Romina Iriarte

Hospital Británico de Buenos Aires

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Mariano Forrester

Servicio Geológico Minero Argentino

Hernán Trimarchi

Hospital Británico de Buenos Aires

Fernando Lombi

Hospital Británico

Vanesa Pomeranz

Hospital Británico de Buenos Aires

Alexis Muryan

Hospital Británico de Buenos Aires

Tatiana Rengel

Hospital Británico de Buenos Aires

Matías Paulero

Hospital Británico

Pablo Young

Hospital Británico de Buenos Aires

Romina Canzonieri

Hospital Británico de Buenos Aires

Amalia Schiel

Hospital Británico de Buenos Aires

Cooperative Institutions

Hospital Británico de Buenos Aires

Hospital Británico

University of Buenos Aires

Consejo Nacional de Investigaciones Científicas y Técnicas

Sociedad Española de Nefrología

Hospital Italiano de Buenos Aires

Universidad Autónoma de Madrid

Hospital Universitario Fundación Jiménez Díaz

Centro de Educación Médica e Investigaciones Clínicas Norberto Quirno

Instituto de Salud Carlos III

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Microangiopatía trombótica e injuria renal aguda en el primer trimestre de embarazo

Fronteras en Medicina (2018)

Ivan González-Hoyos Fernando Lombi Mariano Forrester Vanesa Pomeranz Romina Iriarte

La microangiopatía trombótica acompañada de injuria renal aguda (IRA) en el embarazo es un desafío diagnóstico y terapéutico.Presentamos el caso clínico de una mujer de 29 años de edad cursando el primer trimestre del embarazo, que presentó IRA, anemia hemolítica microangiopática y plaquetopenia, que se correlacionaron con hallazgos compatibles con microangiopatía trombótica (MAT) severa en la punción biopsia renal.Se decidió realizar un estudio genético para las mutaciones del complemento evidenciándose deleción heterocigota de los genes CFHR3/CFHR1 y anticuerpos anti factor H del complemento positivos, haciéndose el diagnóstico de síndrome urémico hemolítico atípico (SUHa).El tratamiento con plasmaféresis y recambio plasmático permitió una evolución clínica favorable de la paciente y estabilización de la función renal.

10.31954/rfem/201803/0154-0157

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Expression of uPAR in Urinary Podocytes of Patients with Fabry Disease

International Journal of Nephrology (2017)

Hernán Trimarchi Romina Canzonieri Amalia Schiel Juan Politei Cristian Costales-Collaguazo

Background. Despite enzyme replacement therapy, Fabry nephropathy still progresses. Podocyturia is an irreversible event that antedates proteinuria and leads to chronic renal failure. We evaluated a potential mechanism of podocyte detachment via the expression of the urokinase-type Plasminogen Activator Receptor (uPAR) in urinary podocytes of Fabry patients. Methods. This is a cross-sectional study that included controls (n = 20) and Fabry patients (n = 44) either untreated (n = 23) or treated with agalsidase-β (n = 21). Variables. Variables are estimated glomerular filtration rate (eGFR), urinary protein : creatinine ratio, and urinary uPAR+ podocyte : creatinine ratio. uPAR mRNA expression in response to lyso-Gb3, a bioactive glycolipid accumulated in Fabry disease, was studied in cultured human podocytes. Results. Controls and Fabry patients had similar age, gender, and renal function. Urinary uPAR+ podocytes were higher in patients than in controls. Untreated patients were significantly younger; had more females, and presented lower urinary protein : creatinine ratios and significantly higher urinary uPAR+ podocytes than treated subjects. In treated patients, urinary uPAR+ podocytes correlated with urinary protein : creatinine ratio (ρ = 0.5; p = 0.02). Lyso-Gb3 at concentrations found in the circulation of Fabry patients increased uPAR expression in cultured podocytes. Conclusions. Urinary podocytes expressing uPAR are increased in Fabry patients, especially in untreated patients. The potential contribution of uPAR expression to podocyte detachment merits further studies.

10.1155/2017/1287289

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Citations (10)

Erratum to: Podocyturia is significantly elevated in untreated vs treated Fabry adult patients

Journal of Nephrology (2016)

Hernán Trimarchi Romina Canzonieri Amalia Schiel Juan Politei Aníbal Stern

10.1007/s40620-016-0293-6

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WCN24-2592 GENETIC DIAGNOSIS OF CHRONIC KIDNEY DISEASE: A SINGLE-CENTER STUDY

Kidney International Reports (2024)

E. Rodríguez Flores Mariana Ursino Mariano Forrester Romina Iriarte Fernando Lombi

Chronic kidney disease (CKD) has an estimated global prevalence of 10%, 20% of which are attributed to genetic causes. Late diagnosis hampers the implementation of preventive nephroprotective regimens, leading to increased morbidity and mortality in this population

Center (category theory)

10.1016/j.ekir.2024.02.731

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Belatacept and mediastinal histoplasmosis in a kidney transplant patient

Journal of Nephropathology (2016)

Hernán Trimarchi Tatiana Rengel J. Matthew Andrews Matías Paulero Alejandro Iotti

