Martin F. Reiner

University Hospital of Zurich

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Jürg H. Beer

Kantonsspital Baden

Giovanni G. Camici

University of Zurich

Simona Stivala

University Hospital of Basel

Thomas F. Lüscher

Royal Brompton & Harefield NHS Foundation Trust

Nicole R. Bonetti

University Hospital of Zurich

Nicolas Rodondi

University of Bern

David Conen

McMaster University

S Gobbato

University of Zurich

Gianluigi Savarese

Karolinska University Hospital

Alexander Akhmedov

University of Zurich

Cooperative Institutions

Manchester Metropolitan University

133

University of Zurich

109

University Hospital of Zurich

University of Salford

Istituti di Ricovero e Cura a Carattere Scientifico

Universidad de Granada

Centro Cardiologico Monzino

Inserm

King's College London

Swiss Integrative Center for Human Health

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Acute kidney injury associated with COVID-19: a prognostic factor for pulmonary embolism or co-incidence?

European Heart Journal (2020)

Seyed Soheil Saeedi Saravi Massimo Barbagallo Martin F. Reiner Hans Ruedi Schmid Jonas Rutishauser

An 81-year-old gentleman presented with fever (39.1 C), cough, dysuria, and urinary tract infection, which warranted antibiotic therapy.Medical history included insulin-dependent type 2 diabetes mellitus, arterial hypertension, and third-degree atrioventricular block with an implanted pacemaker.The patient was intubated and required mechanical ventilation for severe respiratory failure (Horowitz index of 64.2 mmHg) 6 days after hospitalization.SARS-CoV-2 polymerase chain reaction (PCR) test on nasopharyngeal swabs was positive and chest computed tomography (CT) illustrated bilateral ground-glass opacities (Panel A).Laboratory tests showed a remarkable increase in the inflammatory cytokine interleukin-6 (270.6 pg/mL) and C-reactive protein (CRP; 222.7 mg/L).In the second week, he developed acute kidney injury (AKI) [creatinine, 296 lmol/L; blood urea nitrogen (BUN), 14.6 lmol/L, and estimated glomerular filtration rate (eGFR) 16 mL/ min/1.73m 2 ], and consequently continuous haemodialysis was initiated.Fifteen days later, D-dimer levels were strikingly elevated (15 293 lg/L), and CT pulmonary angiography revealed segmental pulmonary embolism (PE) in the right upper lobe (Panel B) without signs of right ventricular failure (Supplementary material online, Video 1).ECG showed new onset of atrial fibrillation (Panel C).Anticoagulation with unfractionated heparin was implemented.The patient remained in the intensive care unit until recovery of pulmonary function, but dialysis continued for 24 days to be prepared for discharge.Although causes of PE and AKI are multifactorial, common mechanisms such as the proinflammatory cytokine storm, endothelial injury, hypercoagulability, and direct infection of both endothelial and epithelial cells in the kidney may underlie a prognostic and predictive role for AKI for PE in patients with severe COVID-19.

2019-20 coronavirus outbreak

Pulmonary Injury

10.1093/eurheartj/ehaa637

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In response to the comment by Hechler et al .: Amotosalen/UVA pathogen inactivation technology reduces platelet activatability, induces apoptosis and accelerates clearance.

Haematologica (2017)

Simona Stivala S Gobbato Laura Infanti Martin F. Reiner Nicole R. Bonetti

We would like to thank B. Hechler and colleagues for the interest shown in our paper on the effects of the Amotosalen/UVA on platelet function, and we are pleased to take the opportunity to reply to their comments. They note correctly that the results of our study are divergent from their

10.3324/haematol.2017.181818

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[Retroperitoneal fibrosis and portal hypertension].

PubMed (1993)

S Réalini Martin F. Reiner S Bernasconi E Pedrinis

A patient is described in whom retroperitoneal fibrosis manifested itself by bleeding from ruptured varices and pain in the left flank and lumbar region. The clinical diagnosis was confirmed by axial computerized tomography and MRI, while the histology from a mesenteric biopsy taken during splenectomy was considered insufficiently consistent with the diagnosis of retroperitoneal fibrosis. Treatment with prednisone resulted in relief of lumbar and flank pain a well as in prevention of further digestive tract hemorrhage. A review of the literature since 1966 shows 16 articles describing the association of retroperitoneal fibrosis and portal hypertension manifesting itself by hemorrhage from bleeding varices.

