Search

Flexible pipes are modular constructions made up of several layers. They are broadly employed in oilgas industry, playing an important role in the Brazilian Pre-Salt production. Under specific conditions, seawater can ingress and this contact with metallic middle layers can significantly lead to a service life reduction of these layers, especially due to a mechanism known as CO

Fibrogenesis markers, such as alpha-actin (AA), CD163 (macrophages), and E-cadherin, have been studied as chronic kidney allograft injury (CAI) predictors, a major cause of allograft failure. OBJECTIVE: Investigate the value of these markers in predicting CAI and initiation of dialysis. MATERIALS AND METHODS: Retrospective analysis of 26 kidney allograft biopsies (from 22 patients with CAI) during 2 years, evaluating intensity and percentage of marked cells on glomeruli and tubulointerstitial compartment. At the time of the biopsy, patients were 45.5 ± 15.8 years and 4.2 years after transplant, and they had a mean glomerular filtration rate (GFR) of 25.8 ± 9.9 mL/min. From an average of 8.5 glomeruli per biopsy, there was ≤25% sclerosis in 17 cases, 26% to 50% in 5, and >50% in 4. Interstitial fibrosis or tubular atrophy affected ≤25% of cortical area in 14 cases, 26% to 50% in 8, and >50% in 2. Twelve patients started dialysis 5.8 ± 4.7 years after transplant, with an average GFR 20.9 mL/min at the time of the biopsy. RESULTS: There was a higher intensity and percentage of CD163-marked cells in the tubulointerstitial compartment in advanced interstitial fibrosis. We found an association between intensity of AA in the tubulointerstitial compartment and initiation of dialysis (P = .003) and a negative correlation between intensity of E-cadherin loss and GFR (r = -0.56, P = .012). CONCLUSIONS: In our study, intensity of tubulointerstitial AA was shown to be a predictor of initiation of dialysis, and E-cadherin loss intensity was associated to CAI progression. However, prospective and larger studies are needed to evaluate the predictive value of these markers. info:eu-repo/semantics/publishedVersion

INTRODUCTION: There is a high incidence of nephrotic proteinuria in renal transplant recipients, which is an accurate predictor of graft loss. Despite this, its histologic correlates and prognostic implications are still not well characterized. We assessed the clinical and histological correlates of kidney transplantation patients with nephrotic range proteinuria. METHODS: We have retrospectively analyzed clinical and histological data from 50 kidney transplantation biopsy specimens from 44 renal transplant recipients with nephrotic range proteinuria between 2006 and 2015. The median follow-up time was 93 months (range, 14 months to 190 months). RESULTS: The mean age of the patients was 45.2 ± 13.7 years and our cohort included 86% recipients of deceased-donor grafts. The maintenance immunosuppressive regimen included calcineurin inhibitors in 68% and mammalian target of rapamycin inhibitors in 32% of patients. The average proteinuria was 6.9 ± 3.8 g/d and 52% of patients presented with nephrotic syndrome. The main histological findings were transplant glomerulopathy (22%), de novo glomerular disease (22%), and recurrence of primary disease (22%). Tubular atrophy and interstitial fibrosis was present in 78% of the biopsy specimens. Thirty-one patients (62%) lost the graft at follow-up. There was no statistically significant difference between the histologic diagnosis nor the proteinuria levels and the outcome of the graft. CONCLUSIONS: The main causes of nephrotic range proteinuria in patients undergoing biopsy were transplant glomerulopathy, recurrence of the underlying disease, and de novo glomerulonephritis. Nephrotic range proteinuria was related to a high rate of graft loss. info:eu-repo/semantics/publishedVersion

