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1.
Int. j. morphol ; 38(3): 585-591, June 2020. graf
Article in English | LILACS | ID: biblio-1098291

ABSTRACT

Acetaminophen (also called paracetamol, or APAP) induced nephrotoxicity is reported after accidental or intentional ingestion of an overdose of the drug. Renal tubular ultrastructural alterations induced by APAP overdose associated with the induction of biomarkers of kidney injury have not been investigated before. Also, we investigated whether the combined polyphenolic anti-inflammatory and antioxidants agents, resveratrol (RES) and quercetin (QUR) can protect against APAP-induced acute kidney injury. The model group of rats received a single dose of APAP (2 g/kg), whereas the protective group of rats was pre-treated for 7 days with combined doses of RES (30 mg/kg) and QUR (50 mg/kg) before being given a single dose of APAP. All rats were then sacrificed one day post APAP ingestion. Harvested kidney tissues were prepared for transmission electron microscopy (TEM) staining and blood samples were assayed for urea, creatinine, and biomarkers of inflammation and oxidative stress. TEM images and blood chemistry analysis showed that APAP overdose induced kidney damage as demonstrated by substantial alterations to the proximal convoluted tubule ultrastructure, and a significant (p<0.05) increase in urea, creatinine, tumor necrosis factor-alpha (TNF-a), and malondialdehyde (MDA) blood levels, which were protected by RES+QUR. These findings indicate that APAP induces alterations to the renal tubular ultrastructure, which is inhibited by resveratrol plus quercetin, which also decreases blood levels of kidney injury biomarkers.


El objetivo de este trabajo fue estudiar la nefrotoxicidad inducida por acetaminofeno (también llamado paracetamol o APAP) después de la ingestión accidental o intencional de una sobredosis de la droga. Las alteraciones ultraestructurales tubulares renales inducidas por sobredosis de APAP asociadas con la inducción de biomarcadores de daño renal no se han investigado. Además, estudiamos si los agentes combinados antiinflamatorios y antioxidantes polifenólicos, el resveratrol (RES) y la quercetina (QUR) pueden proteger contra la lesión renal aguda inducida por APAP. El grupo modelo de ratas recibió una dosis única de APAP (2 g / kg), mientras que el grupo protector de ratas se trató previamente durante 7 días con dosis combinadas de RES (30 mg / kg) y QUR (50 mg / kg) antes de recibir una dosis única de APAP. Todas las ratas se sacrificaron un día después de la ingestión de APAP. Los tejidos renales fueron preparados para el análisis a través de la microscopía electrónica de transmisión (MET). En las muestras de sangre se determinaron la urea, creatinina y los biomarcadores de inflamación y estrés oxidativo. Las imágenes MET y el análisis químico de la sangre mostraron que la sobredosis de APAP inducía daño renal, como lo demuestran las alteraciones sustanciales en la ultraestructura del túbulo contorneado proximal, y además, de un aumento significativo (p <0,05) de la urea, creatinina, factor de necrosis tumoral alfa y niveles sanguíneos de malondialdehído, protegidos por RES + QUR. Estos hallazgos indican que APAP induce alteraciones en la ultraestructura tubular renal, inhibida por el resveratrol más quercetina, que también disminuye los niveles sanguíneos de biomarcadores de daño renal.


Subject(s)
Animals , Rats , Quercetin/administration & dosage , Resveratrol/administration & dosage , Kidney Tubules/drug effects , Acetaminophen/toxicity , Quercetin/pharmacology , Urea/blood , Rats, Sprague-Dawley , Creatinine/blood , Microscopy, Electron, Transmission , Disease Models, Animal , Drug Overdose , Resveratrol/pharmacology , Kidney Tubules/pathology , Anti-Inflammatory Agents/administration & dosage , Antioxidants/administration & dosage
2.
Int. j. morphol ; 37(3): 1049-1057, Sept. 2019. graf
Article in English | LILACS | ID: biblio-1012395

ABSTRACT

SUMMARY: Titanium dioxide nanoparticles (TiO2 NPs) are widely used in many commercial products, nanomedicine, agriculture, personal care products, different industries and pharmaceutical preparations with potential risk in human health and the environment. The current work was conducted to investigate the renal damage that might be induced by the acute toxicity TiO2 NPs. A total of 40 healthy male adult Wistar albino rats (Rattus norvegicus) were exposed to TiO2 NPs (126, 252, 378 mg/kg bw) for 24 and 48 h. Fresh portions of the kidneys from each rat were processed for histological and histochemical alterations. In comparison with respective control rats, exposure to TiO2 NPs has marked the following glomerular, tubular and interstitial alterations including the followings: glomerular congestion, Bowman's capsule swelling and dilatation, inflamed glomeruli, renal tubules cloudy swelling, karyorrhexis, karyolysis, infiltration of inflammatory cells, congestion, necrosis, hydropic degeneration, dilatation and congestion of blood vessels, hyaline droplets and hyaline casts precipitation, interstitial edema and fibrosis. From the findings of the current work one may conclude that TiO2 NPs are capable of inducing kidney damage with more insulation in the cortex and the proximal convoluted tubules than the medulla and the distal ones respectively. In addition, it might be concluded that renal damage induced by these nanomaterials is dose and duration of exposure dependent. Further hematological, biochemical, immunohistochemical, and ultra-structural studies are recommended.


