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      Shear-Wave Elastography Variability Analysis and Relation with Kidney Allograft Dysfunction: A Single-Center Study

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          Abstract

          Shear-wave elastography (SWE) showed the absence or presence of significant differences among stable kidney allograft function and allograft dysfunction. We evaluated the variability of kidney allograft stiffness in relation to allograft dysfunction, respectively, in terms of a correlation of stiffness with patients’ characteristics. A single-center prospective study on patients who had undergone renal transplantation was conducted between October 2017 and November 2018. Patients were clinically classified as having a stable allograft function or allograft dysfunction. SWE examinations performed by the same radiologist with a LOGIQ E9 were evaluated. Ten measurements were done for Young’s modulus (kPa) at the level of allograft cortex and another ten at the level of medulla. Eighty-three SWE examinations from 63 patients, 69 stable allografts, and 14 allografts with dysfunction were included in the analysis. The intra-examinations stiffness showed high variability, with the quantile covariation coefficient ranging from 2.21% to 45.04%. The inter-examinations stiffness showed heterogeneity (from 28.66% to 42.38%). The kidney allograft cortex stiffness showed significantly higher values in cases with dysfunction (median = 28.70 kPa, interquartile range (IQR) = (25.68–31.98) kPa) as compared to those with stable function (median = 20.99 kPa, interquartile range = (16.08–27.68) kPa; p-value = 0.0142). Allograft tissue stiffness (both cortex and medulla) was significantly negatively correlated with body mass index (−0.44, p-value < 0.0001 for allograft cortex and −0.42, p-value = 0.0001 for allograft medulla), and positively correlated with Proteinuria/Creatinuria ratio (0.33, p-value = 0.0021 for allograft cortex and 0.28, p-value = 0.0105 for allograft medulla) but remained statistically significant only in cases with stable function. The cortical tissue stiffness proved significantly higher values for patients with allograft dysfunction as compared to patients with stable function, but to evolve as an additional tool for the evaluation of patients with a kidney transplant and to change the clinical practice, more extensive studies are needed.

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          The natural history of chronic allograft nephropathy.

          With improved immunosuppression and early allograft survival, chronic allograft nephropathy has become the dominant cause of kidney-transplant failure. We evaluated the natural history of chronic allograft nephropathy in a prospective study of 120 recipients with type 1 diabetes, all but 1 of whom had received kidney-pancreas transplants. We obtained 961 kidney-transplant-biopsy specimens taken regularly from the time of transplantation to 10 years thereafter. Two distinctive phases of injury were evident as chronic allograft nephropathy evolved. An initial phase of early tubulointerstitial damage from ischemic injury (P<0.05), prior severe rejection (P<0.01), and subclinical rejection (P<0.01) predicted mild disease by one year, which was present in 94.2 percent of patients. Early subclinical rejection was common (affecting 45.7 percent of biopsy specimens at three months), and the risk was increased by the occurrence of a prior episode of severe rejection and reduced by tacrolimus and mycophenolate therapy (both P<0.05) and gradually abated after one year. Both subclinical rejection and chronic rejection were associated with increased tubulointerstitial damage (P<0.01). Beyond one year, a later phase of chronic allograft nephropathy was characterized by microvascular and glomerular injury. Chronic rejection (defined as persistent subclinical rejection for two years or longer) was uncommon (5.8 percent). Progressive high-grade arteriolar hyalinosis with luminal narrowing, increasing glomerulosclerosis, and additional tubulointerstitial damage was accompanied by the use of calcineurin inhibitors. Nephrotoxicity, implicated in late ongoing injury, was almost universal at 10 years, even in grafts with excellent early histologic findings. By 10 years, severe chronic allograft nephropathy was present in 58.4 percent of patients, with sclerosis in 37.3 percent of glomeruli. Tubulointerstitial and glomerular damage, once established, was irreversible, resulting in declining renal function and graft failure. Chronic allograft nephropathy represents cumulative and incremental damage to nephrons from time-dependent immunologic and nonimmunologic causes. Copyright 2003 Massachusetts Medical Society
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            Supersonic shear imaging: a new technique for soft tissue elasticity mapping

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              The Banff 2015 Kidney Meeting Report: Current Challenges in Rejection Classification and Prospects for Adopting Molecular Pathology

