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1.
Acta cir. bras ; 32(5): 334-341, May 2017. tab, graf
Article Dans Anglais | LILACS | ID: biblio-837710

Résumé

Abstract Purpose: To investigate the glomerular number after different warm ischemia times. Methods: Thirty two pigs were assigned into four groups. Three groups (G10, G20, and G30) were treated with 10, 20, and 30 minutes of left renal warm ischemia. The sham group underwent the same surgery without renal ischemia. The animals were euthanized after 3 weeks, and the kidneys were collected. Right kidneys were used as controls. The kidney weight, volume, cortical-medullar ratio, glomerular volumetric density, volume-weighted mean glomerular volume, and the total number of glomeruli per kidney were obtained. Serum creatinine levels were assessed pre and postoperatively. Results: Serum creatinine levels did not differ among the groups. All parameters were similar for the sham, G10, and G20 groups upon comparison of the right and left organs. The G30 group pigs' left kidneys had lower weight, volume, and cortical-medullar ratio and 24.6% less glomeruli compared to the right kidney. A negative correlation was found between warm ischemia time and glomerular number. Conclusions: About one quarter of glomeruli was lost after 30 minutes of renal warm ischemia. No glomeruli loss was detected before 20 minutes of warm ischemia. However, progressive glomerular loss was associated with increasing warm ischemia time.


Sujets)
Animaux , Mâle , Ischémie chaude/effets indésirables , Rein/vascularisation , Cortex rénal/vascularisation , Glomérule rénal/vascularisation , Facteurs temps , Répartition aléatoire , Créatinine/sang , Modèles animaux , Sus scrofa , Rein/chirurgie , Rein/physiopathologie , Cortex rénal/physiopathologie , Glomérule rénal/chirurgie , Glomérule rénal/physiopathologie
2.
Acta cir. bras ; 31(11): 753-758, Nov. 2016. tab, graf
Article Dans Anglais | LILACS | ID: biblio-827658

Résumé

ABSTRACT PURPOSE: To evaluate the glomerular loss after arteriovenous or arterial warm ischemia in a swine model. METHODS: Twenty four pigs were divided into Group Sham (submitted to all surgical steps except the renal ischemia), Group AV (submitted to 30 minutes of warm ischemia by arteriovenous clamping of left kidney vessels), and Group A (submitted to 30 minutes of ischemia by arterial clamping). Right kidneys were used as controls. Weigh, volume, cortical volume, glomerular volumetric density (Vv[Glom]), volume-weighted glomerular volume (VWGV), and the total number of glomeruli were measured for each organ. RESULTS: Group AV showed a 24.5% reduction in its left kidney Vv[Glom] and a 25.4% reduction in the VWGV, when compared to the right kidney. Reductions were also observed when compared to kidneys of sham group. There was a reduction of 19.2% in the total number of glomeruli in AV kidneys. No difference was observed in any parameters analyzed on the left kidneys from group A. CONCLUSIONS: Renal warm ischemia of 30 minutes by arterial clamping did not caused significant glomerular damage, but arteriovenous clamping caused significant glomerular loss in a swine model. Clamping only the renal artery should be considered to minimize renal injury after partial nephrectomies.


Sujets)
Animaux , Mâle , Artère rénale/chirurgie , Laparoscopie/méthodes , Ischémie chaude/méthodes , Glomérule rénal/vascularisation , Néphrectomie/méthodes , Taille d'organe , Suidae , Modèles animaux de maladie humaine , Glomérule rénal/anatomie et histologie , Glomérule rénal/physiopathologie
3.
Medicina (B.Aires) ; 71(5): 413-419, oct. 2011. ilus, graf, tab
Article Dans Espagnol | LILACS | ID: lil-633889