Texto completo: acesso restrito. p.176–184 Submitted by Suelen Reis (suelen_suzane@hotmail.com) on 2013-01-18T11:08:37Z No. of bitstreams: 1 Silva.pdf: 257229 bytes, checksum: 726a11e8b6867f6f8665f2016da6652a (MD5) Made available in DSpace on 2013-01-18T11:08:37Z (GMT). No. of bitstreams: 1 Silva.pdf: 257229 bytes, checksum: 726a11e8b6867f6f8665f2016da6652a (MD5) Previous issue date: 1999 The aim of the present study was to investigate the effect of acute third ventricle injections of zinc on the brain control of renal sodium and potassium excretion. Adult Wistar male rats received third ventricle injections of zinc acetate in three different doses (0.03, 0.3 and 3.0 nmol/rat). Third ventricle administration of zinc acetate provoked a significant intensification of natriuresis and kaliuresis as compared to sodium acetate-treated controls. When rats were pretreated with losartan, a selective angiotensin II AT1 receptor antagonist (10.8 nmol/rat into the third ventricle 10 min before central zinc injection) the increase in both natriuresis and kaliuresis was abolished. Furthermore, pretreatment with gadolinium, a calcium channel blocker (0.3 nmol/rat into the third ventricle 20 min before central zinc injection), also blunted the increase in renal sodium and potassium excretion seen in animals receiving zinc alone. In a group of rats receiving the same water load used in the previous experiments, the injection of zinc acetate into the third ventricle (3.0 nmol/rat) did not modify arterial blood pressure. It is suggested that zinc in the central nervous system may be involved in the control of renal sodium and potassium excretion by a mechanism unrelated to blood pressure increase. It is also shown that both natriuretic and kaliuretic actions of zinc depend on AT1 receptor activation. Whatever should be the mechanism(s) related to the central effects of zinc here evidenced, the functional integrity of calcium channels is required.

Texto completo: acesso restrito. p.749–754 Submitted by Suelen Reis (suelen_suzane@hotmail.com) on 2013-02-01T11:57:25Z No. of bitstreams: 1 -SILVA.pdf: 252821 bytes, checksum: 841efc1839f806a8b2ad9e05d8af69b7 (MD5) Made available in DSpace on 2013-02-01T11:57:25Z (GMT). No. of bitstreams: 1 -SILVA.pdf: 252821 bytes, checksum: 841efc1839f806a8b2ad9e05d8af69b7 (MD5) Previous issue date: 1997 DE CASTRO-E-SILVA, E., C. SARMENTO, T. A. NASCIMENTO, C. P. LUZ, T. SOARES, C. A. MARINHO, M. CUNHA, C. BULCÃO, I. R. DE OLIVEIRA AND J. B. FREGONEZE. Effect of third ventricle administration of L-694,247, a selective 5-HT1D receptor agonist, on water intake in rats. PHARMACOL BIOCHEM BEHAV 57[4]749–754, 1997.—L-694,247, a selective 5-HT1D receptor agonist, injected directly into the third ventricle (2.5, 5.0, and 10.0 μg/rat) of dehydrated rats induced a dose-dependent partial blockade of water intake. Injected in this way, the compound abolishes drinking behavior induced by third ventricle administration of carbachol (2 μg/rat), angiotensin II (5 ng/rat), and isoproterenol (40 μg/rat). In addition, intraventricular injections of L-694,247 did not modify water intake in normohydrated rats. The effects of L-694,247 are due to a specific interaction with 5-HT1D receptors, because its inhibitory effect on water intake in dehydrated rats is blocked by the previous administration of a 5-HT1D antagonist, GR 127935 (5 μg/rat), directly into the third ventricle. It is concluded that central 5-HT1D receptor activation disrupts the functional integrity of central pathways related to drinking behavior.

