L E Voyer

University of Buenos Aires

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Caupolicán Alvarado

Hospital Pedro de Elizalde

Silvia Corti

Hospital Pedro de Elizalde

Alejandro Balestracci

Hospital Pedro de Elizalde

Mònica Tous

Administración Nacional de Laboratorios e Institutos de Salud

G Bruno

Hospital Pedro de Elizalde

Raquel Eva Wainsztein

Hospital Pedro de Elizalde

Rqquel Wainstein

Hospital Pedro de Elizalde

Ismael Toledo

Hospital Pedro de Elizalde

Takashi Yoshida

Shizuoka City Shimizu Hospital

N Leardini

Administración Nacional de Laboratorios e Institutos de Salud

Cooperative Institutions

Hospital Pedro de Elizalde

University of Buenos Aires

Administración Nacional de Laboratorios e Institutos de Salud

Consejo Nacional de Investigaciones Científicas y Técnicas

Academia Nacional de Medicina

Boston Children's Hospital

Sociedad Española de Nefrología

Universidad Nacional de La Plata

Garrahan Hospital

Institut Pasteur

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Folate Metabolism. Polymorphisms of Methylentetrahydrofolate Reductase. Concurrent Factor in Pathogenic Effects

American Journal of Biomedical Science & Research (2023)

L E Voyer

Human schistosomiasis is a parasitic infection that affects close to a quarter of a million people in 78 nations and the number of people at risk may be projected to 800 million. The disease is caused by Schistosoma parasites, which are blood flukes that infect humans through the skin when they come into contact with contaminated water. Schistosomiasis causes a range of symptoms, including abdominal pain, diarrhea, and blood in the urine. One of the less well-known effects of schistosomiasis is its impact on male reproductive features, germ cells and immune components in the testis. Despite the testicular cells are well equipped with innate and effective local defenses mechanisms against invading parasites. Various pathogens such as Schistosoma parasites, succeeded in hijacking the immune-privileged state of the testis and to evade systemic immune surveillance. Some pathogens can even remain in the testes for long periods of time, disrupting thus local immune homeostasis and affecting testicular function and male fertility. This article presents an overview of the Schistosoma parasites strategies used to jeopardize the testis immune priviledge.

Schistosoma

Parasitic Disease

10.34297/ajbsr.2023.19.002577

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Maillard reaction. Pathogenic effects.

SCIREA Journal of Clinical Medicine (2021)

L E Voyer Caupolicán Alvarado

Maillard reaction.Pathogenic effects.Certain organoleptic modifications by way of processing and cooking foods at high temperatures in dry heat, make them especially appetizing and object of addiction.It results from Mayllard reaction, or glycation, consisting on the non-enzymatic union between carbonyl groups, mainly from reducing sugars as glucose and fructose, with the amino groups of proteins and nucleic acids.In addition of physical changes, also the chemical structure and function of these compounds are changed.Besides exogenous glycation generated during the cooking of foods, recently in situ glycation has been reported in the intestinal lumen during digestion, when certain non-glycated foods are combined with fructose at the time of ingestion.In addition, endogenous glycation, which correlates in the extracellular mainly with blood glucose and in the intracellular with glycolysis metabolites and fructose, is especially significant.Since the 70s, with the frequent sucrose replacement by fructose, much more reactive than glucose, the presence of glycation products in processed foods and soft drinks increased.Pathogenic effects of these compounds, also called glycotoxins, are known to contribute to oxidative stress and inflammation.This

10.54647/cm32348

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Fetal renal maldevelopment with oligohydramnios following maternal use of piroxicam

Pediatric Nephrology (1994)

L E Voyer Ricardo Drut J. M�ndez

Renal cortex

Intervillous space

10.1007/bf00858136

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Citations (44)

Haemolytic uraemic syndrome associated with faecal cytotoxin and verotoxin neutralizing antibodies

Pediatric Nephrology (1988)

Adriana A. Novillo L E Voyer Roberto Cravioto Mar�a C. Freire Graciela Casta�o

Seroconversion

Haemolytic-uraemic syndrome

Vero cell

Nephrology

10.1007/bf00858679

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Citations (27)

[DETERMINATION OF WATER AND ELECTROLYTES IN TISSUE. PRELIMINARY REPORT].

PubMed (1964)

L E Voyer Orestes Humberto Gutiérrez Pérez

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Nephrotic syndrome due to immunoglobulin M mesangial glomerulonephritis preceding juvenile idiopathic arthritis.

PubMed (2013)

L E Voyer Caupolicán Alvarado Rubén Cuttica Alejandro Balestracci Marta Zardini

The association between nephrotic syndrome and juvenile idiopathic arthritis have rarely been described in pediatric patients. We report a child with steroid-responsive nephrotic syndrome, with frequent relapses, who presented with a new relapse of nephrotic syndrome associated with arthritis and uveitis at 21 months in remission after treatment with chlorambucil. Juvenile idiopathic arthritis was diagnosed and kidney biopsy examination showed mesangial glomerulonephritis with immunoglobulin M deposits. To our knowledge, only 2 cases of nephrotic syndrome preceding juvenile idiopathic arthritis have been reported, one without histopathology assessment and the other with minimal change disease. Although mesangial glomerulonephritis with nephrotic syndrome and juvenile idiopathic arthritis could have been coincidental, the immune pathogenic mechanism accepted for both diseases suggests they could be related.