In transplantation immunosuppression enhances the appearance of opportunist infections. An ideal balance between the prevention of rejection, the lowest risk of infections and the highest rates of graft survival is a continuous challenge. Lower doses of immunosuppression may diminish the risk of infections, metabolic and hemodynamic complications or even of malignancy, but may expose patients to episodes of acute rejection. New drugs are being developed to improve graft survival at the lowest risk of side effects. Belatacept has recently been introduced in kidney transplantation to inhibit the co-ligand signal of T cell stimulation. It is a drug with a safe profile, is well-tolerated and appears to improve long-term survival of kidney grafts. However, there may be an increase in opportunistic infections which may be facilitated by T cell depression, as Aspergillus sp., Cryptococcus neoformans or tuberculosis.We describe a 59-year-old female who developed fever, clinical wasting and a mediastinal mass 31 months after receiving a living non-related kidney transplant while on belatacept therapy. A mediastinal node biopsy disclosed the presence of Histoplasma capsulatum. Infection successfully resolved after appropriate antifungal treatment.To our knowledge, this is the first reported case of Histoplasma capsulatum in a kidney transplanted patient on belatacept therapy.

Immunosuppression

Belatacept

Histoplasma

10.15171/jnp.2016.15

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Is There a Role for Mammalian Target of Rapamycin Inhibition in Renal Failure due to Mesangioproliferative Nephrotic Syndrome?

International Journal of Nephrology (2012)

Hernán Trimarchi Mariano Forrester Fernando Lombi Vanesa Pomeranz Romina Iriarte

Primary glomerulonephritis stands as the third most important cause of end-stage renal disease, suggesting that appropriate treatment may not be as effective as intended to be. Moreover, proteinuria, the hallmark of glomerular damage and a prognostic marker of renal damage progression, is frequently resistant to thorough control. In addition, proteinuria may be the common end pathway in which different pathogenetic mechanisms may converge. This explains why immunosuppressive and nonimmunosuppressive approaches are partly not sufficient to halt disease progression. One of the commonest causes of primary glomerulonephritis is mesangioproliferative glomerulonephritis. Among the triggered intracellular pathways involved in mesangial cell proliferation, the mammalian target of rapamycin (mTOR) plays a critical role in cell growth, in turn regulated by many cytokines, disbalanced by the altered glomerulopathy itself. However, when inhibition of mTOR was studied in rodents and in humans with primary glomerulonephritis the results were contradictory. In light of these controversial data, we propose an explanation for these results, to dilucidate under which circumstances mTOR inhibition should be considered to treat glomerular proteinuria and finally to propose mTOR inhibitors to be prospectively assessed in clinical trials in patients with primary mesangioproliferative glomerulonephritis, for which a satisfactory standard immunosuppressive regimen is still pending.

Glomerulopathy

Regimen

10.1155/2012/427060

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Mucin-1 Gene Mutation and the Kidney: The Link between Autosomal Dominant Tubulointerstitial Kidney Disease and Focal and Segmental Glomerulosclerosis

Case Reports in Nephrology (2018)

Hernán Trimarchi Matías Paulero Tatiana Rengel Ivan González-Hoyos Mariano Forrester

Glomerular diseases are one of the most frequent causes of chronic kidney disease, focal and segmental glomerulosclerosis being one of the commonest glomerulopathies. However, the etiology of this glomerular entity, which merely depicts a morphologic pattern of disease, is often not established and, in most of the patients, remains unknown. Nephrologists tend to assume focal and segmental glomerulosclerosis as a definitive diagnosis. However, despite the increasing knowledge developed in the field, genetic causes of glomerular diseases are currently identified in fewer than 10% of chronic kidney disease subjects. Moreover, unexplained familial clustering among dialysis patients suggests that genetic causes may be underrecognized. Secondary focal and segmental glomerulosclerosis due to genetic mutations mainly located in the podocyte and slit diaphragm can occur from childbirth to adulthood with different clinical presentations, ranging from mild proteinuria and normal renal function to nephrotic syndrome and renal failure. However, this histopathological pattern can also be due to primary defects outside the glomerulus. The present report illustrates an adult case of secondary focal and segmental glomerulosclerosis with a dominant tubulointerstitial damage that led to the pursue of its cause at the tubular level. In this patient with an undiagnosed family history of adult kidney disease, a genetic study unraveled a mutation in the mucin-1 gene and a final diagnosis of adult dominant tubular kidney disease-MUC1 was made.

