Abstract

Ultrafiltration coefficient and glomerular capillary resistance in a model of immune complex glomerulonephritis. Decreased ultrafiltration coefficient, L p A or K f , was documented previously in micropuncture studies of glomerulonephritis in rats. Observations were made immediately following an injection of antiglomerular basement membrane (anti-GBM) antibody, later in the course of glomerulonephritis, and during the chronic phase of Heymann nephritis. To gain further insight into the basis of reduced glomerular filtration rate in immune-complex glomerulonephritis, we studied the anatomic, physiologic, and rheologic properties of isolated glomeruli from female Buffalo rats with nephritis which developed during infection with Trypanosoma rhodesiense . Immune-complex mediated glomerulonephritis was present 2 weeks after inoculation and progressed throughout the 4 weeks of study. Renal insufficiency occurred, with serum creatinine concentrations rising to 5 to 10 times control values by week 4. Mesangial hypercellularity, mesangial electron dense deposits, and endothelial cell swelling were observed. Increased numbers of mononuclear cells were present within the glomerulus. Total glomerular water volume was greater in nephritic than in normal animals. Increased cell volume accounted for most of the volume increment. When filtration into the capillaries was induced in vitro by imposing an oncotic gradient of 6.5mm Hg or greater across the capillary wall, rapid and uniform erythrocyte movement occurred within the capillaries of control glomeruli and erythrocytes were ejected into the medium. In contrast, a transcapillary gradient of 30 to 40mm Hg was required to produce erythrocyte movement in glomeruli from nephritic animals studied 4 weeks after inoculation. The ultrafiltration coefficient of nephritic glomeruli was estimated in vitro and was not different from that of control glomeruli (5.81 ± 0.35 vs. 6.21 ± 0.49 nl/minmm Hg). An impairment of capillary perfusion may be responsible for the decreased rate of glomerular filtration observed in this model of glomerulonephritis. Evaluation in vitro du coefficient d'ultrafiltration et de la resistance capillaire glomerulaire dans un modele de glomerulonephrite des comples immuns. La diminution du coefficient d'ultrafiltration, L p A ou K f , a ete etablie precedement au cours de travaux utilisant les microponctions chez des rats atteints de glomerulonephrite, immediatement apres l'injection d'anti-corps anti-membrane basale glomerulaire (anti-GBM) et, ulterieurement, au cours de l'evolution de glomerulonephrite et durant la phase chronique de la nephrite de Heymann. Afin d'obtenir plus d'informations sur les fondements de la diminution du debit de filtration glomerulaire au cours de la nephrite des complexes immuns, nous avons etudie les proprietes anatomiques, physiologiques, et biologiques des glomerules isoles de rats femelles de la souche Buffalo atteints de nephrite developpee au cours de l'infection par Trypanosoma rhodesiense . Une glomerulonephrite des complexes immuns existait deux semaines apres l'inoculation et evoluait pendant les 4 semaines de l'etude. Il existait une insuffisance renale et la creatinine serique atteignait des valeurs 5 a 10 fois plus grandes que les controles a la 4 semaine. L'hypercellularite mesangiale, sous la forme de depots denses mesangiaux en microscopie electronique, et le gonflement des cellules endotheliales ont ete observes. Le nombre des cellules mononuclees du glomerule etait augmente. Le volume total d'eau du glomerule etait plus grand chez les animaux atteints de nephrite que chez les controles. L'augmentation du volume cellulaire rendait compte de la plus grande partie de l'augmentation de volume. Quand la filtration dans les capillaires a ete declenchee par l'imposition d'un gradient oncotique de 6,5mm Hg ou plus a travers la paroi capillaire, un mouvement rapide et uniforme des erythrocytes est apparu et les erythrocytes ont ete ejectes dans le milieu. Par contre, pour les glomerules provenant d'animaux nephritiques, etudies quatre semaines apres l'inoculation, un gradient de 30 a 40mm Hg etait necessaire pour produire un mouvement des erythrocytes. Le coefficient d'ultrafiltration des glomerules d'animaux nephritiques a ete evalue in vitro et n'est pas different de celui des animaux controles (5,81 ± 0,35 vs. 6,21 ± 0,49 nl/minmm Hg). L'alteration de la perfusion capillaire est responsable de la diminution du debit de filtration glomerulaire observee dans ce modele de glomerulonephrite.

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