiologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Open in new tab Download slide Open in new tab Download slide OBJECTIVES Cardiopulmonary bypass (CPB) use is an essential strategy for many cardiovascular surgeries. However, its use and duration have been associated with a higher rate of postoperative complications, such as low cardiac output syndrome due to myocardial oedema and dysfunction. Though Aquaporin water channels have been implicated in myocardial water balance, their specific role in this clinical scenario has not been established. METHODS In a consecutive study of 17 patients with severe aortic stenosis undergoing aortic valve replacement surgery, 2 myocardial biopsies of the left ventricle were taken: 1 before and 1 after CPB use. Sociodemographic, clinical and laboratory data were collected. Western blot and immunohistochemistry studies were performed. RESULTS After CPB use, there was a mean increase of ∼62% in Aquaporin 1 protein levels (P  = 0.001) and a mean reduction of ∼38% in Aquaporin 4 protein levels (P  = 0.030). In immunohistochemistry assays, Aquaporin 1 was found lining small blood vessels, while Aquaporin 4 formed a circular label in cardiomyocytes. There were no changes in the localization of either protein following CPB use. During the observed on-pump time interval, there was a 1.7%/min mean increase in Aquaporin 1 (P  = 0.021) and a 2.5%/min mean decrease in Aquaporin 4 (P  = 0.018). Myocardial interstitial oedema increased by 42% (95% confidence interval 31–54%) after CPB use. Patients who developed low cardiac output syndrome were in the upper half of the median percentage change of Aquaporin expression. CONCLUSION Time-dependent changes in cardiac Aquaporin expression may be associated with myocardial oedema and dysfunction related to CPB use. [ABSTRACT FROM AUTHOR]

We investigated the effect of ovariectomy(oVx) on renal and systemic hemodynamic, electrolyte excretion and total and dephosphorylated Na+,K+-ATPase α1 subunit (t-d-NKA) in normotensive Wistar rats under a normal sodium (NS, 0.24%) or high sodium (HS, 1%) intake versus intact female (IF). On NS intake, t-d-NKA was higher in oVx rats and overexpressed in the thick ascending limbs ( P < .01 vs. IF) and renal plasma flow was increased. On HS intake, oVx rats maintained a greater dephosphorylated NKA, excreted less sodium, and developed arterial hypertension (134 ± 4 vs. IF 112 ± 5 mm Hg, P < .05). Sodium load caused salt-sensitive hypertension in oVx Wistar rats. [ABSTRACT FROM AUTHOR]

In Argentina, hemolytic uremic syndrome (HUS) constitutes the most frequent cause of acute renal failure in children. Approximately 2%-4% of patients die during the acute phase, and one-third of the 96% who survive are at risk of chronic renal sequelae. Little information is available about the direct effect of Shiga toxin type 2 (Stx2) on the onset of proteinuria and the evolution of toxin-mediated glomerular or tubular injury. In this work, rats were injected intraperitoneally with recombinant Escherichia coli culture supernatant containing Stx2 (sStx2; 20 μg/kg body weight) to induce HUS. Functional, immunoblotting, and immunohistochemistry studies were carried out to determine alterations in slit diaphragm proteins and the proximal tubule endocytic system at 48 hours post-inoculation. We detected a significant increase in microalbuminuria, without changes in the proteinuria values compared to the control rats. In immunoperoxidase studies, the renal tubules and glomerular mesangium showed an increased expression of transforming growth factor β1(TGF-β1). The expression of megalin was decreased by immunoperoxidase and the cytoplasm showed a granular pattern of megalin expression by immunofluorescence techniques. Western blot analysis performed in the renal cortex from sStx2-treated and control rats using anti-nephrin and anti-podocalyxin antibodies showed a decreased expression of these proteins. We suggest that the alterations in slit diaphragm proteins and megalin expression could be related to the development of microalbuminuria in response to lethal doses of Stx2. [ABSTRACT FROM AUTHOR]

Introduction: The renal infarct is an infrequent disease and with high diagnostic difficulty that can simulate a renoureteral colic in its presentation and if it is not diagnosed it can lead to significant morbidity. The acute obstruction of the renal artery will produce necrosis of parenchim, that can become irreversible if it is not solved suitably in a short period of time (two hours). We presented a case of renal infarct emphasizing the difficulty to make a precocious diagnosis, given to its LF, and the manifold patient with pictures of acute abdominal pain that to newspaper are received in the hospitable services of urgency. Methods: Patient man of 45 years old with pain in left flank of abrupt beginning, colic type with sensation of abdominal distension. Only antecedent of importance intense tabachism during 30 years approximately 30 daily cigarettes. They are made: Blood chemistry panel, EGO, as well as X-ray, ultrasonography and computed tomography scan with hypodense area in the intravenous resisted phase partly previous of the inferior pole of the left kidney thus angioresonance with gadolineo with occlusion of segmental arteries is asked for previous and inferior. Conclusions: The renal infarct must be considered in the diagnosis differential of the acute flank pain, after discarding more frequent causes like the secondary renoureteral colico to litiasis and the inflammatory-infectious pathology, mainly in patients with cardiovascular pathology. The application of a precocious treatment but the possible thing is decisive at the time of obtaining the recovery of renal parenchim affected. [ABSTRACT FROM AUTHOR]

Copyright of Boletin del Colegio Mexicano de Urologia is the property of Colegio Mexicano de Urologia A.C. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Urea transport depends on the diffusion through cell membrane and the facilitated urea transport. Two groups of urea transporters (UT-A and UT-B) have been identified in mammals, and both are involved in intrarenal recycling of urea. The aim of our study was to examine the renal urea handling in rats with chronic renal failure (CRF)., Methods: CRF rats were induced by 5/6 nephrectomy followed by a high-protein (HP) diet to increase the progressive loss of renal function for 5 months. Functional studies on water and urea handling were performed. RT-PCR, immunoblotting and immunohistochemistry were used to identify UT-A proteins in remnant kidney., Results: A significant decrease in creatinine clearance consistent with development of CRF was observed. The remnant kidneys were hypertrophied, and total renal mass was increased. Urine production increased markedly, whereas urine osmolality and solute-free water reabsorption decreased significantly. Fractional urea excretion was increased reaching values of 105% -/+ 8%. UT-A protein was localized in pars recta by immunohistochemical studies, and it was identified as UT-A2 in outer medulla from remnant kidneys by RT-PCR and immunoblotting., Conclusion: In uremic rats, an urea transporter type UT-A2 was expressed in the pars recta, suggesting a possible relation with the fractional urea excretion increase. This expression may be a consequence of an adaptive mechanism in the handling of urea during development of CRF. Further studies will be necessary to elucidate the contribution of this mechanism to renal damage observed in the progression of CRF.