Glomerulosclerosis

Slit diaphragm

Podocin

Nephrology

10.1155/2018/9514917

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Citations (1)

In IgA Nephropathy, Glomerulosclerosis Is Associated with Increased Urinary CD80 Excretion and Urokinase-Type Plasminogen Activator Receptor-Positive Podocyturia

Nephron Extra (2017)

Hernán Trimarchi Romina Canzonieri Amalia Schiel Cristian Costales-Collaguazo Aníbal Stern

Podocyturia may determine the evolution to podocytopenia, glomerulosclerosis, and renal failure. According to the Oxford classification of IgA nephropathy (IgAN), the S1 lesion describes glomerulosclerosis. Urokinase-type plasminogen activator receptor (uPAR) participates in podocyte attachment, while CD80 increases in glomerulosclerosis. We measured uPAR-positive urinary podocytes and urinary CD80 (uCD80) in controls and in IgAN subjects with M1E0S0T0 and M1E0S1T0 Oxford scores to assess a potential association between podocyturia, inflammation, and glomerulosclerosis.The groups were as follows: controls (G1), n = 20 and IgAN group (G2), n = 39, subdivided into M1E0S0T0 (G2A), n = 21 and M1E0S1T0 (G2B), n = 18. Among the included variables, we determined uPAR-positive podocytes/gram of urinary creatinine (gUrCr) and uCD80 ng/gUrCr. Biopsies with interstitial fibrosis and tubular atrophy <10% were included.Groups were not different in age and gender; urinary protein-creatinine (uP/C) ratio, Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equation, uPAR-positive podocytes/gUrCr, and uCD80 were significantly increased in G2 versus G1. G2A and G2B were not different in age, gender, hypertension, and follow-up. G2B displayed significantly higher uP/C, uPAR-positive podocytes, uCD80, and lower CKD-EPI versus G2A. Strong significant correlations were encountered between uCD80 and podocyturia in G2A and G2B. However, when G1 was compared to G2A and G2B separately, the differences with respect to uP/C, uPAR-positive podocytes, and podocyturia were significantly stronger versus G2B than versus G2A.IgAN presents elevated uCD80 excretion and uPAR-positive podocyturia, while CD80 correlates with podocyturia. Glomerulosclerosis (S1) at the time of biopsy is associated with higher uP/C, lower renal function, increased uPAR-positive podocyturia, and CD80 excretion, and is independent of M1. In IgAN, uPAR may participate in podocyte detachment.

Glomerulosclerosis

SuPAR

10.1159/000473888

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Citations (10)

Early decrease in the podocalyxin to synaptopodin ratio in urinary Fabry podocytes

Clinical Kidney Journal (2018)

Hernán Trimarchi Romina Canzonieri Cristian Costales-Collaguazo Juan Politei Aníbal Stern

In Fabry nephropathy, podocyturia is an early event that may lead to glomerulosclerosis and chronic kidney disease. The glycocalyx is a potential podocyte damaged compartment in glomerulopathies. We investigated glycocalyx podocalyxin in urinary detached podocytes compared with cytoplasmic synaptopodin.This was a cross-sectional study including 68 individuals: Controls (n = 20) and Fabry patients (n = 48), 15 untreated and 33 treated. Variables included age, gender, urinary protein/creatinine ratio (UPCR), estimated glomerular filtration rate (eGFR), lyso-triasocylsphingosine (lyso-Gb3) levels and enzyme replacement therapy (ERT). Podocyturia was assessed by immunofluorescence and podocyte subpopulations were analyzed.Fabry patients displayed higher podocyturia than controls. Fabry treated subjects (n = 33) presented significantly higher UPCR compared with untreated ones (n = 15); podocyturia, eGFR and lyso-Gb3 levels were not different. All control podocytes colocalized synaptopodin and podocalyxin; 13 Fabry patients (27%) colocalized these proteins, while 35 (73%) were only synaptopodin positive. No podocalyxin-positive/synaptopodin-negative cells were encountered. In Fabry patients, podocyturia was significantly higher and proteinuria lower in those that colocalized.Fabry patients present higher podocyturia and a presumably more damaged glycocalyx assessed by podocalyxin. Treated patients had significant higher proteinuria suggesting ERT is initiated late, at advanced stages. The degree of podocalyxin-negative podocytes was similar in both groups, but colocalization was associated with lower proteinuria. Podocyturia assessed by podocalyxin alone may be underestimated. The implications of podocyte glycocalyx damage deserve further investigations.

Podocalyxin

Synaptopodin

Glycocalyx

Glomerulosclerosis

Globotriaosylceramide

10.1093/ckj/sfy053

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Citations (16)

WCN24-2542 HEMODYNAMIC INESTABILITY IN DIALYSIS AS A PREDICTOR OF MORTALITY IN CRITICALLY ILL PATIENTS

Kidney International Reports (2024)

Leonel Langellotti Carolina Lozina Briant Gauna Eugenia M. Flores Jose Diaz Gongora

Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased short- and long-term morbidity, hospital mortality, and chronic kidney disease with the risk of chronic dialysis. The incidence of AKI in the intensive care unit (ICU) ranges from approximately 30% to 60% of critically ill patients.Renal support therapy (RST) is a cornerstone of treatment in critically ill patients; however, its application is not without adverse events, including hemodynamic instability and the risk of chronic dialysis.Intradialytic hemodynamic instability in critically ill patients is a possible and potentially life-threatening condition, in a potential risk of ESRD.Objective: To correlate episodes of arterial hypotension during Renal Support Therapy (RST) in patients admitted to the Intensive Care Unit (ICU) and assess their impact on patient outcomes.

10.1016/j.ekir.2024.02.110

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