Abstract Glucagon is a major regulator of metabolism and drugs targeting the glucagon receptor (GCGR) are being developed. Insight into tissue and cell-specific expression of the GCGR is important to understand the biology of glucagon and to differentiate between direct and indirect actions of glucagon. However, it has been challenging to localize the GCGR in tissue due to low expression levels and lack of specific methods. Immunohistochemistry has frequently been used for GCGR localization, but antibodies targeting G-protein-coupled-receptors may be inaccurate. We evaluated all currently commercially available GCGR antibodies. The antibody, ab75240 (Antibody no. 11) was found to perform best among the twelve antibodies tested and using this antibody we found expression of the GCGR in the kidney, liver, preadipocytes, pancreas, and heart. Three antibody-independent approaches all confirmed the presence of the GCGR within the pancreas, liver and the kidneys. GCGR expression should be evaluated by both antibody and antibody-independent approaches.

Glucagon receptor

10.1038/s42003-022-04242-7

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SUN-026 THE RADICAL NEPHRECTOMY PARADOX: THE UNEXPECTED AKI RISK

Kidney International Reports (2020)

Francesco Trevisani Federico Di Marco Giacomo Dell’Antonio Antonello Pani Alessandro Larcher

Acute Kidney Injury (AKI) following radical nephrectomy (RN) is associated with an increased risk of morbidity and mortality due to the prolonged hospitalization for renal impairment, heart failure and sepsis. Several studies have identified, as possible risk factors, age, gender, comorbidities, and basal eGFR. However, in clinical practice does not exist a clear protocol able to stratify patients upon risk of AKI after surgery. Aim of our study was to investigate the most prominent risk factors for AKI among clinical features, in order to better tailor the medical approach before and after operation.

Clinical Practice

10.1016/j.ekir.2020.02.548

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SGLT2i and postglomerular vasodilation

Kidney International (2020)

María José Soler Esteban Porrini Beatriz Fernández‐Fernández Alberto Ortíz

Dapagliflozin

Canagliflozin

10.1016/j.kint.2020.01.007

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SP236THE RADICAL NEPHRECTOMY PARADOX: THE UNEXPECTED AKI'S RISK

Nephrology Dialysis Transplantation (2019)

Francesco Trevisani Federico Di Marco Umberto Capitanio Arianna Bettiga Riccardo Vago

10.1093/ndt/gfz103.sp236

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Issue Information

Transplant International (2021)

María Teresa Angus Hann Dimitri Sneiders Hermien Hartog Minoli A. Perera

10.1111/tri.13647

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Increased SGK1 activity potentiates mineralocorticoid/NaCl-induced kidney injury

AJP Renal Physiology (2021)

Catalina Sierra‐Ramos Silvia Velázquez-García Ayşe Gökçe Keşküş Arianna Vastola-Mascolo Ana Elena Rodríguez-Rodríguez

Serum and glucocorticoid-regulated kinase 1 (SGK1) stimulates aldosterone-dependent renal Na+ reabsorption and modulates blood pressure. In addition, genetic ablation or pharmacological inhibition of SGK1 limits the development of kidney inflammation and fibrosis in response to excess mineralocorticoid signaling. In this work, we tested the hypothesis that a systemic increase in SGK1 activity would potentiate mineralocorticoid/salt-induced hypertension and kidney injury. To that end, we used a transgenic mouse model with increased SGK1 activity. Mineralocorticoid/salt-induced hypertension and kidney damage was induced by unilateral nephrectomy and treatment with deoxycorticosterone acetate and NaCl in the drinking water for 6 wk. Our results show that although SGK1 activation did not induce significantly higher blood pressure, it produced a mild increase in glomerular filtration rate, increased albuminuria, and exacerbated glomerular hypertrophy and fibrosis. Transcriptomic analysis showed that extracellular matrix- and immune response-related terms were enriched in the downregulated and upregulated genes, respectively, in transgenic mice. In conclusion, we propose that systemically increased SGK1 activity is a risk factor for the development of mineralocorticoid-dependent kidney injury in the context of low renal mass and independently of blood pressure.NEW & NOTEWORTHY Increased activity of the protein kinase serum and glucocorticoid-regulated kinase 1 may be a risk factor for accelerated renal damage. Serum and glucocorticoid-regulated kinase 1 expression could be a marker for the rapid progression toward chronic kidney disease and a potential therapeutic target to slow down the process.

SGK1

Mineralocorticoid

Epithelial sodium channel

10.1152/ajprenal.00505.2020

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SP666ESTIMATED GFR TO EVALUATE RENAL FUNCTION IN PREDIALYSIS PATIENTS: A SHOT IN THE DARK

Nephrology Dialysis Transplantation (2017)

Beatriz Escamilla Eduardo Gallego‐Valcarce Natalia Negrín‐Mena María Soledad Gil Gabarrón Sergio Luis‐Lima

10.1093/ndt/gfx154.sp666

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