FREGONEZE, J. B., C. P. LUZ, C. SARMENTO, V. GONZALEZ, P. OLIVEIRA, P. SANTANA, JR., C. A. MARINHO, L. CASTRO, T. NASCIMENTO, S. DE PAULA, A. K. S. LIMA, I. R. DE OLIVEIRA AND E. DE CASTRO-E-SILVA. Central lead administration induces natriuretic and kaliuretic effects in rats. PHYSIOL BEHAV 65 (2) 321–326, 1998.—The aim of the present experiments was to discern whether central acute lead injections affect brain control of renal function. Adult Wistar male rats received third-ventricle injections of lead acetate in three different doses (0.03, 0.3, and 3.0 nmol/rat). Lead acetate induced a significant increase in renal excretion of sodium and potassium. Pretreatment with losartan, a selective angiotensin II AT1 receptor antagonist (10.8 nmol/rat into the third ventricle 10 min before central lead injection), inhibits lead-induced natriuretic and kaliuretic effects. In addition, pretreatment with gadolinium, a calcium-channel blocker (0.3 nmol/rat into the third ventricle 20 min before central lead administration), reversed the increase in renal excretion of sodium and potassium provoked by central lead administration. Taken together, the data presented here suggest that lead injected into the third ventricle increases renal excretion of sodium and potassium by a mechanism that depends on the functional integrity of central angiotensin II AT1 receptors and calcium channels.

Texto completo: acesso restrito. p.265–272 Submitted by Suelen Reis (suelen_suzane@hotmail.com) on 2013-01-29T15:39:12Z No. of bitstreams: 1 Luz.pdf: 199179 bytes, checksum: fd7c374e74f869bbcd00897897fe528f (MD5) Made available in DSpace on 2013-01-29T15:39:12Z (GMT). No. of bitstreams: 1 Luz.pdf: 199179 bytes, checksum: fd7c374e74f869bbcd00897897fe528f (MD5) Previous issue date: 1998 We studied the acute effects of cadmium third ventricle injections on renal excretion of water, sodium and potassium in rats previously submitted to an oral water load equivalent to 10% of their body weight. Injections of cadmium chloride (0.03, 0.3, and 3.0 nmol/rat) significantly increased sodium and potassium renal excretion without changing urine flow. Pretreatment with losartan, an angiotensin II AT1 receptor antagonist (10.8 nmol/rat into the third ventricle 10 min before central cadmium administration) inhibits the natriuretic effect of this metal, being unable to reverse its kaliuretic effect. Pretreatment with gadolinium, a calcium-channel blocker (0.3 nmol/rat into the third ventricle 20 min before central cadmium administration) abolishes both the natriuretic and the kaliuretic response of cadmium. The data clearly show that cadmium injections into the third ventricle disturb central regulation of renal function leading to an increased renal loss of sodium and potassium. It is also evident that the natriuretic action of the metal depends on an increase in brain angiotensin II release. Also, the functional integrity of calcium channels is required for the expression of both the natriuretic and the kaliuretic effects of the metal.

We have previously demonstrated that acute third ventricle injections of both Pb2+ and Cd2+ impair the dipsogenic response elicited by three different situations: dehydration and central cholinergic or angiotensinergic stimulation. ß-Adrenergic activation is part of the multifactorial integrated systems operating in drinking behavior control in the central nervous system. In the present study acute third ventricle injections of Pb2+ (3, 30 and 300 pmol/rat) or Cd2+ (0.3, 3 and 30 pmol/rat) blocked the dipsogenic response induced by third ventricle injections of isoproterenol (ISO; 160 nmol/rat) in a dose-dependent manner. Normohydrated animals receiving ISO + NaAc (sodium acetate) or saline (controls) displayed a high water intake after 120 min (ISO + saline = 5.78 ± 0.54 ml/100 g; ISO + NaAc = 6.00 ± 0.6 ml/100 g). After the same period, animals receiving ISO but pretreated with PbAc at the highest dose employed (300 pmol/rat) drank 0.78 ± 0.23 ml/100 g while those receiving ISO and pretreated with the highest dose of CdCl2 (30 pmol/rat) presented a water intake of 0.7 ± 0.30 ml/100 g. Third ventricle injections of CdCl2 (3 nmol/rat) or PbAc (3 nmol/rat) did not modify food intake in rats deprived of food for 24 h. Thus, general central nervous system depression explaining the antidipsogenic action of the metals can be safely excluded. It is concluded that both Pb2+ and Cd2+ inhibit water intake induced by central ß-adrenergic stimulation