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Project Context and Objectives: Project Context More than rare kidney diseases have been described, with an overall prevalence of about cases per , total population. In contrast to many other rare diseases, patients with inherited or acquired kidney disorders rarely die when their disease progresses but - thanks to progress in organ replacement therapy - may remain alive for many years. However, this apparent advantage is frequently bought at the expense of severely compromised health with poor quality of life, and causes a tremendous cumulative cost burden to health care systems.

At the outset of the EURenOmics project, the diagnostic and therapeutic management of rare kidney diseases was highly unsatisfactory. Key unsolved issues included the inability fo explain the underlying inherited or acquired abnormality responsible for the disease phenotype, predict the individual risk and rate of disease progression, or quantitate the risk of relatives to develop the same disorder.

Despite progress in gene discovery, the genetic and molecular basis of disease was still unknown in the majority of patients. On the other hand, there was preliminary evidence suggesting that different initial events may converge to common pathways of disease progression.

Neither the clinical heterogeneity within individual disorders nor the commonalities between clinically disparate kidney diseases were well understood, and clinically applicable technologies for the molecular characterisation of diseases and their risk of progression were lacking. Specific therapies effectively targeting disease activity and progression were, with a few notable exceptions, unavailable or limited to poorly defined disease subgroups; in the latter cases, biomarkers predicting individual susceptibility to pharmacotherapy were lacking.

Finally, the lack of suitable disease models for many kidney disorders was conceived as a major barrier to progress in therapeutic development. Urine is a readily available non-invasive bio resource to study molecular readouts directly derived from the organ of interest, the kidney.

Recent technological progress in exosome isolation from urine and amniotic fluid even has created the opportunity to study non-invasively cellular biomaterials originating from the diseased tissues. The availability of such samples greatly facilitates the development of biomarkers. These disease entities were felt paradigmatic for the clinical challenges described above.

WP3: Membranous Nephropathy Objectives Our project objectives were i to establish a large database of deeply phenotyped patients and related bioresources, ii to identify pathogenic B-cell epitopes, novel antigens and gene variants responsible for disease initiation, progression, and recurrence in the graft, iii to characterize T-cell epitopes and T-cell regulation, iv to develop proprietary assays for the identified biomarkers and assess their diagnostic and predictive values in large cohorts, and v to develop new therapeutic strategies and more personalized care and monitoring of patients with MN.

Work strategy Task 1: Identification of CAKUT genes by next generation sequencing - Exome sequencing of familial, syndromic and severe bilateral cases Task 2: Establishment of the transcriptional networks driving renal development analysis - In vivo ChIP-Seq analysis for key transcription factors involved in mouse kidney development Task 3: Functional characterization of CAKUT genes - In vivo-morpholino knockdown, ex vivo organ cultures, gene-targeting in animal models and iPSC Task 4: Use of amniotic fluid -omics and advanced imaging to predict postnatal renal function - Peptidomic, miRNomic and metabolomic profiling of fetuses with favourable vs.

Semi-automatic conversion and analysis of high-throughput data to standardize -omics data including genomic, epigenetic and transcriptomic profiles by array and sequencing techniques, proteomic and metabolomic analyses and comprehensive clinical data Task 2: Provide direct knowledge-based network analyses, co-citation analyses and relevance filtering of individual data with network-based stratification of entire patient cohorts. Screen disease-specific data sets for pathway perturbations and putative causal events using knowledge integration and extraction.

Identify common networks correlating with a given disease, disease stage, or phenotype. Task 3: Screen clinical and molecular datasets procured in task1 and 2 for common elements during renal disease. The website was constantly updated to disseminate news, inform about upcoming events and keep track of all publications emerging from the project. Meeting registrations were handled via the website as well. The Coordinator was also instrumental in establishing and strengthening collaborative links between partners within the consortium and in associating interested external research groups to the project.

Over the years, strong collaborative ties were established with numerous European and international scientists, who were granted the status of Asscociated Partners. This included issues such as central Omics data storage EBI-EGA, Metabolights data archives and data sharing, establishing an inventory of biobanks, harmonization of phenotyping, and the development of generic ethics documents.