RESUMEN: Las nanopartículas de dióxido de titanio (TiO2 NP) se usan ampliamente en muchos productos comerciales, nanomedicina, agricultura, productos para el cuidado personal, diferentes industrias y preparaciones farmacéuticas con riesgo potencial para la salud humana y el medio ambiente. El trabajo actual se realizó para investigar el daño renal que podría ser inducido por la toxicidad aguda NP de TiO2. Un total de 40 ratas Wistar albinas adultas sanas (Rattus norvegicus) fueron expuestas a TiO2 NP (126, 252, 378 mg / kg de peso corporal) durante 24 y 48 h. Las muestras de los riñones de las ratas se procesaron para estudios histológicos e histoquímicos. En comparación con las ratas control, la exposición de las ratas a TiO2 NP presentaron las siguientes alteraciones glomerulares, tubulares e intersticiales: congestión glomerular, dilatación de la cápsula de Bowman, inflamación glomerular, túbulos renales aumentados, cariorrexis, cariólisis, infiltración de células inflamatorias, congestión, necrosis, degeneración hidrópica, dilatación y congestión de vasos sanguíneos, gotas y precipitaciones hialina, edema intersticial y fibrosis. A partir de los hallazgos del trabajo actual, se puede concluir que las NP de TiO 2 son capaces de inducir daño renal con más aislamiento en la corteza y en los túbulos contorneados proximales que en la médula y los túbulos contorneados distales, respectivamente. Además, se podría concluir que el daño renal inducido por estos nanomateriales depende de la dosis y la duración de la exposición. Se recomiendan estudios adicionales hematológicos, bioquímicos, inmunohistoquímicos y ultraestructurales.


Subject(s)
Animals , Rats , Titanium/toxicity , Nanoparticles/toxicity , Kidney/drug effects , Rats, Wistar , Kidney/pathology , Kidney Glomerulus/drug effects , Kidney Glomerulus/pathology , Kidney Tubules/drug effects , Kidney Tubules/pathology , Necrosis/chemically induced
3.
Clinics ; 72(2): 95-102, Feb. 2017. tab, graf
Article in English | LILACS | ID: biblio-840044

ABSTRACT

OBJECTIVES: Henoch-Schönlein purpura nephritis and immunoglobulin A nephropathy are two diseases with similar clinical presentations but very different prognoses. Transforming growth factor β1 and monocyte chemoattractant protein-1 have been associated with the development of tissue fibrosis. We examined the development of tubulointerstitial fibrosis and its relationship with Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in these patients. METHODS: Renal tissue samples were collected by renal biopsy from 50 children with Henoch-Schönlein purpura nephritis and 50 children with immunoglobulin A nephropathy. Hematoxylin and eosin and Masson's trichrome-stained tissues were examined using light microscopy. Tubulointerstitial fibrosis was graded using the method described by Bohle et al. (1). The immunohistochemical detection of Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was correlated with the tubulointerstitial fibrosis grade. Clinical Trial registration number: ZJCH-2012-0105. RESULTS: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in the renal tissues was significantly greater in the patients with immunoglobulin A nephropathy than in the patients with Henoch-Schönlein purpura nephritis (both p<0.001). The immunoglobulin A nephropathy patients had a higher tubulointerstitial fibrosis grade than the Henoch-Schönlein purpura nephritis patients (p<0.001). The tubulointerstitial fibrosis grade was in accordance with the Transforming growth factor β1 and monocyte chemoattractant protein-1 expression levels in both diseases (both p<0.001). CONCLUSION: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was associated with the development of immunoglobulin A nephropathy and Henoch-Schönlein purpura nephritis. Further studies are needed to better evaluate this association.


Subject(s)
Humans , Male , Female , Child, Preschool , Child , Adolescent , Purpura, Schoenlein-Henoch/metabolism , Chemokine CCL2/metabolism , Transforming Growth Factor beta1/metabolism , Glomerulonephritis, IGA/metabolism , Kidney Tubules/metabolism , Prognosis , Purpura, Schoenlein-Henoch/pathology , Fibrosis , Glomerulonephritis, IGA/pathology , Kidney Tubules/pathology
4.
Article in English | WPRIM | ID: wpr-56138

ABSTRACT

Tenofovir disoproxil fumarate (TDF) is effective against chronic hepatitis B (CHB) infection and its use is increasing rapidly worldwide. However, it has been established that TDF is associated with renal toxicity in human immunodeficiency virus-infected patients, while severe or symptomatic TDF-associated nephrotoxicity has rarely been reported in patients with CHB. Here we present two patients with TDF-associated nephrotoxicity who were being treated for CHB infection. The first patient was found to have clinical manifestations of proximal renal tubular dysfunction and histopathologic evidence of acute tubular necrosis at 5 months after starting TDF treatment. The second patient developed acute kidney injury at 17 days after commencing TDF, and he was found to have membranoproliferative glomerulonephritis with acute tubular injury. The renal function improved in both patients after discontinuing TDF. We discuss the risk factors for TDF-associated renal toxicity and present recommendations for monitoring renal function during TDF therapy.


