Figure 6 Schematic of an analysis of a new biopsy

Slides:

Advertisements

Similar presentations

Michael Mengel Department of Laboratory Medicine and Pathology

Advertisements

Tuesday Case Conference May Biopsy finding LM –Glomeruli are normal in size to mildly enlarged Mild enlargement of the mesangial areas with occasional.

Slide 1PUBLICATIONS Racusen/Solez meeting report for AJT. Racusen/Solez meeting report for AJT. Manuscript on antibody-mediated rejection. Manuscript on.

Pathology of Renal Transplantation

Figure 1 Schematic representation of idiopathic nephrotic syndrome,

U # /121 Cad Tx 14/05/2004 Creatinine early December US normal.

FIGURE 1: Urinary proteome analysis in nephrology

Nat. Rev. Nephrol. doi: /nrneph

Figure 5 A layered approach to the follow-up of patients with acute kidney disease (AKD) Figure 5 | A layered approach to the follow-up of patients with.

Figure 4 Interplay between acute kidney injury (AKI),

Figure 3 LncRNAs in kidney disease

Figure 6 Effects of adiponectin on podocyte function

Figure 6 Approach to drug management in patients with acute kidney disease (AKD) Figure 6 | Approach to drug management in patients with acute kidney disease.

Figure 2 Physiological changes in the renal system in pregnancy

Figure 1 Pulmonary oedema in AKI

Nat. Rev. Nephrol. doi: /nrneph

a b c d e Supplemental figure 4

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Pathologic features of obesity-related glomerulopathy (ORG)

Nat. Rev. Nephrol. doi: /nrneph

Figure 6 The bioavailability of phosphate differs according to the protein source Figure 6 | The bioavailability of phosphate differs according to the.

Figure 7 The efficacy of phosphate-binder therapy

Case 5 Helmut Hopfer Institute of Pathology, University Hospital Basel

Figure 3 Putative actions of glucagon-like peptide 1 (GLP-1)

Figure 2 Expression of complement activation products in renal samples

Figure 2 The network of chronic diseases and their mutual influences

Figure 1 The burden of chronic kidney disease (CKD)

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Societal costs for the care of patients with chronic kidney disease in the UK Figure 3 | Societal costs for the care of patients with chronic.

Figure 2 Podocyte dysfunction is a common feature of renal injury

Figure 2 The association between CD8+ T‑cell density of the tumour

Figure 1 Suggested biopsy-avoiding diagnostic pathway for coeliac disease Figure 1 | Suggested biopsy-avoiding diagnostic pathway for coeliac disease.

Figure 2 Milestones in paediatric acute kidney injury (AKI) research

Figure 1 Acute kidney injury and chronic kidney disease

Figure 2 The continuum of acute kidney injury (AKI),

Nat. Rev. Nephrol. doi: /nrneph

Figure 4 Model of changes in the serum levels

Figure 1 Associations between baseline cerebrospinal fluid

Figure 2 Roles of mTOR complexes in the kidney

Nat. Rev. Nephrol. doi: /nrneph

Figure 5 Potential roles of phosphate and fibroblast growth factor 23 (FGF-23) in the development of cardiovascular disease in patients with chronic kidney.

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Emerging models of antibody-mediated rejection (ABMR) and

Figure 4 The molecular configuration of the CD20 molecule

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Loss of the glycocalyx leads to podocyte and kidney injury

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro

Figure 3 Hypothetical trajectories of acute kidney disease (AKD)

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Potential strategy for belatacept-based

Figure 5 The nephron-centric model of renal transplant fibrosis based on the injury-related molecular events observed in biopsy samples in the first year.

Figure 1 Identification of anti-HLA antibodies

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Regulation of TGF-β1/Smad signalling by microRNAs (miRs) in tissue fibrosis Figure 3 | Regulation of TGF-β1/Smad signalling by microRNAs (miRs)

Figure 2 Sources of data to characterize the ADPKD clinical phenotype

Nat. Rev. Nephrol. doi: /nrneph

Payan Schober et al. Am J Nephrol 2017;45: (DOI: / )

Figure 3 Preventive strategies for CSA-AKI

Figure 4 The relationship between the time-dependent changes in the expression of immunoglobulin, mast cell, acute kidney injury (AKI), and fibrillar collagen.

Expression of connective tissue growth factor in human renal fibrosis

Figure 4 Intracellular distribution and

Figure 1 Worldwide distribution of disease burden attributable to environmental risks in 2012 Figure 1 | Worldwide distribution of disease burden attributable.

primary Sjögren syndrome

Post-transplant membranous glomerulonephritis as a manifestation of chronic antibody-mediated rejection Hyeon Joo Jeong, Beom Jin Lim, Myoung Soo Kima,

Nat. Rev. Nephrol. doi: /nrneph

Overview of the cellular and molecular basis of kidney fibrosis

Algorithm for management of drug-induced acute interstitial nephritis

Relationship between time from diagnosis of type 2 diabetes to renal biopsy and the proportion of biopsies with any diabetic nephropathy (DN) and any non-diabetic.

Presentation transcript:

Figure 6 Schematic of an analysis of a new biopsy sample in relation to a reference set of samples from indication biopsies Figure 6 | Schematic of an analysis of a new biopsy sample in relation to a reference set of samples from indication biopsies. Each symbol represents one of 530 biopsy samples from a reference set (the details of which have been published46). The samples are coloured by their histologic diagnosis but distributed by their molecular features as determined using principal component analysis. The principal component analysis is based on four molecular classifier scores (T cell-mediated rejection (TCMR), antibody-mediated rejection (ABMR), all rejection and tubular atrophy and interstitial fibrosis (TA/IF)), and the transcript scores for parenchymal and acute kidney injury (AKI). ABMR cases are distributed in the top half of the graph, TCMR on the lower right, and normal cases on the left side. The biopsy sample of interest (yellow triangle) has a histologic diagnosis of ABMR. Prognosis (survival) can be predicted based on the actual outcomes of cases that share the highest molecular similarity to this sample in the Reference Set. In this example, the nearest neighbours to the sample biopsy had ABMR-related conventional and molecular phenotypes; only 43% of patients with this pattern had functioning kidneys at 3 years post biopsy. BK, BK polyomavirus; GN, glomerulonephritis; PC1, principal component 1 (accounts for 47% of total molecular variance in the reference set); PC2, principal component 2 (accounts for 21% of total molecular variance in the reference set); TG, transplant glomerulopathy. Halloran, P. F. et al. (2016) Molecular assessment of disease states in kidney transplant biopsy samples Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.85