Towards the end of the project, EURenOmics partners started using the RD-Connect exome analysis pipeline and have uploaded sequencing data to the central platform. Seventy-nine responses were received, and the results indicate a very positive outcome of this project. The mean scores are given in Table 1 below. This was achieved in families and causative mutations were found in This allowed the identification of mutations in 11 new genes and 2 strong candidates genes.

Nat Genet Functional studies using cell and animal models were performed in most cases and allow the identification of new pathophysiologic mechanisms underlying SRNS. Regulation of microtubule dynamics and organization Huynh Cong E et al. J Am Soc Nephrol. Partner 2a identified a homozygous missense mutation in the ciliary gene TTC21B which unexpectedly causes a dual phenotype of both primary tubulointerstitial and glomerular lesions, describing a new class of primary tubulo-glomerular disorders that might be due to mutations in ciliary genes.

The product of the TTC21B gene, IFT, mainly localizes at the base of the primary cilium in developing podocytes, whereas it relocalises along the extended microtubule MT network in nonciliated adult podocytes, suggesting a role in the regulation of MT organization and dynamics in mature podocytes. Such a tubulo-glomerular disorder was also described by Partner 7 who demonstrated the presence of glomerular lesions in patients with mutations in ANKS6, also encoding a ciliary protein Taskiran EZ et al.

Partner 2a experiments and those of other teams, in various cell models and in zebrafish, clearly suggest a role for WDR73 in cell survival, MT regulation and neuronal progenitor proliferation and differentiation. Indeed, WDR73 is recruited at the spindle poles and MT aster during mitosis, a behavior similar to proteins mutated in primary microcephaly.

Nat Genet. Very recently, Partner 2a identified, in collaboration with the group of F. These genes encode the four subunits of the KEOPS complex, a very ancient and essential multi-protein complex that catalyses a universal chemical modification on tRNA, the formation of a Nthreonylcarbamoyladenosine t6A at position 37 in ANN decoding tRNAs, necessary for translation initiation and translational efficiency.

Functional in vitro and in vivo studies of these mutations led to the identification of alterations in multiple cellular processes, such as proliferation, apoptosis, migration and protein translation. Some of these altered cellular processes are known to contribute to the pathogenesis of SRNS or microcephaly.

Potential digenic inheritance Partner 2a in collaboration with M. Partner 2a also identified two homozygous missense variants in two candidate genes, ADD3 and KAT2B, both expressed in podocytes, in a consanguinous family with a complex phenotype associating SRNS, cardiomyopathy and neurological impairment.

ADD3 and KAT2B encodes adducing gamma, an important regulator of the actin cytoskeleton, and the lysine acetyl transferase2B involved in histone acetylation, respectively. However, the results suggest that ADD3 mutations are responsible for the neurological manifestations, cataracts and skeletal defects whereas KAT2B mutations are responsible for the heart and kidney phenotype, either alone or on a susceptible genetic background ADD3 mutation.

Characterization of two new candidate genes in zebrafish: successful data-sharing strategy. Functional studies in podocyte cell lines and zebrafish allowed to confirm the pathogenic role of these mutations in the podocyte. Unfortunately, only one family was found mutated for each of these candidate genes by Partner 2a.

However, during the course of EURenOmics, a list of all rare potentially pathogenic variants identified by exome sequencing in the families without identified disease-causing gene mutations has been established and made available to the partners. Deciphering the functional role of podocin Tory K et al. Podocyte cell models have also been instrumental to identify a novel mechanism of mutation pathogenicity. Podocin, encoded by the NPHS2 gene, is a membrane-associated component of the slit diaphragm in podocytes.

Partner 2a demonstrated that the pathogenicity of the NPHS2 variant, p. RQ is dependent on the trans-associated mutations: specific-C-terminal missense mutations exert a dominant negative effect on podocin RQ resulting in its abnormal oligodimerization and mislocalization explaining the pathogenicity of this variant when it is associated only with certain specific mutations.

