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      Call for Papers: Digital Platforms and Artificial Intelligence in Dementia

      Submit here by August 31, 2025

      About Dementia and Geriatric Cognitive Disorders: 2.2 Impact Factor I 4.7 CiteScore I 0.809 Scimago Journal & Country Rank (SJR)

      Call for Papers: Epidemiology of CKD and its Complications

      Submit here by August 31, 2024

      About Kidney and Blood Pressure Research: 2.3 Impact Factor I 4.8 CiteScore I 0.674 Scimago Journal & Country Rank (SJR)

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      Kidney Histopathology Features of Suspected Intra-Kidney Venous Thromboembolism in Patients with Primary Glomerulonephritis

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          Abstract

          Introduction

          Renal vein thromboembolism is a severe complication of nephrotic syndrome. Small thrombus in the intra-kidney venous system cannot be recognized by ultrasonography. The current study was to investigate the kidney pathological features of intra-kidney venous thrombus and their values in clinical practice.

          Methods

          Kidney pathological features of glomerular capillary dilatation and congestion, peritubular capillary dilatation and congestion, and intraglomerular neutrophil infiltration were screened and scored during kidney biopsy information interpretation. Eighty-four consecutive patients with these features and primary glomerulonephritis were analyzed, comparing to another 84 control patients without these features who were matched according to the pathological types of glomerulonephritis.

          Results

          In the patients with pathological features of suspected intra-kidney venous thrombus, the levels of proteinuria (5.2 vs. 3.2 g/24 h, p = 0.005), serum creatinine (80.9 vs. 71.2 μmol/L, p < 0.001), platelet count (274.0 vs. 254.5 ×10<sup>9</sup>/L, p = 0.020), D-dimer (0.2 vs. 0.2 mg/L, p = 0.002), and fibrin degradation products (1.9 vs. 1.0 mg/L, p = 0.003) were significantly higher than those in control patients. The levels of serum albumin (24.2 vs. 28.6 g/L, p = 0.003) and eGFR (92.1 vs. 103.9 mL/min/1.73 m<sup>2</sup>, p < 0.001) were significantly lower. The scores of these pathological features were positively correlated with the levels of D-dimer (r = 0.21, p = 0.05). During follow-up, 9 (10.7%) patients with pathological features of suspected intra-kidney venous thrombus developed venous thromboembolism, which was significantly more than that of control patients (0%, p = 0.006).

          Conclusions

          Kidney pathological features could indicate intra-kidney venous thromboembolism, and their scores represent the possibility of thrombus. The notice of these features may provide clinical alerts for venous thromboembolism possibility.

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          Most cited references40

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          A new equation to estimate glomerular filtration rate.

          Equations to estimate glomerular filtration rate (GFR) are routinely used to assess kidney function. Current equations have limited precision and systematically underestimate measured GFR at higher values. To develop a new estimating equation for GFR: the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. Cross-sectional analysis with separate pooled data sets for equation development and validation and a representative sample of the U.S. population for prevalence estimates. Research studies and clinical populations ("studies") with measured GFR and NHANES (National Health and Nutrition Examination Survey), 1999 to 2006. 8254 participants in 10 studies (equation development data set) and 3896 participants in 16 studies (validation data set). Prevalence estimates were based on 16,032 participants in NHANES. GFR, measured as the clearance of exogenous filtration markers (iothalamate in the development data set; iothalamate and other markers in the validation data set), and linear regression to estimate the logarithm of measured GFR from standardized creatinine levels, sex, race, and age. In the validation data set, the CKD-EPI equation performed better than the Modification of Diet in Renal Disease Study equation, especially at higher GFR (P < 0.001 for all subsequent comparisons), with less bias (median difference between measured and estimated GFR, 2.5 vs. 5.5 mL/min per 1.73 m(2)), improved precision (interquartile range [IQR] of the differences, 16.6 vs. 18.3 mL/min per 1.73 m(2)), and greater accuracy (percentage of estimated GFR within 30% of measured GFR, 84.1% vs. 80.6%). In NHANES, the median estimated GFR was 94.5 mL/min per 1.73 m(2) (IQR, 79.7 to 108.1) vs. 85.0 (IQR, 72.9 to 98.5) mL/min per 1.73 m(2), and the prevalence of chronic kidney disease was 11.5% (95% CI, 10.6% to 12.4%) versus 13.1% (CI, 12.1% to 14.0%). The sample contained a limited number of elderly people and racial and ethnic minorities with measured GFR. The CKD-EPI creatinine equation is more accurate than the Modification of Diet in Renal Disease Study equation and could replace it for routine clinical use. National Institute of Diabetes and Digestive and Kidney Diseases.
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            KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases

