Glomerular filtration and tubular reabsorption during anuria in postischemic acute renal failure

AbstractGlomerular filtration and tubular reabsorption during anuria in postischemic acute renal failure. Complete occlusion of the left renal artery for 60min in the rat produced anuric acute renal failure after 1 day. Using fluorescence microscopy, a television system combined with double slit densitometry, and micropuncture techniques, tubular pressure and tubular flow rates were determined in different segments of superficial nephrons. Intratubular pressures in proximal convolutions of the postischemic kidney were largely heterogeneous due to abnormally increased flow resistance in proximal tubules which were filled with loose obstructive material. Proximal tubular pressure in the control kidney was independent of the site of its measurement and had a mean value of 14.1mm Hg. In the postischemic kidney pressure decreased gradually along the proximal tubule, its value in the early and late segments being 16.3 and 9.7mm Hg, respectively. Low pressure in late proximal convolutions excludes a significant flow impediment due to obstruction in more distal segments. The mean nephron filtration rate (SNGFR) obtained by extrapolation of tubular flow data was 62% of the control value, whereas tubular reabsorption was estimated to be 50% above normal. Reduced SNGFR and increased outflux caused a total reabsorption of tubular fluid within 60% of proximal convoluted tubule length. The partial reduction of SNGFR can be explained by increased pressure in early proximal convolutions and reduced glomerular plasma flow known for these kidneys, without postulating a change in glomerular permeability. Tubular obstruction and increased passive outflux in proximal tubules due to cellular damage appear to be crucial mechanisms responsible for the loss of renal function in this model of acute renal failure.Filtration glomérulaire et réabsorption tubulaire pendant l'anurie due à une insuffisance rénale aiguë postischémique. Une occlusion complète de l'artère rénale gauche pendant 60min chez le rat a entraîné une insuffisance rénale aiguë anurique après 1 jour. En utilisant la microscopie par fluorescence, un système de télévision combiné avec une densitométrie à double faisceau, et des techniques de microponction, la pression tubulaire et les débits tubulaires ont été déterminés dans différents segments de néphrons superficiels. Les pressions intratubulaires dans les convolutions proximales du rein postischémique étaient largement hétérogènes, en raison d'une augmentation anormale de la résistance au flux dans les tubules proximaux qui étaient remplis avec un matériau lâche obstructif. La pression tubulaire proximale dans le rein contrôle était indépendante du lieu de sa mesure et avait une valeur moyenne de 14,1mm Hg. Dans le rein postischémique, la pression diminuait graduellement le long du tubule proximal, ses valeurs dans les segments proximal et terminal étant 16,3 et 9,7mm Hg, respectivement. La faible pression dans les convolutions proximales tardives exclut un ralentissement significatif du flux par obstruction dans les segments plus distaux. La filtration glomérulaire moyenne par néphron (SNGFR), obtenue par extrapolation des valeurs de flux tubulaire était de 62% de la valeur contrôle, tandis que la réabsorption tubulaire était estimée à 50% au-dessus de la normale. La réduction de SNGFR et l'augmentation du flux sortant entraînaient une réabsorption totale du liquide tubulaire dès 60% de la longueur du tubule contourné proximal. Cette réduction partielle de SNGFR peut être expliquée par l'augmentation de pression dans les convolutions proximales précoces et la réduction du flux plasmatique glomérulaire connue dans ces reins, sans postuler de modification de la perméabilité glomérulaire. L'obstruction tubulaire et l'augmentation passive du flux sortant dans les tubules proximaux par l'altération cellulaire semblent être des mécanismes cruciaux responsables de la perte de la fonction rénale dans ce modèle d'insuffisance rénale aiguë

Robotic-assisted radical cystectomy vs open radical cystectomy: systematic review and meta-analysis

To perform an updated systematic review and meta-analysis evaluating patient important outcomes for patients undergoing robot-assisted radical cystectomy (RARC) and open radical cystectomy (ORC). Multiple scientific databases were searched up to July 2018 for randomized controlled trials that compared RARC and ORC. The primary outcomes of interest were: disease progression, major (Clavien III-V) complications and 90-day quality of life. The quality of evidence was evaluated according to the framework in the Cochrane Handbook for Systematic Reviews of Interventions. Five studies with a total of 540 participants were included in this review. There was no difference between RARC and ORC for disease progression [RR 0.94, 95%CI 0.69-1.29], major complications [RR 1.06, 95%CI 0.75-1.49] or quality-of-life [SMD -0.03, 95%CI -0.27-0.21]. However, RARC demonstrated a reduced risk of requiring a perioperative blood transfusion [RR 0.58, 95%CI 0.43-0.80] and had a marginally lower duration of hospital stay [RR -0.63 days, 95%CI -1.21- -0.05]. Operative time was longer in the RARC group [MD 68.51 minutes, 95%CI 30.55-105.48]. There was no statistically significant difference in local recurrence rates between the procedures [RR 2.08, 95%CI 0.96-4.50], but this difference may be clinically significant and favors ORC. The overall quality of evidence was judged to be moderate. Surgical approach does not have a considerable impact on oncological, safety and quality-of-life outcomes for patients undergoing radical cystectomy. The benefits conferred by RARC are the decreased need for blood transfusion and an earlier discharge from hospital

Endothelin ETA receptor blockade with darusentan increases sodium and potassium excretion in aging rats

This study investigated whether intrarenal endothelin-1(ET-1) contributes to sodium excretion in aged rats. Metabolic function studies were performed in male Wistar rats (3 and 24 months) treated with placebo or the orally active ET(A) receptor antagonist darusentan (20 mg/kg/d) for 4 weeks. Mean arterial pressure was measured using an intra-arterial catheter. Electrolytes, aldosterone levels, renin activity, and angiotensin converting enzyme activity were determined in plasma, and mRNA expression of epithelial sodium channel (ENaC) and Na(+), K(+)-ATPase subunits was measured in the renal cortex and medulla. Aging was associated with a marked decrease in urinary excretion of sodium, chloride, and potassium (all P < 0.001) as well as renin activity (P < 0.05), but had no significant effect on gene expression of ENaC or Na(+), K(+)-ATPase subunits. In aged rats, darusentan treatment increased ion excretion (P < 0.05), reduced cortical gene expression of alphaENaC and alpha(1)-Na(+), K(+)-ATPase (both P < 0.05), and increased plasma aldosterone levels (P < 0.01). These data demonstrate a decrease of sodium and potassium excretion in aged rats, changes that are partly sensitive to ETA receptor blockade. Treatment with darusentan also reduced cortical expression of alphaENaC and alpha(1)-Na(+), K(+)-ATPase and increased plasma aldosterone levels independently of blood pressure, electrolytes, renin activity, or angiotensin converting enzyme activity. These findings may provide new pathogenetic links between aging and sodium sensitivity