Flank pain

Retroperitoneal Hemorrhage

Flank

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Amotosalen/ultraviolet A pathogen inactivation technology reduces platelet activatability, induces apoptosis and accelerates clearance

Haematologica (2017)

Simona Stivala S Gobbato Laura Infanti Martin F. Reiner Nicole R. Bonetti

Amotosalen and ultraviolet A (UVA) photochemical-based pathogen reduction using the Intercept™ Blood System (IBS) is an effective and established technology for platelet and plasma components, which is adopted in more than 40 countries worldwide. Several reports point towards a reduced platelet function after Amotosalen/UVA exposure. The study herein was undertaken to identify the mechanisms responsible for the early impairment of platelet function by the IBS. Twenty-five platelet apheresis units were collected from healthy volunteers following standard procedures and split into 2 components, 1 untreated and the other treated with Amotosalen/UVA. Platelet impedance aggregation in response to collagen and thrombin was reduced by 80% and 60%, respectively, in IBS-treated units at day 1 of storage. Glycoprotein Ib (GpIb) levels were significantly lower in IBS samples and soluble glycocalicin correspondingly augmented; furthermore, GpIbα was significantly more desialylated as shown by Erythrina Cristagalli Lectin (ECL) binding. The pro-apoptotic Bak protein was significantly increased, as well as the MAPK p38 phosphorylation and caspase-3 cleavage. Stored IBS-treated platelets injected into immune-deficient nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice showed a faster clearance. We conclude that the IBS induces platelet p38 activation, GpIb shedding and platelet apoptosis through a caspase-dependent mechanism, thus reducing platelet function and survival. These mechanisms are of relevance in transfusion medicine, where the IBS increases patient safety at the expense of platelet function and survival.

10.3324/haematol.2017.164137

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Citations (55)

[Cholesterol crystal embolisms: an exciting search for "pearls"].

PubMed (1997)

Brenno Balestra Martin F. Reiner G Noseda

This article is meant to increase the interest in an often forgotten clinical entity. Cholesterol emboli are in the majority of cases only diagnosed at post-mortem examination. Even though the triad livedo reticularis, renal failure and eosinophilia constitutes its most prominent feature, the variable clinical manifestations of this disorder with multiorgan involvement ("pseudovasculitis") make the search for cholesterol crystals particularly exciting. The discovery of 10 cases of cholesterol emboli over 2 years in a regional hospital's internal medicine department demonstrates that this occurrence is not rarely and that its accurate identification can be particularly relevant. It is important to recognize this disease since it is often iatrogenic, affects elderly people with atherosclerosis of the large vessels and causes high morbidity and mortality.

Livedo reticularis

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Both PU.1 and nuclear factor-kappa B mediate lipopolysaccharide- induced HIV-1 long terminal repeat transcription in macrophages.

PubMed (1998)

Tracey Lodie Martin F. Reiner Salvatore J. Coniglio Gregory A. Viglianti Matthew J. Fenton

We recently reported that LPS stimulation of monocytic cells leads to the activation of PU.1, a member of the Ets family of transcription factors. Phosphorylation of PU.1 by protein kinase CK2 was found to up-regulate its trans-activation function, but not its DNA binding activity. Previous studies suggested that Ets proteins could bind to NF-kappa B motifs at the tetrameric core sequence TTCC. In macrophages, LPS-inducible HIV-1 gene expression is mediated in part by binding of NF-kappa B to identical tandem binding sites located within the long terminal repeat (LTR). Thus, we performed additional studies to determine whether PU.1 also played a role in regulating HIV-1 gene expression in macrophages. Our functional studies revealed that activation of the HIV-1 LTR in LPS-stimulated cells requires both NF-kappa B and PU.1. Extensive mutagenesis of the HIV-1 LTR revealed that PU.1-dependent activation requires the Ets motif within the upstream NF-kappa B site, whereas NF-kappa B itself binds to the downstream site. We also found that insertion of five additional nucleotides between the NF-kappa B sites abolished LPS inducibility, suggesting a direct interaction between factors that bind these sites. Lastly, we found that mutation of PU.1 at serine 148, which prevents its phosphorylation by CK2, blocked its ability to activate the HIV-1 LTR in response to LPS. These effects were promoter specific because PU.1 did not affect LPS-inducible activation of a distinct NF-kappa B-dependent promoter. While these data do not demonstrate direct binding of PU.1 to the HIV-1 LTR, they illustrate a novel role for PU.1 in activation of the HIV-1 LTR by LPS.