More recently, this work was completed by the demonstration that some distal C-terminal truncating mutations are endocytosed and that this internalization can be prevented by the coexpression of membranous podocin variants suggesting the possibility of interallelic complementation in compound heterozygous patients Straner P, submitted — This work has been performed mainly by K.

In parallel, Partner 2a studied podocin biogenesis, trafficking and degradation, in particular for the mutant p. RQ is massively degraded by the proteasome, whereas the wild-type podocin is degraded by both the proteasome and the lysosome. Task 2: Mapping the epigenetic landscape of podocytes in vivo By combining ChIP-Seq analysis with genomic profiling in model systems e.

Moreover, we showed that one of its targets - Magi2 - is essential for podocyte foot-process development. This gene has therefore been included as a novel candidate involved in screening protocol for SNRS. Indeed, mutations in MAGI2 have recently been identified in patients suffering from nephrotic syndrome. Task 4a: Deep phenotyping towards new disease ontology for SRNS A consortium-wide Renal Phenome Database was established, which incorporates relevant clinical family history, disease features at first manifestation, treatment response features, disease progression to renal failure , histopathological and genetic information.

The database contains information from more than SRNS patients from 72 specialized units in 21 countries, including those of partners 2a, 4 and 7. The results of NGS gene panel screening see Task 4b were included in the Renal Phenome Database to allow efficient genotype-phenotype analysis. Slides from almost digitalized biopsies of SRNS patients were stored on the central server. The collected comprehensive phenotype information resulted in two landmark publications Trautmann et al. The first publication described the age distribution, clinical and histopathological features, responsiveness to immunosuppressive therapy and post-transplant recurrence risk, stratified by the genetic diagnosis.

The second publication informed about the long-term outcomes of SRNS. Immunosuppression responsiveness, presence of a genetic diagnosis, histopathological diagnosis, as well as age, serum albumin concentration, and CKD stage at disease onset all independently affected the risk to develop end-stage renal disease. Notably, patients with familial SRNS in whom no genetic diagnosis could be established showed an intermediate long-term course and some of them were immunosuppression-sensitive.

In addition to these global analyses of the entire cohort, several cohorts with specific genetic diagnoses were characterized in the course of the project. The publications described the largest patient cohorts by far ever compiled for these rare diseases. Disease prevalence, phenotype spectrum, and genotype-phenotype correlations of 61 patients with WT1 nephropathy were reported relative to WT1-negative SRNS patients Lipska et al.

Kidney Int We concluded that there is a wide range of expressivity, solid genotype-phenotype associations, and a high risk and significance of extrarenal complications in WT1-associated nephropathy and suggested that all SRNS children should undergo WT1 gene screening.

In the first clinical report of ADCK4 nephropathy following the original description of this podocyte limited podocytopathy, we identified 26 patients among consecutively screened cases Korkmaz et al. JASN Renal biopsy specimens uniformly showed FSGS.

In a subsequent analysis of 28 Turkish patients Atmaca M et al. Pediatr Nephrol , partner 7 reported treatment with CoQ10 supplementation in 8 patients who were diagnosed early in the disease course with asymptomatic proteinuria. Hypothesizing that NGS gene panel sequencing may unsurface oligosymptomatic cases of SIOD with potentially milder disease courses, we analysed the renal and extrarenal phenotypic spectrum and genotype-phenotype associations in 34 patients, the largest SMARCAL1-associated nephropathy cohort to date.

Whereas patients diagnosed by phenotype more frequently developed severe extrarenal complications cerebral ischemic events, septicemia and were more likely to die before age 10 years than patients identified by SRNS-gene panel screening 88 vs.

Also, 10 of 11 children diagnosed unsuspectedly by NGS were small at diagnosis and all showed progressive growth failure. Severe phenotypes were usually associated with biallelic truncating mutations and milder phenotypes with biallelic missense mutations. Tasks 4b and 5a: Development and implementation of rapid genetic diagnostic tools A diagnostic kit for SRNS gene testing by NGS has been successfully set up and implemented by Partner Altogether, during the whole project, the Multiplicom assay has been tested in unrelated patients using the MiSeq technology Illumina Partners 1, 2a and two associate partners and patients were tested using the Ion Torrent Technology Partners 4 and 7.

