Capillary permeability to protein as a factor in the control of plasma volume

Wraight, E. P.

doi:10.1113/jphysiol.1974.sp010468

Cited by 39 publications

(14 citation statements)

References 16 publications

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“…In addition, there is a reduction of the hydrostatic pressure gradient by lowering the capillary blood pressure and increasing the interstitial pressure [14]. Experimental data on the effect of hypoalbuminemia on the capillary permeability are controversial: Wraight et al showed a decreased glomerular permeability to proteins in rats made acutely hypoalbuminemic after plasmapheresis [24] whereas Fujihara et al demonstrated enhanced glomerular permeability to macromolecules in the (chronic)…”

Section: Discussionmentioning

confidence: 99%

A boy with congenital analbuminemia and steroid-sensitive idiopathic nephrotic syndrome: an experiment of nature

2007

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Section: Discussionmentioning

confidence: 99%

A boy with congenital analbuminemia and steroid-sensitive idiopathic nephrotic syndrome: an experiment of nature

2007

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“…Furthermore, the acceleration of lymph flow tends to maintain a normal transcapillary colloid-osmotic pressure gradient [3]. A factor that normally contributes to the control of fluid filtration is a decrease in intrinsic capillary permeability to proteins, a phenomenon occurring under conditions of hypoalbuminemia [15]. The intrinsic permeability of the capillary to proteins (‘vascular permeability’) is assessed as the osmotic reflection coefficient in the Starling forces equation; it may be altered by numerous mediators such as histamine, endotoxins, anaphylatoxins, catecholamines, estrogens, progesterone, insulin and cytokines (VEGF, IL-1, IL-2, TNF-α and vascular permeability factor, VPF) [6, 16, 17, 18, 19].…”

Section: Discussionmentioning

confidence: 99%

Vascular Hyperpermeability in Nephrotic Edema

Rostoker¹,

Béhar

Lagrue

2000

Nephron

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Background/Aim: There is increasing evidence that hypoalbuminemia and the inability of the renal distal tubule to excrete salt are not the only factors responsible for nephrotic edema. We tested the possibility that vascular hyperpermeability also plays a role in the pathophysiology of nephrotic edema in human primary glomerulonephritis. Methods: We investigated the capillary permeability by means of a standardized test using albumin labelled with technetium (^99mTc-albumin) in 20 healthy adults and in 101 nephrotic adult patients comprising 60 patients with idiopathic nephrotic syndrome (INS; minimal-change nephropathy and segmental glomerulosclerosis), 32 with idiopathic membranous nephropathy (IMN) and 9 patients with idiopathic type I membranoproliferative glomerulonephritis (MPGN). The patients and healthy controls were also compared with a group of women (n = 25) with idiopathic cyclic edema, a disease in which an increase in capillary permeability plays a pivotal role. The capillary permeability measured by the Landis isotope test is normal in edematous patients with cardiac and renal impairment unrelated to glomerular disease, cirrhosis, hypothyroidism, lymphatic obstruction and diuretic abuse. As values were not normally distributed, nonparametric analysis of variance was used (Kruskal-Wallis test), and patient groups were compared with healthy controls and with women with idiopathic cyclic edema by means of the two-tailed nonparametric Mann-Whitney test. The effects of high-dose steroids and Ginkgo biloba extract (Tanakan^®; an agent able to improve capillary permeability) were analyzed by means of the two-tailed nonparametric Wilcoxon test. Results: The capillary permeability was significantly increased (Mann-Whitney test) in each glomerular disease group compared with the healthy controls. ^99mTc-albumin extravasation values (%; median and range in parentheses were the following: healthy controls 0 (0–8.4); idiopathic cyclic edema patients 11.5 (8–24), p < 0.001; INS 20 (0–50), p < 0.0001; IMN 12.5 (0–40), p < 0.001, and MPGN 10 (0–40), p < 0.05. An increase in capillary permeability exceeding the upper limit of control values ( >8% of ^99mTc-albumin extravasation) was observed in 88% of INS, in 53% of IMN and in 44% of MPGN patients. The increase in capillary permeability (%) was greater in idiopathic nephrotic patients than in idiopathic cyclic edema patients (p < 0.005, Mann-Whitney test) and was markedly reduced in nephrotic patients receiving high-dose steroids (n = 8) [before 25 (8–40); after 0 (0–25), p < 0.005 (Wilcoxon’s test)] and high doses of G. biloba extract (n = 16) [before 30 (8–50); after 2.5 (0–20, p < 0.0005 (Wilcoxon’s test)]. Conclusions: We conclude that capillary permeability is severely altered in most of the nephrotic patients with primary glomerulonephritis. These results strongly suggest that the capillary hyperpermeability plays a role in the pathophysiology of nephrotic edema in primary glomerular disease, especially in INS. We postu...

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“…Acute changes in plasma albumin concentra tion, for example by infusion of hyperoncotic albumin [7] or plasmapheresis [8], will certainly affect the blood vol ume. However, with a time lag of several hours or days [7,[26][27][28]] such changes will be largely abolished due to redistribution of the extracellular albumin mass along the pathways outlined above.…”

Section: Discussionmentioning

confidence: 99%

Lowered Protein Content of Tissue Fluid in Patients with the Nephrotic Syndrome: Observations during Disease and Recovery

Koomans¹,

Kortlandt²,

Geers³

et al. 1985

Nephron

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To find out why most patients with the nephrotic syndrome maintain a normal blood volume despite a reduced plasma colloid osmotic pressure (COP), we measured the transcapillary (plasma-tissue fluid) COP difference in 12 patients with the nephrotic syndrome, as well as in 6 patients during complete (n = 3) and partial (n = 3) recovery. Subcutaneous nylon wicks were used to collect tissue fluid. The albumin content was also measured. The albumin content and COP were lowered in both plasma and tissue fluid in the nephrotic phase, and rose gradually during recovery. During these changes the transcapillary COP difference only rose slightly: from 6.2 ± 1.7 mm Hg when the plasma COP was below 10 mm Hg (n = 11) to 8.7 ± 1.5 mm Hg when the plasma COP exceeded 20 mm Hg (n = 12). These observations indicate that in hypoproteinemia preservation of the intravascular volume is strongly dependent on maintenance of the difference in oncotic pressure across the capillary wall.

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Capillary permeability to protein as a factor in the control of plasma volume

Cited by 39 publications

References 16 publications

A boy with congenital analbuminemia and steroid-sensitive idiopathic nephrotic syndrome: an experiment of nature

A boy with congenital analbuminemia and steroid-sensitive idiopathic nephrotic syndrome: an experiment of nature

Vascular Hyperpermeability in Nephrotic Edema

Lowered Protein Content of Tissue Fluid in Patients with the Nephrotic Syndrome: Observations during Disease and Recovery

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