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Background Diabetic kidney disease (DKD) remains one of the leading causes of premature death in diabetes. DKD is classified on albuminuria and reduced kidney function (estimated glomerular filtration rate (eGFR)) but these have modest value for predicting future renal status. There is an unmet need for biomarkers that can be used in clinical settings which also improve prediction of renal decline on top of routinely available data, particularly in the early stages. The iBEAt study of the BEAt-DKD project aims to determine whether renal imaging biomarkers (magnetic resonance imaging (MRI) and ultrasound (US)) provide insight into the pathogenesis and heterogeneity of DKD (primary aim) and whether they have potential as prognostic biomarkers in DKD (secondary aim). Methods iBEAt is a prospective multi-centre observational cohort study recruiting 500 patients with type 2 diabetes (T2D) and eGFR ≥30 ml/min/1.73m 2 . At baseline, blood and urine will be collected, clinical examinations will be performed, and medical history will be obtained. These assessments will be repeated annually for 3 years. At baseline each participant will also undergo quantitative renal MRI and US with central processing of MRI images. Biological samples will be stored in a central laboratory for biomarker and validation studies, and data in a central data depository. Data analysis will explore the potential associations between imaging biomarkers and renal function, and whether the imaging biomarkers improve the prediction of DKD progression. Ancillary substudies will: (1) validate imaging biomarkers against renal histopathology; (2) validate MRI based renal blood flow measurements against H 2 O 15 positron-emission tomography (PET); (3) validate methods for (semi-)automated processing of renal MRI; (4) examine longitudinal changes in imaging biomarkers; (5) examine whether glycocalyx and microvascular measures are associated with imaging biomarkers and eGFR decline; (6) explore whether the findings in T2D can be extrapolated to type 1 diabetes. Discussion iBEAt is the largest DKD imaging study to date and will provide valuable insights into the progression and heterogeneity of DKD. The results may contribute to a more personalised approach to DKD management in patients with T2D. Trial registration Clinicaltrials.gov ( NCT03716401 ).

Background Patients with chronic kidney disease (CKD) experience abnormality of intracardiac blood flow status during early-stages of disease. Left ventricular energy loss (EL) derived from vector flow mapping (VFM) represents fluid energy lost as heat in left ventricle and had been used to detect intracardiac blood flow efficiency. We aimed to evaluate the left ventricular EL in stage 1–3 CKD patients, and explored whether hypertension, a main cardiovascular risk, deteriorate the abnormality of intracardiac blood flow status. Methods Transthoracic echocardiography was performed in 41 controls and 48 patients with stages 1–3 CKD. CKD patients consisted a subgroup with no hypertension, a subgroup with well-controlled hypertension and a subgroup with poorly controlled hypertension. The EL were calculated in the left ventricle using VFM analysis from the apical 3-chamber view. Furthermore, the correlation and stepwise multiple regression analysis were used to explore the potential independent predictors of left ventricular EL. Results Compared with controls, stage 1–3 CKD patients showed increased left ventricular EL during total diastole, late diastole, total systole, isovolumic contraction and ejection. CKD patients with poorly controlled hypertension had higher left ventricular EL compared to the other CKD subgroups. Additionally, the ratio of mitral early filling wave peak velocity and early mitral annular peak velocity on septal side, mitral early filling wave peak velocity, and left ventricular mass index were independent predictors of the diastolic EL; whereas systolic blood pressure and left ventricular mass index were independent predictors of the systolic EL. Conclusions Left ventricular EL was a useful echocardiographic parameter to evaluate the impaired intracardiac blood flow efficiency in patients with stages 1–3 CKD. Hypertension was a crucial contributor for intracardiac blood flow abnormality. This study might provide valuable clinical data to discern cardiac dysfunction and reduce the cardiovascular risk in early-stage CKD.

End-stage renal disease is associated with an increased incidence of renal cell neoplasms. Among these, recent studies have identified tumors with unusual histological patterns that do not fit into the categories recognized in the current classification system. These tumors often occur in kidneys with acquired cystic disease and are composed mainly of large eosinophilic cells arranged in solid, cribriform, acinar, or papillary patterns. They also contain deposits of calcium oxalate crystals. We investigated three eosinophilic epithelial tumors arising in kidneys with acquired cystic disease from three patients. Each of the tumors was composed of large eosinophilic cells arranged in solid, acinar, or tubulocystic architecture. Deposits of calcium oxalate crystals were present in each tumor. Hale's colloidal stain showed a positive cytoplasmic reaction in one of the neoplasms. Immunohistochemistry displayed positive results for CD10 (3/3), AE1/AE3 (3/3), alpha-methylacyl-CoA racemase (2/3), CAM5.2 (2/3), and vimentin (1/3). Reactions for epithelial membrane antigen, cytokeratin 7, and high molecular weight cytokeratin (34βE12) were negative. Fluorescence in situ hybridization analysis showed no losses or gains of chromosomes 1, 2, 6, 10, or 17 in one tumor. There were gains of chromosomes 1, 2, and 6 in two tumors. One of these tumors also showed gains of chromosome 10. Eosinophilic renal cell tumors associated with acquired cystic disease have immunophenotypes and genetic profiles distinct from the renal cell neoplasms recognized in the current classification of renal cell neoplasia, and should be considered as a distinct clinicopathologic entity in the spectrum of renal cell neoplasia.