              The XIII Banff meeting, held in conjunction the Canadian Society of Transplantation in Vancouver, Canada, reviewed the clinical impact of updates of C4d‐negative antibody‐mediated rejection (ABMR) from the 2013 meeting, reports from active Banff Working Groups, the relationships of donor‐specific antibody tests (anti‐HLA and non‐HLA) with transplant histopathology, and questions of molecular transplant diagnostics. The use of transcriptome gene sets, their resultant diagnostic classifiers, or common key genes to supplement the diagnosis and classification of rejection requires further consensus agreement and validation in biopsies. Newly introduced concepts include the i‐IFTA score, comprising inflammation within areas of fibrosis and atrophy and acceptance of transplant arteriolopathy within the descriptions of chronic active T cell–mediated rejection (TCMR) or chronic ABMR. The pattern of mixed TCMR and ABMR was increasingly recognized. This report also includes improved definitions of TCMR and ABMR in pancreas transplants with specification of vascular lesions and prospects for defining a vascularized composite allograft rejection classification. The goal of the Banff process is ongoing integration of advances in histologic, serologic, and molecular diagnostic techniques to produce a consensus‐based reporting system that offers precise composite scores, accurate routine diagnostics, and applicability to next‐generation clinical trials.
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                Author and article information

                Journal
                Diagnostics (Basel)
                Diagnostics (Basel)
                diagnostics
                Diagnostics
                MDPI
                2075-4418
                13 January 2020
                January 2020
                : 10
                : 1
                : 41
                Affiliations
                [1 ]Department of Medical Informatics and Biostatistics, Iuliu Hațieganu University of Medicine and Pharmacy Cluj-Napoca, Louis Pasteur Str., no. 6, 400349 Cluj-Napoca, Romania; miancu@ 123456umfcluj.ro
                [2 ]Department of Urology, Iuliu Hațieganu University of Medicine and Pharmacy Cluj-Napoca, Clinicilor Str., no. 4-6, 400006 Cluj-Napoca, Romania; ramona.contis@ 123456gmail.com
                [3 ]Department of Renal Transplantation, Clinical Institute of Urology and Renal Transplantation, Clinicilor Str., no. 4-6, 400006 Cluj-Napoca, Romania; dralinaelec@ 123456gmail.com (A.D.E.); munteana2@ 123456yahoo.com (A.M.M.); iacob.gheorghita@ 123456gmail.com (G.I.)
                [4 ]Department of Medical Imaging, Iuliu Hațieganu University of Medicine and Pharmacy Cluj-Napoca, Croitorilor Str., no. 19-23, 400162 Cluj-Napoca, Romania; mihaiaso@ 123456gmail.com (M.A.S.); Razvan.Zaro@ 123456umfcluj.ro (R.Z.);
                [5 ]Department of Medical Imaging, “Prof. Dr. Octavian Fodor” Regional Institute of Gastroenterology and Hepatology, Constanța Str., no. 5, 400162 Cluj-Napoca, Romania
                [6 ]Department of Anatomy, Iuliu Hațieganu University of Medicine and Pharmacy Cluj-Napoca, Clinicilor Str., no. 3-5, 400006 Cluj-Napoca, Romania; ignat.radu@ 123456umfcluj.ro
                Author notes
                [* ]Correspondence: sbolboaca@ 123456umfcluj.ro (S.D.B.); ioan.elec@ 123456gmail.com (F.I.E.); rbadea@ 123456umfcluj.ro (R.I.B.); Tel.: +40-374-834-506 (S.D.B.); +40-722-822-740 (F.I.E.); +40-264-439-889 (R.I.B.)
                Author information
                https://orcid.org/0000-0002-2342-4311
                https://orcid.org/0000-0001-8162-121X
                https://orcid.org/0000-0002-4557-5364
                Article
                diagnostics-10-00041
                10.3390/diagnostics10010041
                7169400
                31941112
                87bf3662-dd52-41fb-8357-23ea9cd79cea
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 04 December 2019
                : 10 January 2020
                Categories
                Article

                kidney stiffness,kidney transplantation,shear wave elastography (swe),allograft dysfunction,estimated glomerular filtration rate (egfr),ultrasound

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