Gianluigi Ardissino

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

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Sara Testa

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Francesca Tel

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Fabio Paglialonga

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Valentina Capone

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Massimo Cugno

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Patrizia Salice

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Giovanni Montini

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Ilaria Possenti

Azienda Ospedaliera Nazionale SS. Antonio e Biagio e Cesare Arrigo

Valeria Daccò

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Alberto Edefonti

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Cooperative Institutions

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

276

Istituti di Ricovero e Cura a Carattere Scientifico

225

University of Milan

215

Ospedale Maggiore

184

RELX Group (United States)

Boston Children's Hospital

Istituto Giannina Gaslini

Inserm

Pediatric Nephrology of Alabama

Bambino Gesù Children's Hospital

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Soluble Toll-Like Receptor 4 Impairs the Interaction of Shiga Toxin 2a with Human Serum Amyloid P Component

Toxins (2018)

Maurizio Brigotti Valentina Arfilli Domenica Carnicelli Francesca Ricci Pier Luigi Tazzari

Shiga toxin 2a (Stx2a) is the main virulence factor produced by pathogenic Escherichia coli strains (Stx-producing E. coli, STEC) responsible for hemorrhagic colitis and the life-threatening sequela hemolytic uremic syndrome in children. The toxin released in the intestine by STEC targets the globotriaosylceramide receptor (Gb3Cer) present on the endothelial cells of the brain and the kidney after a transient blood phase during which Stx2a interacts with blood components, such as neutrophils, which, conversely, recognize Stx through Toll-like receptor 4 (TLR4). Among non-cellular blood constituents, human amyloid P component (HuSAP) is considered a negative modulating factor that specifically binds Stx2a and impairs its toxic action. Here, we show that the soluble extracellular domain of TLR4 inhibits the binding of Stx2a to neutrophils, assessed by indirect flow cytometric analysis. Moreover, by using human sensitive Gb3Cer-expressing cells (Raji cells) we found that the complex Stx2a/soluble TLR4 escaped from capture by HuSAP allowing the toxin to target and damage human cells, as assayed by measuring translation inhibition, the typical Stx-induced functional impairment. Thus, soluble TLR4 stood out as a positive modulating factor for Stx2a. In the paper, these findings have been discussed in the context of the pathogenesis of hemolytic uremic syndrome.

Virulence factor

10.3390/toxins10090379

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Citations (9)

Kinetics of Mature Platelet Fraction as a Tool for Predicting the Time Course of Shiga Toxin-Producing Escherichia coli-Associated Hemolytic Uremic Syndrome (STEC-HUS)

Journal of the American Society of Nephrology (2023)

Gianluigi Ardissino Thomas Ria Maria Cristina Mancuso Valentina Capone Laura Daprai

Ardissino, Gianluigi; Ria, Thomas; Mancuso, Maria Cristina; Capone, Valentina; Daprai, Laura; Amico, Valeria; Spanu, Francesco Author Information

Uremic Toxins

10.1681/asn.20233411s1759a

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Glucose Control in Post-hemolytic-Uremic Syndrome Diabetes: A New Approach Offered by Sensor-Augmented Pump Therapy

Frontiers in Pediatrics (2022)

Valeria Grancini Federica Vianello Santo Colosimo Alessia Gaglio Veronica Resi

We report the case of a 3-year-old girl admitted to her town emergency department for fever (39°C) associated with diarrhea, generalized edema, oliguria, and drowsiness. The blood test revealed metabolic acidosis, leucocytosis, increased inflammatory markers, anemia, thrombocytopenia, and acute kidney failure. Based on the diagnosis of hemolytic-uremic syndrome, the patient was referred to a third-level children hospital. Assisted ventilation, hemodialysis, and parenteral nutrition were instituted. The blood glucose levels increased above 200 mg/dl with peaks at 500 mg/dl. Islet auto-antibodies were negative and C-peptide was undetectable, thus ruling out the diagnosis of type 1 diabetes. Multiple-daily-injection insulin therapy was then instituted with the following regimen: Detemir 2 U once daily and Aspart 0.5 U if blood glucose >200 mg/dl. Despite the very low insulin dosage, the patient experienced frequent and severe hypoglycemic events during the following 24 h and was therefore switched to sensor-augmented pump therapy. Optimal glucose control was achieved without further hypoglycemic episodes. Moreover, thanks to the possibility to customize insulin therapy hour by hour during the day and the use of a pre-low glucose suspend system, glucose control was maintained even despite the continuous modifications in the nutritional scheme due to the multiple complications that arose during hospitalization. This rare case of post-hemolytic-uremic syndrome diabetes, treated with sensor-augmented therapy from its outbreak, suggests for the first time the potential of this therapeutic strategy in achieving glucose control without significant hypoglycemic episodes in children with secondary forms of diabetes associated with very low insulin requirement.