We identified several promising candidate peptides and miRNAs that may serve as biomarkers differentiating patients with intensified immunosuppression sensitive disease from genetic and non-genetic multidrug resistant disease. Furthermore, it appears that ISS-responsive SRNS patients in remission can be distinguished from unaffected healthy individuals by their urinary peptidome signature and possibly also by their exosomal miRNA signatures. The results obtained in these seminal studies are being further evaluated by a detailed assessment of the specific functions of the identified peptides and miRNAs, as well as by prospective validation of the reproducibility and the diagnostic and prognostic value of the identified marker signatures.

In the current contract Partner 2a established the first steps towards the identification of new therapies for hereditary NS linked to mutations in NPHS2 and NPHS1, the two major genes responsible for SRNS in children and encoding for podocin and nephrin, respectively. Some mutants of these proteins are retained in the ER or in cytoplasmic vesicles instead of being localized at the plasma membrane PM. We thus established podocyte cell lines expressing two types of podocin mutants localized either in the ER or in cytoplasmic vesicles or one ER-retained nephrin mutant and set up cell-based assays designed for high-content screening of compound libraries, based on immunofluorescence analyses of the subcellular location of these proteins collaboration with Biophenics, the Institut Curie Screening Facility and Imagopole, the Pasteur Dynamic Imaging Platform, Paris.

Following these steps, primary hits will be confirmed in triplicates in the conditions of the screen and tested in a dose-response experiment when appropriate. Soon after induction the mice develop nephrotic range proteinuria, which peaks after 4 weeks. The animals develop progressive glomerulosclerosis and die within 4 months from renal failure. Four-week intervention studies were performed by Partner 1 in this model to test nephroprotective effects of candidate pharmacological compounds: the ACE inhibitor Ramipril, the AT1 receptor blocker Candesartan and their combination, the Endothelin-1 type A receptor blocker Atrasentan based on RAS-independent antiproteinuric action in humans both alone and in combination with Candesartan, the calcineurin inhibitor Tacrolimus based on published in vitro findings , the protease inhibitor Bortezomib based on promising in vitro findings by partner 1 , the non-specific chaperone compound 4-phenyl butyric acid, and the vasopressin 2 receptor antagonist Tolvaptan based on published nephroprotective actions in rodents.

RAS blockade with Ramipril and Candesartan showed excellent antiproteinuric efficacy. The antiproteinuric effect was maximized with combined RAS blockade, which was subsequently used for extended studies and demonstrated to mitigate podocyte loss, glomerulosclerosis and tubulointerstitial fibrosis and to improve renal function and animal survival.

Delayed treatment still lowered proteinuria but the beneficial effects on histopathology, renal function and animal survival were less impressive. Treatment withdrawal abolished the antiproteinuric effect. The other tested compounds were largely ineffective or seven exhibited significant toxicity. WP3: Membranous Nephropathy Establishment of a large database of deeply phenotyped patients and bioresources The Nijmegen, Paris and Manchester groups in collaboration with Prague have assembled the largest cohort world-wide of deeply phenotyped patients with iMN and the related biobank.

We have written SOPs for biobanking and build database templates. The database is functioning online since September 1st www. We have been able to collect the data of almost patients with MN in our registry. Long-term follow-up will allow analysis of outcome data in relation to baseline characteristics, treatment, and follow-up parameters. This registry can be pivotal in establishing ongoing collaborative studies in the recently installed European Reference Network for Rare Kidney Disease.

In addition, the registry will allow continuation of biomarkers discovery studies, using clearly defined phenotypes i. The Nijmegen group has performed a proof of principle study to illustrate the potential of using database data. In total, rituximab treated patients were compared to patients who received cyclophosphamide. The results showed that Rituximab is safer than cyclophosphamide, and its use may be beneficial in some, but not all patients with MN.

