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Anemia is a frequent, yet increasingly recognized, comorbidity in diabetes mellitus (DM), with prevalence often driven by multifactorial mechanisms. Hematinic deficiencies, common in this population, may arise from associated comorbidities or medications, such as metformin, as well as other drugs commonly employed for DM-related conditions. Among contributing factors, diabetic kidney disease (DKD) plays a pivotal role, with anemia developing more frequently and being more pronounced in earlier stages, than in CKD of other causes.

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Fibronectin glomerulopathy (FG) is caused by fibronectin 1 () gene mutations. A renal biopsy was performed on a 4-year-old girl with incidentally discovered proteinuria (150 mg/dL); her family history of renal disease was negative. Markedly enlarged glomeruli (mean glomerular diameter: 196 μm; age-matched controls: 140 μm), α-SMA-positive and Ki-67-positive mesangial cell proliferation (glomerular proliferation index 1.

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Simplified Outcome Prediction in Patients Undergoing Transcatheter Tricuspid Valve Intervention by Survival Tree-Based Modelling.

JACC Adv

January 2025

Department of General and Interventional Cardiology, Heart and Diabetes Center North Rhine-Westphalia, Ruhr University Bochum, Bad Oeynhausen, Germany. Electronic address:

Background: Patients with severe tricuspid regurgitation (TR) typically present with heterogeneity in the extent of cardiac dysfunction and extra-cardiac comorbidities, which play a decisive role for survival after transcatheter tricuspid valve intervention (TTVI).

Objectives: This aim of this study was to create a survival tree-based model to determine the cardiac and extra-cardiac features associated with 2-year survival after TTVI.

Methods: The study included 918 patients (derivation set, n = 631; validation set, n = 287) undergoing TTVI for severe TR.

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Chronic kidney disease affects ~10% of people worldwide and there are no disease modifying therapeutics that address the underlying cause of any form of kidney disease. Genome wide association studies have identified the G1 and G2 variants in the apolipoprotein L1 (APOL1) gene as major contributors to a subtype of proteinuric kidney disease now referred to as APOL1-mediated kidney disease (AMKD). We hypothesized that inhibition of APOL1 could have therapeutic potential for this genetically-defined form of kidney disease.

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Background: Diabetes often causes diabetic nephropathy (DN), a serious long-term complication. It is characterized by chronic proteinuria, hypertension, and kidney function decline, can progress to end-stage renal disease, lowering patients' quality of life and lifespan. Inflammation and apoptosis are key to DN development.

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