Insulin pump

Oliguria

Blood glucose monitoring

10.3389/fped.2022.882319

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Citations (1)

Hemoglobinuria for the Early Identification of Atypical Hemolytic Uremic Syndrome Relapse: Data from the ItalKId-HUS Network

Journal of the American Society of Nephrology (2020)

Gianluigi Ardissino Marta Brambilla Fabio Paglialonga Sara Testa Valentina Capone

Ardissino, Gianluigi; Brambilla, Marta; Paglialonga, Fabio; Testa, Sara; Capone, Valentina; Vergori, Antonio; Cresseri, Donata C.; Montini, Giovanni Author Information

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Hemoglobinuria

10.1681/asn.20203110s1709c

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Metabolic Factors in the Renal Response to Amino Acid Infusion

American Journal of Nephrology (1998)

Aldo Claris-Appiani Gianluigi Ardissino Amedea Silvia Tirelli Valeria Daccò Carlo Corbetta

In order to investigate the renal effects of amino acids (AA) with different metabolic fate, we compared the changes in glomerular and tubular function, nitrogen metabolism and glucoregulatory hormones in 7 volunteers during two infusions, one of a complete solution of amino acids (MIX-AA), which included five AA electively metabolized at the splanchnic level, and the other of a solution containing only essential AA (EAA), which escape splanchnic metabolism. MIX-AA increased GFR and RPF (from 104 ± 6 to 122 ± 13 and from 488 ± 46 to 572 ± 34 ml/min/1.73 m<sup>2</sup>), stimulated splanchnic metabolism as demonstrated by rises in urinary urea excretion (from 20.7 ± 2 to 30.6 ± 7.5 mg/min/1.73 m<sup>2</sup>) and the plasma glucagon/insulin ratio (from 21.4 ± 13 to 26.7 ± 15), and caused increases in fractional excretion of AA, FeNa and free-water clearance. During MIX-AA infusion significant correlations were observed between the individual values of GFR and the urea excretion rate (r = 0.66), and between GFR modifications (ΔGFR) and the plasma glucagon/plasma insulin ratio (r = 0.40). No change in renal function, urea excretion and the glucagon/insulin ratio was observed with EAA. An intermediate splanchnic step (increased plasma glucagon/insulin ratio and ureagenesis) seems necessary in the pathway leading to the nonessential AA-induced rise in GFR; this might stimulate an ultimate intrarenal pathway (possibly involving the diluting segment) via a still undefined mechanism.

10.1159/000013377

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Citations (13)

Urea percentiles in children with chronic renal failure

Pediatric Nephrology (2003)

Giovanni Montini Lorena Pisanello Sara Testa Valeria Daccò Luca Dello Strologo

Nephrology

Chronic renal failure

10.1007/s00467-003-1071-y

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Citations (4)

Late Onset Cobalamin Disorder and Hemolytic Uremic Syndrome: A Rare Cause of Nephrotic Syndrome

Case Reports in Pediatrics (2017)

Gianluigi Ardissino Michela Perrone Francesca Tel Sara Testa Amelia Morrone

Hemolytic uremic syndrome (HUS) is an unrare and severe thrombotic microangiopathy (TMA) caused by several pathogenetic mechanisms among which Shiga toxin-producing Escherichia coli infections and complement dysregulation are the most common. However, very rarely and particularly in neonates and infants, disorders of cobalamin metabolism (CblC) can present with or be complicated by TMA. Herein we describe a case of atypical HUS (aHUS) related to CblC disease which first presented in a previously healthy boy at age of 13.6 years. The clinical picture was initially dominated by nephrotic range proteinuria and severe hypertension followed by renal failure. The specific treatment with high dose of hydroxycobalamin rapidly obtained the remission of TMA and the complete recovery of renal function. We conclude that plasma homocysteine and methionine determinations together with urine organic acid analysis should be included in the diagnostic work-up of any patient with TMA and/or nephrotic syndrome regardless of age.

Thrombotic microangiopathy

Eculizumab

10.1155/2017/2794060

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Citations (13)

Atypical hemolytic uremic syndrome and C3 glomerulopathy: conclusions from a “Kidney Disease: Improving Global Outcomes” (KDIGO) Controversies Conference

Kidney International (2016)

Timothy H.J. Goodship H. Terence Cook Fádi Fakhouri Fernando C. Fervenza Véronique Frémeaux‐Bacchi

In both atypical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy (C3G) complement plays a primary role in disease pathogenesis. Herein we report the outcome of a 2015 Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference where key issues in the management of these 2 diseases were considered by a global panel of experts. Areas addressed included renal pathology, clinical phenotype and assessment, genetic drivers of disease, acquired drivers of disease, and treatment strategies. In order to help guide clinicians who are caring for such patients, recommendations for best treatment strategies were discussed at length, providing the evidence base underpinning current treatment options. Knowledge gaps were identified and a prioritized research agenda was proposed to resolve outstanding controversial issues.

Glomerulopathy

Eculizumab

10.1016/j.kint.2016.10.005

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Citations (595)

Discontinuation of Eculizumab Treatment in Atypical Hemolytic Uremic Syndrome: An Update

American Journal of Kidney Diseases (2015)

Gianluigi Ardissino Ilaria Possenti Francesca Tel Sara Testa Stefania Salardi

Eculizumab

Discontinuation

10.1053/j.ajkd.2015.04.010

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