Subject(s)
Acute Kidney Injury/etiology , Aged , Antiviral Agents/adverse effects , Creatinine/blood , Glomerular Filtration Rate , Hepatitis B, Chronic/drug therapy , Humans , Kidney Tubules/pathology , Male , Microscopy, Electron , Middle Aged , Necrosis , Risk Factors , Tenofovir/adverse effects
5.
Acta cir. bras ; 29(12): 812-818, 12/2014. tab, graf
Article in English | LILACS | ID: lil-731027

ABSTRACT

PURPOSE: To investigate the effects of acute hyperglycemia on dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury. METHODS: Sprague-Dawley rats were randomly arranged to the normoglycemic (NG) or hyperglycemic group (HG), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and dex (given by dexmedetomidine) groups. Acute hyperglycemia was induced by intraperitoneal injection (i.p.) of 25% glucose (3 g/kg) 45 min before ischemia. Dexmedetomidine (50 μg/kg, i.p.) was administrated 30 min before induction of ischemia. Renal function, histology, apoptosis, expression of Bax, Bcl-2 and phosphorylated AKT (p-AKT) were detected. RESULTS: I/R insult significantly increased the serum levels of blood urea nitrogen and creatinine, apoptotic tubular epithelial cells, expression of Bax and p-AKT, but decreased Bcl-2 expression. All these changes were further enhanced by hyperglycemia (p<0.05). In hyperglycemic condition, there was no statistically difference between the I/R group and Dex group in all the aforementioned detection indexes (p>0.05). CONCLUSION: Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats. .


Subject(s)
Animals , Male , Dexmedetomidine/pharmacology , Hyperglycemia/physiopathology , Ischemic Preconditioning , Ischemia/chemically induced , Kidney/blood supply , Reperfusion Injury/prevention & control , Acute Disease , Apoptosis/drug effects , Blood Glucose , Creatinine/blood , Hyperglycemia/chemically induced , Ischemia/drug therapy , Kidney Tubules/drug effects , Kidney Tubules/pathology , Models, Animal , Nephrectomy , Proto-Oncogene Proteins c-akt/metabolism , Random Allocation , Rats, Sprague-Dawley , Urea/blood
6.
Rev. panam. salud pública ; 36(5): 342-347, nov. 2014. tab
Article in Spanish | LILACS | ID: lil-733238

ABSTRACT

Este trabajo muestra, desde el punto de vista de la normatividad de la Organización Panamericana de la Salud (OPS), el proceso de gestación, la metodología de implementación y los resultados obtenidos de la iniciativa de formación de recursos humanos en salud vía e-learning a través del Campus Virtual de Salud Pública de la Universidad de Guadalajara, México, a seis años de su inicio. Se trata de un informe especial del trabajo realizado por el comité institucional del campus virtual en la región occidental de México para generar un portal de Internet que se ajustara a los lineamientos del Modelo Estratégico establecido por el Nodo México y la OPS para la Región de las Américas. Este Campus Virtual inició sus actividades en el año 2007. Su filosofía es el uso de software libre y la colaboración entre instituciones. El nodo fue implementado en un año y ha logrado capacitar a más de 500 profesionales de la salud a través de cursos virtuales, su plataforma educativa y un repositorio de recursos virtuales de aprendizaje con interoperabilidad con los repositorios de México y de la Región de las Américas. El comité del Campus Virtual de la Universidad de Guadalajara ha intentado respetar lo más posible al modelo propuesto, lo que ha permitido cumplir la mayoría de los objetivos fijados en el plan de trabajo inicial, aunque ha enfrentado una serie de dificultades administrativas y de motivación de sus integrantes.


This paper discusses the gestation process, implementation methodology, and results obtained from the initiative to use e-learning to train human resources for health, six years after the launch of the Virtual Campus of Public Health of the University of Guadalajara (Mexico); the discussion is framed by Pan American Health Organization (PAHO) standards and practices. This is a special report on the work done by the institutional committee of the Virtual Campus in western Mexico to create an Internet portal that follows the guidelines of the strategic model established by Nodo México and PAHO for the Region of the Americas. This Virtual Campus began its activities in 2007, on the basis of the use of free software and institutional collaboration. Since the initial year of implementation of the node, over 500 health professionals have been trained using virtual courses, the node's educational platform, and a repository of virtual learning resources that are interoperable with other repositories in Mexico and the Region of the Americas. The University of Guadalajara Virtual Campus committee has followed the proposed model as much as possible, thereby achieving most of the goals set in the initial work plan, despite a number of administrative challenges and the difficulty of motivating committee members.


Subject(s)
Animals , Dogs , Iron/toxicity , Kidney Tubules/drug effects , Adenylyl Cyclases/metabolism , /metabolism , Cell Line , Cell Division/drug effects , Epithelium/drug effects , Epithelium/pathology , Epithelium/physiology , Ferric Compounds/toxicity , Iron/metabolism , Kidney Tubules/pathology , Kidney Tubules/physiology , LLC-PK1 Cells , Microscopy, Electron , Swine , Wound Healing/drug effects
8.
Medicina (B.Aires) ; 74(3): 254-258, jun. 2014. ilus
Article in Spanish | LILACS | ID: lil-734375