Résumé

La hiperfiltración glomerular y el aumento de la reabsorción de sodio son factores fundamentales para el desarrollo de la unidad feto placentaria. Dichos factores resultan de adaptaciones hemodinámicas y renales en las que participan sistemas vasoactivos. Se pudo demostrar en ratas que la activación del sistema kallicreína kinina (SKK) precede a la instalación de la hiperfiltración glomerular, dado que su inhibición por aprotinina previene el aumento del filtrado glomerular. Además, la inhibición individual o asociada de los efectores específicos del SKK, las prostaglandinas (PGs) y el óxido nítrico (ON), confirman la dependencia del filtrado glomerular del SKK durante la preñez. Encontramos también que el sistema renina angiotensina (SRA) participa en la generación de la hiperfiltración glomerular dado que ésta es afectada por la administración de bloqueantes del SRA. La inhibición máxima sobre el pico de hiperfiltración se obtuvo con el bloqueo de ambos sistemas (SKK y SRA). Además, estrategias para alterar la hiperfiltración glomerular y la reabsorción de sodio de la preñez evidenciaron alteraciones en el desarrollo de la unidad feto placentaria, menor número de crías, mayor cantidad de reabsorciones intrauterinas y retardo en el crecimiento. El tratamiento combinado de inhibidores del SKK asociados a bloqueantes del SRA o de óxido nítrico mostraron los mayores efectos. En consecuencia, demostramos que el SKK juega un rol central en los fenómenos de adaptación que acompañan la preñez normal. La interrelación del SKK con varios sistemas vasoactivos parecería formar una red que participa en las adaptaciones hemodinámicas para un adecuado desarrollo de la gestación y de la unidad feto-placentaria.


Glomerular hyperfiltration and increased sodium reabsorption are key factors for the development of the fetus and placenta in pregnancy. These adjustments result from hemodynamic and renal factors involving vasoactive systems. It was demonstrated in rats that activation of KKS precedes the installation of glomerular hyperfiltration as aprotinin prevents the increase in glomerular filtration. In addition, individual or associated inhibition of specific kallikrein kinin system effectors, prostaglandins (PGs) and nitric oxide (NO), confirm the glomerular filtration rate dependence of KKS during pregnancy. It was also found that the renin-angiotensin system (RAS) contributes to glomerular hyperfiltration as this is affected by the administration of RAS blockers. The peak of hyperfiltration maximum inhibition was obtained by the blockade of both systems (KKS and RAS). In addition, strategies used to alter the glomerular hyperfiltration and increased sodium reabsorption during pregnancy, showed abnormalities in the development of the fetus and placenta, fewer offspring, more fetus resorptions and intrauterine growth retardation. KKS inhibitors associated with RAS or nitric oxide blockers showed the greatest impact. As a consequence, it was demonstrated that KKS plays a central role in the adaptation phenomenom that accompanies normal pregnancy. The interplay of KKS with several vasoactive systems, seem to arrange a network involved in the hemodynamic adaptations to allow the proper development of pregnancy and the fetus and placenta.


Sujets)
Animaux , Femelle , Grossesse , Rats , Débit de filtration glomérulaire/physiologie , Système kallicréine-kinine/physiologie , Système rénine-angiotensine/physiologie , Sodium/métabolisme , Aprotinine/pharmacologie , Système kallicréine-kinine/effets des médicaments et des substances chimiques , Glomérule rénal/vascularisation , Rein/vascularisation , Rein/physiopathologie , Monoxyde d'azote/antagonistes et inhibiteurs , Prostaglandines/physiologie , Rat Wistar , Inhibiteurs de la sérine protéinase/pharmacologie , Chlorure de sodium/pharmacologie , Vasodilatation/physiologie
4.
Indian J Pathol Microbiol ; 2008 Oct-Dec; 51(4): 509-11
Article Dans Anglais | IMSEAR | ID: sea-75571

Résumé

Collapsing glomerulopathy (CG) is a distinct clinicopathological entity characterized by high levels of nephrotic range proteinuria, rapidly progressive renal failure, marked parenchymal injury, and poor response to present therapeutic regimens. Growing awareness has led to the identification of associated conditions other than human immunodeficiency virus (HIV) and idiopathic. We report a case of CG from India in a HIV-negative young female, presenting with heavy proteinuria and rapidly progressing renal failure preceded by a febrile illness.


Sujets)
Adulte , Vaisseaux capillaires/anatomopathologie , Évolution de la maladie , Femelle , Fièvre/complications , Glomérulonéphrite segmentaire et focale/complications , Humains , Insuffisance rénale/étiologie , Glomérule rénal/vascularisation , Syndrome néphrotique/étiologie , Protéinurie/étiologie , Jeune adulte
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