The epitope was sensitive to reduction and SDS denaturation in the isolated ricin domain and the larger fragment containing the ricin, fibronectin type II, first and second C-type lectin domains CTLD. These constructs form the basis for new immunoadsorption therapy for removal of anti-PLA2R.

When the ELISA for each epitope will become commercially available expected soon , this finding will have a major impact on the start of therapy although they need to be confirmed in other prospective studies.

The Paris group has also described arylsulfatase as an exogenous antigen responsible for MN in a young patient treated with the recombinant enzyme for mucopolysaccharidosis type VI. Enzyme replacement therapy ERT could be resumed after tolerance induction therapy. This observation leads to consider the diagnosis of MN in ERT patients when they develop proteinuria and to undertake tolerance induction therapy. Identification of pathogenic gene variants The Nijmegen and Paris groups hypothesized that rare genetic variants within the coding region of the PLA2R1 gene might explain antibody formation.

We detected only few novel rare variants. Thus, the pathophysiology of iMN is unlikely to be explained by rare variants mutations in the coding sequence, including splice sites, of PLA2R1. This haplotype is also at risk for several auto-immune diseases. The Paris group performed the first detailed analysis of genes involved in complement regulation and showed a common haplotype associated with increased risk of primary MN odds ratio 2.

We found that the third lead SNP identified in HLA-D by logistic regression analysis was strongly associated with recurrence in the graft when expressed by the donor. We provided the first evidence derived from genetic studies that in idiopathic MN, activation of the alternative pathway of complement plays a leading role at least in a subpopulation of patients with MBL deficiency.

Analysis of antigen presentation and T-cell response The Manchester group has identified 5 candidate peptides T which they have synthesized and analyzed for solubility in cell culture medium for use in ELISPOT. In collaboration with the Paris group, differences between the HLA peptidomes of healthy volunteers and MN patients were successfully characterized.

Development of proprietary assays for the identified biomarkers and evaluation of their diagnostic and predictive values: towards a new ontology Manchester, Paris, CBC, MTBX and MOS have laid the grounds for robust Omics studies, and already obtained significant data.

For proteomics, the classification of the MN diagnosis resulted in a sensitivity of For the differentiation of MN progressors and non-progressors, 62 peptide biomarkers were used to generate a support vector machine SVM -based classifier, which reached an accuracy of The Bristol group has also identified a soluble isoform of PLA2R sPLA2R , that is expressed in podocytes which binds to the membrane bound receptor and inhibits its signaling.

There is evidence that the production of both the membrane and soluble isoforms is regulated by methylation of the PLA2R1 promoter. Development of a novel diagnostic tool for rapid complete screening of mutations and variants in known renal tubular disease genes TUB MASTR v3 was successfully developed as a diagnostic panel for identification of mutations associated with renal tubulopathies.

The tubulopathies MASTR assay has successfully been used for molecular diagnosis in probands, with documentation of spectacular diagnostic yields. Deep phenotyping of the SLC12A3 Gitelman syndrome carrier state Set-up and recruitment for a clinical study to deeply phenotype heterozygous carriers for mutations of the SLC12A3 gene responsible for Gitelman syndrome.

The multicentre study will compare blood pressure and metabolic status in 80 Gitelman syndrome patients, 80 heterozygous individuals and 80 controls. Recruitment has been achieved and the biological centralized analysis were performed and data quality has been reviewed. Completion of a comprehensive atlas of renal tubulopathy gene expression during Xenopus embryogenesis.

In another pedigree WES disclosed a mut in the gene encoding properdin. Other candidate genes have been identified by WES and are currently under investigation. Functional studies revealed that both mutant proteins form large multimeric complexes with increased avidity for C3 fragments and increased competition with FH.

The purified hybrid protein formed very large multimers that efficiently competed the regulatory activity of FH on cellular surfaces. Functional studies revealed that the hybrid protein acts as a competitive antagonist of FH and activates complement on cell surfaces. Functional studies revealed that the hybrid protein: stabilizes the C3 convertase, reduces FH-mediated decay, forms high molecular mass complexes, interacts with CFHR1, increases complement activation on cell surfaces by enhancing properdin attachment.