ABSTRACT

La muerte celular programada y la fibrosis renal son procesos inherentes a la enfermedad renal crónica y, en tal sentido, ha sido recientemente descripta una clara desregulación de la maquinaria respiratoria mitocondrial en pacientes con enfermedad renal crónica asociada con un aumento del estrés oxidativo. Las células tubulares lesionadas vinculadas a los macrófagos intersticiales y miofibroblastos producen citoquinas y factores de crecimiento que promueven un estado inflamatorio, inducen la apoptosis de las células tubulares y facilitan la acumulación de matriz extracelular. La angiotensina II desempeña un papel central en la fibrogénesis renal y conduce a una rápida progresión de la enfermedad renal crónica. Los niveles crecientes de la angiotensina II inducen citoquinas pro-inflamatorias, la activación de NF-kB, moléculas de adhesión, quimiocinas, factores de crecimiento y estrés oxidativo. Toda la evidencia actual sugiere que la angiotensina II aumenta el estrés oxidativo mitocondrial, regula la inducción de apoptosis y condiciona al estado inflamatorio. Por lo tanto, existiría un papel determinante de las mitocondrias y el estrés oxidativo en el proceso inflamatorio renal. Finalmente, esta revisión resume nuestro actual conocimiento acerca de los posibles mecanismos que contribuirían con la apoptosis modulada por la inflamación y/o el estrés oxidativo durante la enfermedad renal crónica. Además, se propone un nuevo concepto de herramientas anti-inflamatorias que regulan el estrés oxidativo mitocondrial lo cual afectaría directamente al proceso inflamatorio y la apoptosis. Esta idea podría tener consecuencias atractivas sobre el tratamiento de patologías inflamatorias renales y de otras afines.


The apoptosis and renal fibrosis are processes inherent to the chronic kidney disease, and consequently a clear deregulation of the mitochondrial respiratory mechanism has been described in patients with chronic renal disease associated to an increase of the oxidative stress. The injured tubular cells linked to the interstitial macrophages and myofibroblasts produce cytokines and growth factors that encourage an inflammatory condition, inducing the apoptosis of the tubular cells and enabling the accumulation of the extracellular matrix. The angiotensin II has a central role in the renal fibrogenesis leading to a rapid progression of the chronic kidney disease. The growing levels of the angiotensin II induce pro-inflammatory cytokines, the activation of NF-kB, adhesion molecules,chemokines, growth factors, and oxidative stress. The current evidence suggests that the angiotensin II increases the mitochondrial oxidative stress, regulates the induction of the apoptosis and conditions the inflammatory process. Therefore the mitochondria and the oxidative stress would play a determinant role in the renal inflammatory process. Finally, this review summarizes our present knowledge regarding the possible mechanisms that would contribute to the apoptosis conditioned by inflammation and/or oxidative stress during the chronic renal disease. Additionally, a new concept of the anti-inflammatory tools is proposed to regulate the mitochondrial oxidative stress that would directly affect the inflammatory process and apoptosis. This concept could have positive consequences on the treatment of renal inflammatory pathologies and related diseases.


Subject(s)
Animals , Humans , Apoptosis/physiology , Mitochondria/metabolism , Mitochondria/pathology , Nephritis/etiology , Oxidative Stress/physiology , Renal Insufficiency, Chronic/etiology , Angiotensin II/metabolism , Cytoprotection , Ergocalciferols/pharmacology , Kidney Cortex/drug effects , Kidney Cortex/pathology , Kidney Tubules/drug effects , Kidney Tubules/pathology , NF-kappa B/metabolism , Nephritis/metabolism , Renal Insufficiency, Chronic/metabolism , Renal Insufficiency, Chronic/pathology , Vitamins/pharmacology
9.
Rev. Inst. Med. Trop. Säo Paulo ; 56(1): 85-88, Jan-Feb/2014. tab, graf
Article in English | LILACS | ID: lil-702064

ABSTRACT

Renal histology results are very scarce in dengue-associated rhabdomyolysis patients developing acute kidney injury (AKI). We report a case of dengue fever-induced AKI associated to rhabdomyolysis with a renal biopsy showing acute tubular necrosis (ATN) and renal deposition of myoglobin. A 28-year-old patient who presented dengue fever (DF) complicated by severe AKI and rhabdomyolysis is described. The patient required hemodialysis for three weeks. A renal biopsy revealed ATN with positive staining for myoglobin in the renal tubuli. The patient was discharged with recovered renal function. In conclusion, this case report described a biopsy proven ATN associated to DF-induced rhabdomyolysis, in which renal deposition of myoglobin was demonstrated. We suggest that serum creatine phosphokinase should be monitored in DF patients to allow for an early diagnosis of rhabdomyolysis and the institution of renal protective measures.


Resultados de histologia renal são muito escassos em pacientes com rabdomiólise e injúria renal aguda (IRA) associada a dengue. Descrevemos caso de dengue complicado por rabdomiólise e IRA no qual a biópsia renal mostrou necrose tubular aguda (NTA) e deposição renal de mioglobina. Paciente de 28 anos que apresentou dengue complicado por IRA grave e rabdomiólise é descrito. Ele necessitou de diálise por três semanas. A biópsia renal mostrou NTA, com imunohistoquímica fortemente positiva para mioglobina nos túbulos renais. O paciente recebeu alta com recuperação da função renal. Em conclusão, descrevemos caso de dengue complicado por IRA e rabdomiólise, em que a biópsia renal mostrou NTA e deposição de mioglobina. Sugerimos que creatinofosfoquinase deve ser monitorizada em pacientes com dengue para permitir o diagnóstico precoce de rabdomiólise e a instituição de medidas protetoras para o rim.


