The pathologic anatomy of eclampsia, bilateral renal cortical necrosis, pituitary necrosis, and other acute fatal complications of pregnancy, and its possible relationship to the generalized Shwartzman phenomenon

McKay, Donald G.; Merrill, Samuel J.; Weiner, Albert E.; Hertig, Arthur T.; Reid, Duncan E.

doi:10.1016/0002-9378(53)90068-4

Cited by 222 publications

(40 citation statements)

References 8 publications

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“…Jeffcoate (1966) summarized many of the pathological factors known to be associated with pre-eclampsia and affirmed that it was a disease of theories; the possible role of the coagulation and fibrinolytic systems was not included and this aspect has received little attention. In some fatal cases of eclampsia, however, a prominent finding has been widespread fibrin deposition (McKay et al, 1953). Electron microscopical study of tissue obtained by renal biopsy from patients with preeclampsia has revealed swelling of the glomerular capillary endothelium and deposition of an amorphous fibrinoid material within the cells and beneath the basement membrane (Pollak and Nettles, 1960;Altchek, 1961).…”

Section: Discussionmentioning

confidence: 99%

Coagulation and Fibrinolytic Systems in Pre-eclampsia and Eclampsia

Bonnar¹,

McNicol²,

Douglas³

1971

BMJ

181

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SummaryThe coagulation and fibrinolytic mechanisms were investigated in a group of patients with severe pre-eclampsia and eclampsia and the findings were compared with those of healthy women in late pregnancy. In patients with pre-eclampsia the following significant differences were found: (1) greater depression of plasma fibrinolytic activity (euglobulin lysis time) than in normal pregnancy, (2) a higher level of inhibitor to urokinaseinduced lysis, (3) increased levels of serum fibrin degradation products, and (4) reduced platelet counts.In patients with eclampsia a progressive increase of the level of serum fibrin degradation products was found over the three days following eclamptic seizures. No such increase occurred after grand mal seizures in late pregnancy. The findings in this study support the view that intravascular clotting is taking place in pre-eclampsia and that this disturbance of the balance between coagulation and fibrinolysis may be localized to certain areas of the vascular compartment, particularly the placental and renal circulations. Fibrin deposition in the maternal vessels supplying the placenta would impair the placental blood flow, which may explain the placental insufficiency which occurs in pre-eclampsia. Likewise fibrin deposition in the renal vasculature will result in glomerular damage and proteinuria. Hypertension may be related to the renal

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Section: Discussionmentioning

confidence: 99%

Coagulation and Fibrinolytic Systems in Pre-eclampsia and Eclampsia

Bonnar¹,

McNicol²,

Douglas³

1971

BMJ

181

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“…Examples of sudden death syndrome from the medical literature support our hypothesis, including thrombohemorrhagic phenomena (THP), such as anaphylaxis [229,230,[237][238][239], disseminated intravascular coagulation (DIC) [240,241], HELLP syndrome [242], acute liver necrosis [243], Waterhouse-Friderichsen's syndrome, hemolytic uremic anemia, idiopathic pulmonary hemorrhage [244], acute pancreatitis [245], acute pituitary necrosis [246], pseudomembranous colitis, thrombotic thrombocytopenic purpura (TTP), Sanarelli-Shwartzman phenomenon (SSP), Henoch-Schonlein purpura (HSP), eclampsia [238], serum sickness, hemolytic anemia, preeclampsia, and stillbirths [247].…”

Section: Zeta Potential and Cardiovascular Diseasementioning

confidence: 99%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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Abstract:In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome Glossary of TermsAnaphylaxis a severe, rapidly progressing, life-threatening, generalized allergic reaction. Biological equipoise a stable, non-equilibrium, dissipative system synonymous with life. Cholesterol sulfate (Ch-S)quantitatively the most important known sterol sulfate in human plasma where it regulates the activity of the serine proteases, in cell membranes where it has a stabilizing role, and in platelet membranes where it supports platelet adhesion. Coherence domain (CD)a water CD is a collection of liquid water molecules which oscillate in unison in tune with a self-trapped electromagnetic field at a well-defined frequency. The coherent oscillations produce an ensemble of quasi-free electrons, able to collect noise energy from the environment and transform it into high-grade coherent energy in the form of electron vortices. This high-grade energy may then activate biomolecules resonating with the water CD. Colloidal instabilitya property attributed to a colloidal suspension that develops when stabilizing repulsive steric and electrostatic forces between colliding particles are insufficient to prevent their natural tendency to aggregate into masses large enough to precipitate.Colloidal suspension a colloid that has a continuous liquid phase in which a solid is suspended in a liquid, e.g., our flowing blood. Exclusion zone (EZ)a glass-like, gel phase consisting of water CDs resonating in-phase, adjacent to hydrophilic surfaces, several hundred micrometers wide which excludes colloi...

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“…In human cases fibrin thrombi are frequently found in the renal cortex and also in liver, spleen, pituitary, and adrenals and less frequently in lungs, myocardium, brain, and intestine [5]. Extrarenal thrombi were reported in four out of seven cases of renal cortical necrosis in humans [I I].…”

Section: Discussionmentioning

confidence: 99%

Renal Cortical Necrosis in a Cat

Hall

1972

Vet Pathol

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Abstract. An 8-year-old cat had symptoms of advanced renal failure. At postmortem examination it was found to have extensive bilateral renal cortical necrosis that appeared to have been in existence for some weeks. The literature on this type of lesion was reviewed, but no conclusions could be reached on the pathogenesis of this case.Bilateral renal cortical necrosis is well recognized in humans and is usually a sequel to the obstetrical catastrophy of uteroplacental apoplexy. A number of cases, however, have been reported in men, nonpregnant women, and children [lo]. JUBB and KENNEDY [I] state that it is 'not uncommon' in domestic animals. They report cases in cattle, outbreaks in kennels of dogs, and in cats sporadic cases, of which some have been associated with thrombosis of the renal arteries. NORDSTOCA [8], however, reported that only six cases had been diagnosed in the Department of Pathology in the Veterinary College of Norway during a 12-year period. Three cases were in horses, two in cows, and one in a dog, and during the same period the total necropsies of these species were 512, 1,522 and 4,333, respectively. He was unaware of any other description of spontaneously occurring BCN in domestic animals.In the last I3 years in this Department, 368 cats have been subject t o postmortem examination and in only one was renal cortical necrosis diagnosed. Case ReportAn 8-year-old castrated male Siamese cat was presented for postmortem examination. The cat had lost weight for 3 months before death and in the last 3 weeks of life had developed polydipsia, inappetence, and a chronic cough and had become inactive. Towards the

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The pathologic anatomy of eclampsia, bilateral renal cortical necrosis, pituitary necrosis, and other acute fatal complications of pregnancy, and its possible relationship to the generalized Shwartzman phenomenon

Cited by 222 publications

References 8 publications

Coagulation and Fibrinolytic Systems in Pre-eclampsia and Eclampsia

Coagulation and Fibrinolytic Systems in Pre-eclampsia and Eclampsia

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Renal Cortical Necrosis in a Cat

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