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              Cell biology of ischemia/reperfusion injury.

              Disorders characterized by ischemia/reperfusion (I/R), such as myocardial infarction, stroke, and peripheral vascular disease, continue to be among the most frequent causes of debilitating disease and death. Tissue injury and/or death occur as a result of the initial ischemic insult, which is determined primarily by the magnitude and duration of the interruption in the blood supply, and then subsequent damage induced by reperfusion. During prolonged ischemia, ATP levels and intracellular pH decrease as a result of anaerobic metabolism and lactate accumulation. As a consequence, ATPase-dependent ion transport mechanisms become dysfunctional, contributing to increased intracellular and mitochondrial calcium levels (calcium overload), cell swelling and rupture, and cell death by necrotic, necroptotic, apoptotic, and autophagic mechanisms. Although oxygen levels are restored upon reperfusion, a surge in the generation of reactive oxygen species occurs and proinflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury. The pathologic events induced by I/R orchestrate the opening of the mitochondrial permeability transition pore, which appears to represent a common end-effector of the pathologic events initiated by I/R. The aim of this treatise is to provide a comprehensive review of the mechanisms underlying the development of I/R injury, from which it should be apparent that a combination of molecular and cellular approaches targeting multiple pathologic processes to limit the extent of I/R injury must be adopted to enhance resistance to cell death and increase regenerative capacity in order to effect long-lasting repair of ischemic tissues. Copyright © 2012 Elsevier Inc. All rights reserved.

                Author and article information

                Journal
                Kidney Dis (Basel)
                Kidney Dis (Basel)
                KDD
                Kidney Diseases
                S. Karger AG (Allschwilerstrasse 10, P.O. Box · Postfach · Case postale, CH–4009, Basel, Switzerland · Schweiz · Suisse, Phone: +41 61 306 11 11, Fax: +41 61 306 12 34, karger@karger.com )
                2296-9381
                2296-9357
                December 2022
                31 October 2022
                31 October 2022
                : 8
                : 6
                : 478-486
                Affiliations
                [1] aRenal Division, Peking University First Hospital, Institute of Nephrology, Peking University, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease (CKD) Prevention and Treatment, Ministry of Education of China, Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences, Beijing, China
                [2] bLaboratory of Electron Microscopy, Pathological Center, Peking University First Hospital, Beijing, China
                [3] cPeking-Tsinghua Center for Life Sciences, Beijing, China
                Author notes
                Article
                kdd-0008-0478
                10.1159/000527009
                9798834
                36590678
                7d46cd61-43f5-4460-abac-e711cd865998
                Copyright © 2022 by The Author(s). Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Usage and distribution for commercial purposes requires written permission.

                History
                : 30 May 2022
                : 4 September 2022
                : 2022
                Page count
                Figures: 3, Tables: 4, References: 34, Pages: 9
                Funding
                This work was supported by grants of the Natural Science Foundation of China (81870486, 82070732, 82090021) and the CAMS Innovation Fund for Medical Sciences (2019-I2M-5-046).
                Categories
                Research Article

                kidney pathology,intra-kidney venous thromboembolism,venous thromboembolism,scores,glomerulonephritis

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