Subject(s)
Adult , Humans , Male , Acute Kidney Injury/etiology , Dengue/complications , Kidney Tubules/pathology , Rhabdomyolysis/etiology , Acute Kidney Injury/pathology , Biopsy , Necrosis
10.
Clinics ; 67(7): 697-703, July 2012. ilus, graf, tab
Article in English | LILACS | ID: lil-645439

ABSTRACT

OBJECTIVES: The objectives of our study were as follows: 1) to analyze the prognostic value of macrophage infiltration in primary IgA nephropathy (IgAN) and 2) to study the relationship between macrophages and other factors associated with the development of renal fibrosis, including mast cells, TGF-β1, α-SMA and NF-kB. METHODS: We analyzed 62 patients who had been diagnosed with IgAN between 1987 and 2003. Immunohistochemical staining was performed with monoclonal antibodies against CD68 and mast cell tryptase and polyclonal antibodies against TGF-β1, α-SMA and NF-kB p65. We also used Southwestern histochemistry for the in situ detection of activated NF-kB. RESULTS: The infiltration of macrophages into the tubulointerstitial compartment correlated with unfavorable clinical and histological parameters, and a worse clinical course of IgAN was significantly associated with the number of tubulointerstitial macrophages. Kaplan-Meier curves demonstrated that increased macrophage infiltration was associated with decreased renal survival. Moreover, the presence of macrophages was associated with mast cells, tubulointerstitial α-SMA expression and NF-kB activation (IH and Southwestern histochemistry). In the multivariate analysis, the two parameters that correlated with macrophage infiltration, proteinuria and tubulointerstitial injury, were independently associated with an unfavorable clinical course. CONCLUSION: An increased number of macrophages in the tubulointerstitial area may serve as a predictive factor for poor prognosis in patients with IgAN, and these cells were also associated with the expression of pro-fibrotic factors.


Subject(s)
Adult , Female , Humans , Male , Actins/metabolism , Glomerulonephritis, IGA/pathology , Macrophages/physiology , NF-kappa B/metabolism , Biopsy , Biomarkers/metabolism , Fibrosis , Glomerulonephritis, IGA/metabolism , Histocytochemistry , Kidney Tubules/pathology , Macrophages/pathology , Proteinuria/pathology , Transforming Growth Factor beta1/metabolism
11.
Acta cir. bras ; 27(4): 340-345, Apr. 2012. ilus, tab
Article in English | LILACS | ID: lil-622360

ABSTRACT

PURPOSE: To evaluate the effect of N-acetylcysteine, as a renoprotective agent, when administered early after anesthesia induction, against ischemia/reperfusion injury in rats anesthetized with isoflurane. METHODS: Eighteen male Wistar rats weighing > 300g were anesthetized with isoflurane. The internal jugular vein and the left carotid artery were dissected and cannulated. The animals were randomly divided into GAcetyl, receiving intravenous N-acetylcysteine, 300mg/kg, and GIsot, isotonic saline. After 30 minutes, right nephrectomy was performed and the left renal artery was clamped during 45 minutes. The animals were sacrificed after 48 hours and blood samples were taken after anesthetic induction and upon sacrificing of the animals to evaluate blood creatinine. The kidneys were sent for histological analysis. RESULTS: The variation in serum creatinine was 2.33mg/dL ± 2.21 in GAcetyl and 4.38mg/dL ± 2.13 in GIsot (p=0.074). Two animals presented intense tubular necrosis in GAcetyl, compared to 5 in GIsot. Only GAcetyl presented animals free of tubular necrosis (two) and tubular degeneration (one). CONCLUSION: After renal ischemia/reperfusion, the rats which were given N-acetylcysteine presented less variation in serum creatinine and milder kidney injuries than the control group.


OBJETIVO: Avaliar o efeito da N-acetilcisteína na proteção renal contra lesão de isquemia/reperfusão, quando administrada logo após a indução anestésica, em ratos anestesiados com isoflurano. MÉTODOS: Dezoito ratos Wistar machos pesando mais que 300g foram anestesiados com isoflurano. A jugular interna direita e a carótida esquerda foram dissecadas e canuladas. Os animais foram distribuídos aleatoriamente em GAcetil, recebendo N-acetilcisteína por via intravenosa, 300mg/kg, e GIsot, solução salina. Foi realizada nefrectomia direita e clampeamento da artéria renal esquerda por 45 min. Os animais foram sacrificados após 48h, sendo colhidas amostras sanguíneas após a indução anestésica e ao sacrifício dos mesmos para avaliar a creatinina sérica. Realizou-se histologia renal. RESULTADOS: A variação da creatinina foi 2,33mg/dL ± 2,21 no GAcetil e 4,38mg/dL ± 2,13 no GIsot (p=0,074). Dois animais apresentaram necrose tubular intensa no GAcetil, comparados a cinco no GIsot. Apenas GAcetil apresentou animais livres de necrose tubular (dois) e degeneração tubular (um). CONCLUSÃO: Após isquemia/reperfusão renais, os ratos aos quais se administrou N-acetilcisteína apresentaram menor variação na creatinina sérica e lesões renais mais leves que o grupo controle.