Mesangial proliferative glomerulonephritis

Chlorambucil

Juvenile rheumatoid arthritis

Idiopathic Nephrotic Syndrome

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Determination of urinary bicarbonate with the Henderson-Hasselbalch equation

Pediatric Nephrology (2004)

Silvia González‐Gómez L E Voyer Silvia Corti Beatriz E. Quadri Cecilia Gogorza

Bicarbonate

10.1007/s00467-004-1540-y

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Citations (7)

Effect of salicylates on renal gluconeogenesis

The Journal of Pediatrics (1975)

L E Voyer Bolívar Pereyra

Gluconeogenesis

10.1016/s0022-3476(75)80862-6

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Hemolytic uremic syndrome in families ? an argentinian experience

Pediatric Nephrology (1996)

L E Voyer Raquel Eva Wainsztein Beatriz E. Quadri Silvia Corti

Nephrology

Uremic Toxins

10.1007/bf00863451

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Hiperpotasemia transitoria del lactante sin pérdida salina, enfoque fisiopatológico de tres casos

Nefrología (2021)

Caupolicán Alvarado Alejandro Balestracci Ismael Toledo Sandra Mariel Martin Laura Beaudoin

Se reconocen 2 variedades de hiperpotasemia temprana de la infancia (del inglés Early childhood hyperkalemia) según la presencia o no de pérdida salina urinaria. Se trata de una entidad atribuida a un desorden madurativo en los receptores de aldosterona caracterizada por hiperpotasemia, acidosis metabólica hiperclorémica por diminución de la eliminación de amonio y bicarbonaturia, y creatinina normal con retraso de crecimiento. Presentamos 3 pacientes de la forma con ausencia de pérdida salina, a la que denominaremos hiperpotasemia transitoria del lactante sin pérdida salina, y discutimos su fisiopatología con relación a los nuevos conocimientos en el manejo tubular del sodio y el potasio por la aldosterona. En 3 pacientes de entre 30 y 120 días de edad con bronquiolitis y retraso de crecimiento se encontró hiperpotasemia en laboratorio de rutina. Presentaban creatinina normal, excreción fraccionada de potasio disminuida o inapropiadamente normal junto a niveles de aldosterona y renina plasmática inadecuadamente normales para el estado de hiperpotasemia, pero sin pérdida salina. También cursaban con acidosis metabólica hiperclorémica con bicarbonaturia (excreción fraccionada de bicarbonato 0,58-2,2%), anión restante urinario positivo durante acidosis metabólica y capacidad normal para acidificar la orina. En base a estos hallazgos se diagnosticó hiperpotasemia transitoria del lactante sin pérdida salina y se trataron con bicarbonato de sodio e hidroclorotiazida con buena respuesta. El cuadro fue transitorio permitiendo la suspensión del tratamiento. Dado que la hiperpotasemia transitoria del lactante sin pérdida salina es un desorden tubular transitorio con síntomas leves debe tenerse presente en el diagnóstico diferencial de hiperpotasemia en niños pequeños. Two types of early-childhood hyperkalemia had been recognized, according to the presence or absence of urinary salt wasting. This condition was attributed to a maturation disorder of aldosterone receptors and is characterized by sustained hyperkalemia, hyperchloremic metabolic acidosis due to reduced ammonium urinary excretion and bicarbonate loss, and normal creatinine with growth delay. We present three patients of the type without salt wasting, which we will call transient early-childhood hyperkalemia without salt wasting, and discuss its physiopathology according to new insights into sodium and potassium handling by the aldosterone in distal nephron. In three children from 30 to 120-day-old admitted with bronchiolitis and growth delay hyperkalemia was found in routine laboratory. Further studies revealed a normal creatinine with inappropriately normal or low fractional excretion of potassium, accompanied by inadequately normal serum aldosterone and plasma renin activity for their higher plasma potassium levels, but without urine salt wasting. They also presented hyperchloremic metabolic acidosis with fractional excretion of bicarbonate 0.58–2.2%, positive urinary anion gap during metabolic acidosis and normal ability to acidify the urine. Based on these findings a diagnosis of transient early-childhood hyperkalemia without salt wasting was made and they were treated sodium bicarbonate and hydrochlorothiazide with favorable response. The condition was transient in all cases leading to treatment discontinuation. Given that transient early-childhood hyperkalemia without salt wasting is a tubular disorder of transient nature with mild symptoms; it must be keep in mind in the differential diagnosis of hyperkalemia in young children.

Pseudohypoaldosteronism

Urine sodium

10.1016/j.nefro.2020.12.018

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