An analysis of the results of therapy in 67 cases of the hemolytic-uremic syndrome

Kaplan, B.; Katz, J.; Krawitz, S.; Lurie, A.

doi:10.1016/s0022-3476(71)80221-4

Cited by 93 publications

(33 citation statements)

References 17 publications

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“…In our unit (table I) 32 patients were treated from 1957 to 1961 while 436 were managed from 1967 to 1971. Outside Argentina the published cases are from: USA [33]; South Africa [28]; France [20]; United Kingdom [39]; Belgium [35]; The Netherlands [51]; Mexico [19]; Australia [46]; Chile [54]; Switzerland [25]; Canada [31]; Germany [56]; Rhodesia [30]; Czechoslovakia [57]; Uruguay [44] and Italy [58] etc.…”

Section: Incidencementioning

confidence: 99%

“…There is no explanation for the scarcity of reports that describe similar neurologic abnormalities [28,36],…”

Section: Neurologic Involvementmentioning

confidence: 99%

“…Excellent reviews [33,36,43] and many recent papers [13,16,22,28] expressing the growing interest in the syndrome have delineated its clinical characteristics and several aspects of its patho genesis. As a rule, the HUS is a disease of infancy and childhood.…”

Section: Introduction and Definitionmentioning

confidence: 99%

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The Hemolytic-Uremic Syndrome

Ca¹,

Vitacco²,

Mendilaharzu³

et al. 1973

Nephron

249

132

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The clinical and pathological characteristics of the acute stage of the HUS are described on the basis of 678 patients and the study of 52 autopsies and 3 kidney biopsies. The laboratory and pathological studies point to DIC as a basic pathogenic mechanism, probably related to a viral infection. The recent mortality rate has been 6.25% due to the exacting dialysis treatment employed. Heparin was ineffective in the 26 patients in which it was used. 124 patients have a follow-up of more than 5 years and up to 13 years. 60 patients are completely recovered, while 64 have persistent signs of renal disease. Nine other children died in uremia 1–12 years after onset. The pathological findings are discussed on the basis of 6 autopsies and 24 biopsies in 27 patients. This stage of the HUS appears as an important and new aspect of pediatric nephrology.

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Section: Incidencementioning

confidence: 99%

“…There is no explanation for the scarcity of reports that describe similar neurologic abnormalities [28,36],…”

Section: Neurologic Involvementmentioning

confidence: 99%

See 1 more Smart Citation

The Hemolytic-Uremic Syndrome

Ca¹,

Vitacco²,

Mendilaharzu³

et al. 1973

Nephron

249

132

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“…The diversity of therapeutic approaches advocated by various groups, in cluding dialysis [6], anticoagulation [7], and exchange transfusion [8], reflects further the inadequacy of our understanding at present.…”

Section: Introductionmentioning

confidence: 99%

Renal Microangiopathy of the Hemolytic-Uremic Syndrome in Childhood

Riella

George

Hickman

et al. 1976

Nephron

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18 children with clinical and laboratory findings characteristic of the hemolytic-uremic syndrome were retrospectively studied. Thrombocytopenia due to platelet destruction was accompanied by only minimal changes in fibrinogen turnover and fibrinolytic degradation products. The most consistent pathologic feature was severe renal endothelial cell injury, which is postulated to produce both platelet and red cell destruction. Despite initially severe renal damage, 90% of the patients ultimately recovered normal renal function if adequately supported during the acute phase of the disease.

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“…Cabe esperar que el mejor conocirmento de la etiopatogenia Ueve a descubrir los medios de prevenir (10,11,17,18,19) el dano parenquimatoso y de influir en los procesos fibrinoliticos (6, 27) de modo de que la repermeabilizacion de las asas capilares glomerulares comprometidas permita una recuperacion de la funcion renal que sea compatible con una vida normal. …”

unclassified

Síndrome Hemolítico Urémico

Ochoa¹,

Gasc²

1973

Rev. chil. pediatr.

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El sindrome hemolitico uremico (SHU) se caracteriza por la aparicion simultanea de anemia de mecanismo extracorpuscular, nefropatia aguda hematurica y anurica, e hipertension; se acompana de trombopenia y lesiones neurologicas, especialmente en el lactante menor.Definido por Gasser y colaboradores (1), desde esa fecha se nan reportado numerosos casos en la literatura (2,3,4,5,6, 7,8,9, 10) siendo la casuistica mas importanle la del grupo de Gianantonio, en Buenos Aires (7,8). Otras series importantes se han comunicado en otros paises (9, 10, 11).Descrito como cuadro fatal en 1955, la aplicaci6n de mejores metodos de cuidado y, esencialmente el uso de procedimientos de dialisis ha hecho que los pacientes snperen la fase aguda de la enfermedad, poniendose en evidencia los problemas de secuelas que derivan de la nefropatia que produce el SHU.Aun cuando hay numerosos hechos que indican que la etiologia esta relacionada con enfermedad viral, no se ha podido probar con certeza. Hay bastantes casos publicados en que se ha logrado aislar algun virus en enfermos con SHU, pero el hallazgo no es constante, ni se repite el rnismo agente. Asi se ha encontrado evidencia de infection por Coxackie (5, 12), Echo (13) y Myxovirus (9), sin establecerse estrecha relacion causaefecto. Tambien se han encontrado anticuerpos anti-Coxackie en biopsias renales, estudiados por inmunofluorescencia (5). Asimismo apuntan hacia una etiologia viral, la aparici6n de brotes epidemicos en ciertas regiones del mundo, o endemias como seria el caso de Argentina.El mecanismo a traves del cual el o los agentes podrian llevar a la production de los sintomas, tampoco esta claro. Hay dos hipotesis importantes:* Departamento dc Pediatria. Hospital Roberto del Rio.-A) El dafio se produce por coagulaci6n intravascular, sin mediar factores inmuno!6-gicos. -B) La patogenesis seria de tipo inmunologico.A) Son muchos los argumentos a favor de la coagulacion intravascular como factor etiopatogenico. En primer lugar, la relacion estrecha entre la initiation de los sintomas y los procesos de coagulacion intravascular (CIV): gastroenteritis seguida de anemizacion y oligoanuria. Se explicaria bien: la trombocitopenia constante al iniciarse el fen<5me-no; la hem61isis importante que lleva a la anemizacion con morfologia especial de los eritrocitos, a causa de la deformacion que sufren al ser atrapados en las mallas de fibrina resultantes; la sobrevida acortada de plaquetas y g!6bulos rojos, y los altos niveles de hemoglobina plasmatica.Todos estos hechos son propios de hemolisis intravascular, por trastornos en pequenos vasos en diferentes parenquimas entre ellos rinon (14), sistema nervioso, intestine y otros (8), que llevan a alteracion grave de su funcion.Hay tambien evidencias bioquimicas y anatomopatologicas de CIV. Se ha estudiado la coagulacion en el SHU (9, 15) encontrandose, en general, elementos que permiten colocarlo dentro de las coagulopatias por consumo, especiahnente si las determinaciones se realizan en la etapa precoz de la enfermedad. La coagulacion...

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An analysis of the results of therapy in 67 cases of the hemolytic-uremic syndrome

Cited by 93 publications

References 17 publications

The Hemolytic-Uremic Syndrome

The Hemolytic-Uremic Syndrome

Renal Microangiopathy of the Hemolytic-Uremic Syndrome in Childhood

Síndrome Hemolítico Urémico

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