Subject(s)
Animals , Male , Rats , Anesthetics, Inhalation , Acetylcysteine/therapeutic use , Isoflurane , Kidney/blood supply , Reperfusion Injury/prevention & control , Creatinine/blood , Kidney Tubules/drug effects , Kidney Tubules/pathology , Kidney/pathology , Necrosis , Nephrectomy , Random Allocation , Rats, Wistar , Reperfusion Injury/blood
12.
Acta cir. bras ; 25(6): 496-500, nov.-dez. 2010. ilus, tab
Article in English | LILACS | ID: lil-567278

ABSTRACT

PURPOSE: Analyse the histologic changes of rat kidneys perfused with isotonic saline solution (ISS), Euro-Collins solution (ECS) and Euro-Collins solution with diltiazem (ECSD). METHODS: Thirty-six Wistar rats were used divided equally, as follow: group A (ISS), group B (ECS) and group C (ECSD). Through a catheter placed into the abdominal aorta, a renal perfusion was performed using a solution according to the group to which the animal belonged. After the complete perfusion, bilateral nephrectomy was performed and the organs were preserved under hypothermia for five distinct periods of time. Glomerulus and tubule were evaluated through optical microscopy. RESULTS: Renal perfusion with ECS and ECSD proved effectiveness in the preservation of the organs up to 36 hours and an increase in the percentage of injured glomeruli was noticed only in the period of 48 hours. CONCLUSIONS: The results showed that exists an association between the tubular injury and the glomeruli lesion degree; kidneys with a higher degree of tubular damage were related to severe glomerular lesion. Also, the addition of a calcium channel blocker, diltiazem, to the ECS for the renal perfusion does not decrease the percentage of glomerular lesion.


OBJETIVO: Analisar as alterações histológicas nos rins de ratos perfundidos com solução salina isotônica (ISS), solução Euro-Collins (ECS) e solução Euro-Collins com diltiazem (ECSD). MÉTODOS: Foram divididos, de forma igual, 36 ratos Wistar, como se segue: grupo A (ISS), grupo B (ECS), grupo C (ECSD). Através de um cateter localizado na aorta abdominal, foi realizada a perfusão renal com a solução de acordo com o grupo ao qual o animal pertencia. Após a perfusão total, realizou-se nefrectomia bilateral com a preservação dos órgãos sob hipotermia por cinco períodos distintos de tempo. Glomérulos e túbulos foram avaliados por microscopia óptica. RESULTADOS: Tanto a perfusão renal com ECS quanto a com ECSD provaram sua efetividade na preservação dos órgãos em até 36 horas e aumento da porcentagem de glomérulos injuriados foi notada apenas no período de 48 horas. CONCLUSÕES: Os resultados mostraram haver uma correlação entre a injúria tubular e o grau de lesão glomerular; rins com um maior grau de dano tubular foram relacionados com lesão glomerular severa. Além disso, a adição de um bloqueador de canal de cálcio, diltiazem, à ECS para a perfusão renal não diminui a porcentagem de lesão glomerular.


Subject(s)
Animals , Rats , Acute Kidney Injury/drug therapy , Diltiazem/pharmacology , Hypertonic Solutions/pharmacology , Kidney Glomerulus/drug effects , Kidney Tubules/drug effects , Organ Preservation Solutions/pharmacology , Acute Kidney Injury/chemically induced , Disease Models, Animal , Kidney Glomerulus/pathology , Kidney Tubules/pathology , Perfusion/methods , Random Allocation , Rats, Wistar , Statistics, Nonparametric
13.
Int. braz. j. urol ; 36(4): 480-489, July-Aug. 2010. ilus, graf, tab
Article in English | LILACS | ID: lil-562114

ABSTRACT

PURPOSE: Recurrence and persistent side effects of present day treatment for urolithiasis restrict their use, so an alternate solution, using phytotherapy is being sought. The present study attempted to evaluate the antilithiatic properties of Tribulus terrestris commonly called as “gokhru” which is often used in ayurveda to treat various urinary diseases including urolithiasis. MATERIALS AND METHODS: The activity of Tribulus terrestris was investigated on nucleation and the growth of the calcium oxalate (CaOx) crystals as well as on oxalate induced cell injury of NRK 52E renal epithelial cells. RESULTS: Tribulus terrestris extract exhibited a concentration dependent inhibition of nucleation and the growth of CaOx crystals. When NRK-52E cells were injured by exposure to oxalate for 72 h, Tribulus terrestris extract prevented the injury in a dose-dependent manner. On treatment with the different concentrations of the plant, the cell viability increased and lactate dehydrogenase release decreased in a concentration dependent manner. CONCLUSION: The current data suggests that Tribulus terrestris extract not only has a potential to inhibit nucleation and the growth of the CaOx crystals but also has a cytoprotective role. Our results indicate that it could be a potential candidate for phytotherapy against urolithiasis.