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Dietary omega-3 alpha-linolenic acid does not prevent venous thrombosis in mice

Thrombosis and Haemostasis (2014)

Simona Stivala Gianluigi Savarese Giovanni G. Camici Thomas F. Lüscher Denisa Wagner

Summary Venous thromboembolism (VTE) is a leading cause of cardiovascular death. Omega-3 fatty acids (n-3 FA) exhibit protective effects against cardiovascular disease. Others and our group have reported that the plant-derived n-3 FA alpha-linolenic acid (ALA) displays antiinflammatory, anticoagulant and antiplatelet effects, thereby reducing atherosclerosis and arterial thrombosis in mice fed a high ALA diet. Since procoagulant factors such as tissue factor and fibrin as well as platelets and leukocytes are crucially involved in the development of VTE, we investigated possible protective effects of dietary ALA on venous thrombus formation in a mouse model of stenosis- and furthermore, in a mouse model of endothelial injury-induced venous thrombosis. Four week old C57BL/6 mice underwent four weeks of high (7.3g%) or low ALA (0.03g%) treatment before being exposed to inferior vena cava (IVC) stenosis for 48 hours or laser injury of the endothelium of the internal jugular vein (IJV). Thrombus generation frequency, thrombus size and composition (IVC stenosis group) and time to thrombus formation (endothelial injury group) were assessed. In addition, plasma glycocalicin, a marker of platelet activation, platelet P-selectin and activated integrin expression as well as plasma thrombin generation was determined, but did not reveal any significant differences between he groups. Despite its protective properties against arterial thrombus formation, dietary ALA did not protect against venous thrombosis neither in the IVC stenosis nor the endothelial injury model, further indicating that the biological processes involved in arterial and venous thrombosis are different.

alpha-Linolenic acid

Alpha (finance)

10.1160/th14-03-0200

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Citations (11)

Calcium absorption and excretion in the gut in acromegaly

Clinical Endocrinology (1973)

Gunnar Sigurðsson V. Nunziata Martin F. Reiner A Nadarajah G. F. Joplin

Summary In twenty patients with active acromegaly, twenty‐five measurements of radiocalcium absorption and fourteen measurements of gut excretion were made. Calcium absorption in this group was greater than normal, and was positively correlated with both the serum calcium level and the urine calcium output. Endogenous faecal calcium was usually normal. It is suggested that increased calcium absorption from the gut is a major factor in determining any elevation in serum and urine calcium levels in acromegaly.

10.1111/j.1365-2265.1973.tb00418.x

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Citations (29)

The MAP kinase JNK2 mediates cigarette smoke-induced arterial thrombosis

Thrombosis and Haemostasis (2016)

Alexander Breitenstein Simon F. Stämpfli Martin F. Reiner Yi Shi Stephan Sylvest Keller

Despite public awareness of its deleterious effects, smoking remains a major cause of death. Indeed, it is a risk factor for atherothrombotic complications and in line with this, the introduction of smoking ban in public areas reduced smoking-associated cardiovascular complications. Nonetheless, smoking remains a major concern, and molecular mechanisms by which it causes cardiovascular disease are not known. Peripheral blood monocytes from healthy smokers displayed increased JNK2 and tissue factor (TF) gene expression compared to non-smokers (n=15, p<0.05). Similarly, human aortic endothelial cells exposed to cigarette smoke total particulate matter (CS-TPM) revealed increased TF expression mediated by JNK2 (n=4; p<0.05). Wild-type and JNK2-/- mice were exposed to cigarette smoke for two weeks after which arterial thrombosis was investigated. Wild-type mice exposed to smoke displayed reduced time to thrombotic arterial occlusion (n=8; p<0.05) and increased tissue factor activity (n=7; p<0.05) as compared to wild-type controls (n=6), while JNK2-/-mice exposed to smoke maintained an unaltered thrombotic potential (n=8; p=NS) and tissue factor activity (n=8) comparable to that of JNK2-/- and wild-type controls (n=6; p=NS). Smoking caused an increased production of reactive oxygen species (ROS) in wild-type but not in JNK2-/- mice (n=7; p<0.05 for wild-type mice and n=5-6; p=NS for JNK2-/- mice). In conclusion, the MAP kinase JNK2 mediates cigarette smoke-induced TF activation, arterial thrombosis and ROS production. These results underscore a major role of JNK2 in smoke-mediated thrombus formation and may offer an attractive target to prevent smoke-related thrombosis in those subjects which do not manage quitting.

10.1160/th16-05-0351

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Citations (7)

The Intercept Blood System Affects Platelet Function and Survival By Inducing Apoptosis

Blood (2014)

Simona Stivala S Gobbato Martin F. Reiner Sara C. Meyer Thomas F. Lüscher

P-selectin

Annexin A5

10.1182/blood.v124.21.4283.4283

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Citations (3)