Role of Glomerular Basement Membrane Thixotropy and Influence of Glomerular Vascular Pressure in the Pathogenesis of Immune Complex-Induced Glomerulonephritis

Lo, Simpson

doi:10.1159/000182035

Cited by 8 publications

(4 citation statements)

References 18 publications

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“…We ignore the role that prolonged corticosteroid therapy had in this patient (case 5), but the persistence of hypocomplementemia could be related to the effect of steroids on the reticuloendothelial system. Simpson [20] has shown that immune complex deposition is enhanced in animals treated with pressor agents, and as a result glomerulonephritis of increased severity developed.…”

Section: Discussionmentioning

confidence: 99%

Shunt Nephritis: A Report on Five Children

Zamora

Alvarez-Garijo

et al. 1984

Pediatr Neurosurg

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Of 5 children with glomerulonephritis with infected ventriculoatrial shunt, 3 had improved renal function after antibiotic therapy and removal of the infected shunt. 1 patient with endoextracapillary proliferative glomerulonephritis with 70% glomerular crescents developed a rapidly progressive renal insufficiency. Renal failure was successfully managed by hemodialysis and kidney transplantation. 1 patient died from extrarenal causes in the course of a septic episode.

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Section: Discussionmentioning

confidence: 99%

Shunt Nephritis: A Report on Five Children

Zamora

Alvarez-Garijo

et al. 1984

Pediatr Neurosurg

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“…However, work in progress dealing with exercise and postural proteinuria has shown that individuals with normal renal function responded with transient high molecular weight proteinuria after short-term posturing aimed at producing a compressive effect on the kidneys (unpublished observations). The appearance of protein in the urine is considered to indicate that there had been an increase in intraglomerular pressure of such magnitude as to enable some plasma proteins to deform the pressure-dependent basement membrane, and become part of the glomerular filtrate [20], This implies that it is possible to over-ride the electrostatic repulsion of the charge barrier by an increase in intravascular pressure. In an attempt to show how this occurs, a mathematical mode] of glomerular filtration has been developed and has yielded values in close agreement with published values for intraglomerular pressure (in preparation).…”

Section: Blood Viscosity and Renal Functionmentioning

confidence: 99%

A Hypothesis Proposing Increased Blood Viscosity as a Cause of Proteinuria and Increased Vascular Permeability

Simpson¹

1982

Nephron

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Currently accepted concepts of renal and vascular physiology are inadequate to explain the reversible increases in vascular permeability which occur during episodes of increased blood viscosity. On the basis that all basement membranes exhibit biological thixotropy, it has been suggested that basement membranes are pressure dependent. The physiological significance of increased blood viscosity lies in the associated increase in peripheral vascular resistance which develops because of altered blood rheology. In order to overcome the peripheral resistance, intravascular pressure rises, and if adequate pressures develop, plasma proteins may deform and pass through the vascular basement membrane. This is considered to be the mechanism of proteinuria. In the treatment of high blood viscosity disorders it is suggested that the immunosuppressant drug, Thiamphenicol, may be useful because of its ability to induce a reversible dose-related depression of erythropoiesis, and thereby reduce blood viscosity.

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“…However, immune complexes with slight antigen excess are removed from circulation by glomerular mesangial or endothelial cells [16,17]. In advanced renal failure, such complexes may not be removed as readily.…”

Section: Discussionmentioning

confidence: 99%

“…An occurrence of serositis 1-3 weeks after bacterial or viral infection without detect able organisms in an exudate [3,4,12,13] resembles the sequence of events in glomerulonephritis, rheumatic fever, serum sickness, and other immune complex-induced dis eases. One of the functions of healthy kidneys is the removal of CIC with slight antigen excess [16,17], thus CIC levels may be elevated in patients with renal failure. The incidence of pericarditis tends to be lower in patients treated by peritoneal dialysis than by HD [6], which suggests better removal of a purported toxin through the peritoneum than artificial membranes.…”

Section: Introductionmentioning

confidence: 99%

Circulating Immune Complexes: Possible Toxins Responsible for Serositis (Pericarditis, Pleuritis, and Peritonitis) in Renal Failure

Twardowski¹,

Alpert²,

Gupta³

et al. 1983

Nephron

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In 71 patients (41 men, 30 women) with advanced renal failure maintained on hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), or within 8 weeks after the commencement of dialysis therapy (ED), studies were performed searching for evidence of serositis and the blood levels of circulating immune complexes (CIC), measured by the polyethylene glycol precipitation method. Mean CIC levels were elevated in these patients compared to the 58 healthy subjects (mean ± SEM 725 ± 40, and 260 ± 34 µg/ml, respectively). Serositides were significantly more prevalent in ED patients compared to both remaining groups, and tended to occur less frequently in CAPD than in HD patients. CIC levels were significantly lower in CAPD than in ED patients. The levels of CIC were significantly higher in patients with serositis compared to those without evidence of serosal inflammation (mean ± SEM 868 ± 71 and 677 ± 53 µg/ml, respectively). In addition, immune complex-like materials were found in all of 4 effusate samples and in 10 of 27 peritoneal dialysates. It is suggested that immune complexes may be the ‘uremic toxins’ responsible for the serositis of renal failure, and may be secreted into serous effusions. Immune complex-like material can be removed in peritoneal dialysate, which may contribute to the lower CIC levels and lower incidence of serositis in the CAPD patients.

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Role of Glomerular Basement Membrane Thixotropy and Influence of Glomerular Vascular Pressure in the Pathogenesis of Immune Complex-Induced Glomerulonephritis

Cited by 8 publications

References 18 publications

Shunt Nephritis: A Report on Five Children

Shunt Nephritis: A Report on Five Children

A Hypothesis Proposing Increased Blood Viscosity as a Cause of Proteinuria and Increased Vascular Permeability

Circulating Immune Complexes: Possible Toxins Responsible for Serositis (Pericarditis, Pleuritis, and Peritonitis) in Renal Failure

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