Subject(s)
Animals , Rats , Calcium Oxalate/chemistry , Epithelial Cells/drug effects , Kidney Tubules/drug effects , Plant Extracts/pharmacology , Tribulus/chemistry , Urolithiasis , Crystallization , Disease Models, Animal , Epithelial Cells/pathology , Kidney Calculi/chemically induced , Kidney Tubules/cytology , Kidney Tubules/pathology , Phytotherapy , Plant Extracts/therapeutic use , Plant Extracts/toxicity , Tribulus/toxicity , Urolithiasis/prevention & control
14.
Braz. j. med. biol. res ; 43(6): 557-564, June 2010. ilus, tab
Article in English | LILACS | ID: lil-548268

ABSTRACT

Interstitial fibrosis and tubular atrophy (IF/TA) are the most common cause of renal graft failure. Chronic transplant glomerulopathy (CTG) is present in approximately 1.5-3.0 percent of all renal grafts. We retrospectively studied the contribution of CTG and recurrent post-transplant glomerulopathies (RGN) to graft loss. We analyzed 123 patients with chronic renal allograft dysfunction and divided them into three groups: CTG (N = 37), RGN (N = 21), and IF/TA (N = 65). Demographic data were analyzed and the variables related to graft function identified by statistical methods. CTG had a significantly lower allograft survival than IF/TA. In a multivariate analysis, protective factors for allograft outcomes were: use of angiotensin-converting enzyme inhibitor (ACEI; hazard ratio (HR) = 0.12, P = 0.001), mycophenolate mofetil (MMF; HR = 0.17, P = 0.026), hepatitis C virus (HR = 7.29, P = 0.003), delayed graft function (HR = 5.32, P = 0.016), serum creatinine ≥1.5 mg/dL at the 1st year post-transplant (HR = 0.20, P = 0.011), and proteinuria ≥0.5 g/24 h at the 1st year post-transplant (HR = 0.14, P = 0.004). The presence of glomerular damage is a risk factor for allograft loss (HR = 4.55, P = 0.015). The presence of some degree of chronic glomerular damage in addition to the diagnosis of IF/TA was the most important risk factor associated with allograft loss since it could indicate chronic active antibody-mediated rejection. ACEI and MMF were associated with better outcomes, indicating that they might improve graft survival.


Subject(s)
Adult , Female , Humans , Male , Graft Rejection/pathology , Kidney Glomerulus/pathology , Kidney Transplantation/adverse effects , Kidney Tubules/pathology , Atrophy/pathology , Chronic Disease , Fibrosis , Graft Rejection/prevention & control , Immunosuppressive Agents/therapeutic use , Predictive Value of Tests , Retrospective Studies , Risk Factors
15.
Yonsei Medical Journal ; : 105-111, 2009.
Article in English | WPRIM | ID: wpr-83524

ABSTRACT

PURPOSE: Recent studies have showed that epithelial-mesenchymal transition (EMT) is a key process of glomerular and tubulointerstitial pathology in many chronic kidney diseases. However, there are no data of EMT in humane autosomal dominant polycystic kidney disease (ADPKD). PATIENTS AND METHODS: ADPKD kidneys (N = 5) with end stage renal disease (ESRD) and control kidneys (N = 4) were analyzed immnunohistochemically. We evaluated alpha-SMA, E-cadherin, vimentin, TGF-beta1 and Smad 2/3 expression in ADPKD and compared them with those in control kidney. These immunohistochemical findings were quantitatively analyzed by computer-assisted image analyzer and positive tubules (%). RESULTS: There were severe interstitial fibrosis and proliferation of alpha-SMA+ myofibroblasts in ADPKD. Cystic tubular epithelial cells in ADPKD lost epithelial marker (E-cadherin) and expressed mesenchymal markers (alpha-SMA, vimentin). There were significant increases of alpha-SMA (34.3 +/- 11.7% vs 0.9 +/- 1.5%), vimentin (19.9 +/- 3.9% vs 3.3 +/- 1.4%), TGF-beta1 (5.42 +/- 2.83% vs 0%) and Smad 2/3 (3.4 +/- 1.7% vs 0.7 +/- 0.6%) in ADPKD kidneys compared with control kidneys evidenced by computer-assisted image analyzer. When we analyze the positive tubules (%), the results were the same as computer-assisted image analyzer. CONCLUSION: Our results showed that the end stage of ADPKD is associated with TGF-beta, Smad 2/3 and markers of EMT. It suggests that TGF-beta mediated EMT has a role in progression of ADPKD.


Subject(s)
Aged , Biomarkers/metabolism , Cell Division , Disease Progression , Epithelial Cells/pathology , Female , Fibrosis , Humans , Kidney Glomerulus/pathology , Kidney Tubules/pathology , Male , Mesoderm/pathology , Middle Aged , Polycystic Kidney, Autosomal Dominant/metabolism , Transforming Growth Factor beta/metabolism
17.
Medical Sciences Journal of Islamic Azad University. 2007; 17 (3): 127-131
in Persian | IMEMR | ID: emr-100053

ABSTRACT

Influenza virus produces cell death in animals and human. Cell death can be caused by either necrosis or apoptosis. We investigated the types of cell death that occur in chickens infected with avian influenza virus [A/chicken/Iran/772/2000[H9N2]. In an experimental study, 60 SPF chickens aged 3 weeks old were assigned to two groups. The first group was infected with 10[7-5] EID50 of the virus intravenously and the second group was treated with saline normal. 72 hours later, renal tissues were collected and fixed in 10% formalin solution. The prepared microscopic sections with the thickness of 5-6 micron were stained using TUNEL method. There was a significant difference in apoptotic cells of renal tubular tissue between the infected group and controls [p<0.005]. We demonstrated that A/chicken/Iran/772/2000 [H9N2] is able to induce apoptosis in renal tubular cells


Subject(s)
Animals , Apoptosis , Influenza A Virus, H9N2 Subtype , Kidney Tubules/virology , Kidney Tubules/pathology
18.
IJMS-Iranian Journal of Medical Sciences. 2007; 32 (3): 173-176
in English | IMEMR | ID: emr-104640

ABSTRACT

Hexachlorobutadiene [HCBD] is a potent nephrotoxin in rodents, which can cause degeneration, necrosis and regeneration in renal tubular epithelial cells. It has been shown that safranal, the active ingredient of saffron, has a protective effect against ischemic injuries. The aim of this study was to examine the protective effect of safranal against HCBD-induced nephrotoxicity in rats. Method: Thirty Wistar albino rats were randomly divided in five groups. The rats received a single dose of corn oil 1ml/kg [group1], HCBD 50mg/kg [group 2], or safranal at doses of 0.5, 0.25 and 0.1 ml/kg one hour before HCBD [50mg/kg] injection [groups 3-5]. All injections were carried out intraperitoneally. Urine samples were collected one day before, and one day after injections. On day 3 the animals were sacrificed and both kidneys were removed. The right kidney was fixed in formalin for histological examination and the left kidney was homogenized for measuring malondialdehyde [MDA]. Blood samples were taken by cardiac puncture and used for the measurement of urea, creatinine, glucose and protein concentrations. Blood urea concentration in HCBD treated group was significantly higher compared with group 3 [p<0.01] and groups 1 and 4 [p<0.001]. There was no significant difference in urea concen-trations between group 5 and HCBD treated group. Urinary concentration of glucose was significantly higher in group 2, compared with groups 1, 3 and 4 [p<0.001] No significant differences were observed in urinary glucose concentrations between HCBD- and safranal [0.1ml/kg]-treated groups. Concentration of protein was also significantly higher in group 5 than those of other tested groups [p<0.001]. Safranal at doses of 0.25 and 0.5ml/kg has a protective effect against HCBD-induced nephrotoxicity in rats


Subject(s)
Animals, Laboratory , Cyclohexenes , Butadienes/adverse effects , Butadienes/toxicity , Kidney Diseases/etiology , Kidney Diseases/drug therapy , Injections, Intraperitoneal , Nephrectomy , Kidney/pathology , Kidney Tubules/drug effects , Kidney Tubules/pathology , Rats, Wistar , Urea , Creatinine
19.
Journal of Mazandaran University of Medical Sciences. 2007; 17 (61): 88-89
in Persian | IMEMR | ID: emr-83489

ABSTRACT

Thalassemia is a hereditary quantitative hemoglubinopathy which is common in mediteranian area including IRAN. Homos zygotic beta thalassemia patients suffer from severe anemia and complication of the disease in many organs. Studies have shown different results about renal complication and disease. Thus, in this study we investigated renal function of thalassemia Major [TM] patients in comparison with control group. This was a historical cohort Study. The population who TM patients was were admitted to Boalisina hospital, Sari, and control group were brothers and sisters of the patients who were matched in gender and age. Serum and urine markers of renal function were measured and demographic and therapeutic data were gathered from medical records. Analysis of the data was performed using SPSS 11 with statistical test [t, chi square]. The Total of 84 [42 patients and, 42 controls] patients were studied. The Mean age of the patients was 21.3 +/- 5.2 years. Dose of Deferral was 70 +/- 19 mg/kg. The results showed no significant statistical differences in levels of beta2 microglobulin, 24 urine protein, Excretion Fraction of Na and K between case and control group. There was significant differences in levels of serum BUN, creatinin, Potassium and urine potassium and creatinin between case and control group. Gender, level of Hb and serum Ferritin significantly affected the differences between two groups. In this study, evidences of renal tubular damage were not detected in TM patients. There was increase in levels of Bun, serum potassium, uric Acid, specially with severe anemia, high dose desferal and Iron over load


Subject(s)
Humans , Male , Female , Deferoxamine/adverse effects , Kidney Tubules/pathology , Iron Overload , Cohort Studies
20.
Article in English | WPRIM | ID: wpr-32679

ABSTRACT

C1q nephropathy is a proliferative glomerulopathy with extensive mesangial deposition of C1q. A three-year old boy presented with a nephrotic-range proteinuria during an acute phase of Epstein-Barr virus (EBV) infection, and he had a family history of Dent's disease. The renal biopsy findings were compatible with C1q nephropathy. However, EBV in situ hybridization was negative. The CLCN5 gene analysis revealed an R637X hemizygous mutation, which was the same as that detected in his maternal cousin, the proband of the family. The causal relationship between EBV infection and C1q nephropathy remains to be determined. Moreover, the effects of underlying Dent's disease in the process of C1q nephropathy has to be considered.


Subject(s)
Biopsy , Child, Preschool , Epstein-Barr Virus Infections/metabolism , Glomerulonephritis/pathology , Humans , In Situ Hybridization , Infectious Mononucleosis/complications , Kidney Diseases/complications , Kidney Tubules/pathology , Male , Membrane Glycoproteins/chemistry , Mutation , Nephrosis , Proteinuria/complications , Receptors, Complement/chemistry , Treatment Outcome
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