The mutant FHR1 protein strongly competed the binding of FH to cell surfaces, impairing complement regulation. The deletion encompassed ten other genes. Gene silencing in cultured endothelial cells demonstrated that loss of DGKE expression induces endothelial cell activation, increases apoptosis and impairs cell migration and angiogenesis. These findings are relevant to clarify the pathogenesis of aHUS associated with DGKE muts and suggest that in these patients the disease results from impaired endothelial cell proliferation and angiogenesis.

Search determinants of disease penetrance and clinical heterogeneity in mutation carriers The incidence of combined complement gene mutations and the impact of common SNPs in CFH and MCP on disease penetrance were disclosed by a multinational effort in aHUS patients. Functional studies on the CFH hot spot p. RC mutant revealed that the mutant forms complexes with albumin which impair accessibility to all FH functional domains. Studies on the c.

In two independent studies, partners of WP5 provided genetic and clinical characterization of pregnancy-associated aHUS. Another study provided description of prognosis, response to therapies and outcome of kidney transplant in HUS children with DGKE mutations. The new database www. For each variant MAF, predictive comparisons of wild-type and mutant amino acids, examination of evolution-conserved residues across species, and correlations with functional binding sites are reported in the new database.

These tools will help clinicians in interpreting the potential impact of gene variants in the pathogenesis of aHUS and C3G. A multicenter HLA study has been started with more than patients to increase the power of the analysis.

Functional characterization demonstrated that these Abs induced no perturbations in FH cell surface protection but were able to affect the cofactor activity of FH. Epitope mapping identified the N-terminal domain of FH as the major binding site. In adult patients the anti-FH Abs were frequently associated with monoclonal gammopathy. Version one comprised 29 genes. Validation of the assay was done in different DNA samples from patients that had been previously sequenced.

The assay is expected to be commercially available in Q4 of Four academic NGS panels with 7, 14, 15 and 48 genes respectively, have been developed and used to screen overall patients. Finally, an analytical strategy for the complete functional characterization of CFH disease-associated variants have been developed.

Comparison of proteomic profiles among the 4 conditions identified 13 and 2 sequenced peptides selectively upregulated in the urines and in plasma, respectively, of patients with aHUS as compared with IC-MPGN, C3G and controls.

Several miRNA were identified that were up or down-regulated in each condition vs controls. New assays to quantify free eculizumab level during treatment were developed. Finally, a report on response to eculizumab treatment in 29 patients with secondary HUS has been published. Develop in vitro, ex vivo and in vivo models for testing new therapeutic interventions Cell based in vitro and ex-vivo assays, namely FH-dependent hemolytic assays with rabbit and sheep erythrocytes and serum-induced C5b-9 deposition on endothelial cells, were developed.

Novel complement inhibitors, an anti-FB mAb and a fusion protein in which the surface recognition domain of CFH was fused to the bacterial complement inhibitor Sbi have been obtained and showed good complement inhibitory activity by the above tests. The anti-FB mAb given to rats by i.

Three new moAbs were generated against human C3 fragments and inhibited complement activation; two of them by blocking the cleavage of C3 by the AP C3 convertase and one by impeding formation of the AP C3 convertase. Two mAbs against C5a were also obtained which efficiently inhibit neutrophil chemotaxis. All biochemical, hematological and histology features of this novel mouse model are mirroring that seen in human aHUS.

Treatment of the mouse model with an anti-C5 mAb improved mouse survival and prevented weight loss. We identified numerous novel gene variants with in silico predicted pathogenicity. Importantly, we also showed that the contribution of previously implicated genes to CAKUT risk is significantly smaller than expected and that the disease is far more complex than previously assumed Nicolaou, Kidney Int, ; Heidet, J Am Soc Nephrol, These studies significantly add to the literature since the data indicates that detection of novel and likely deleterious variants in any known genes does not by itself imply pathogenicity, as erroneously reported in many recent publications.

This provided new clinical diagnoses after gene testing e. Targeted exome sequencing proved to be an efficient and cost-effective strategy to identify pathogenic mutations and homozygous deletions in known CAKUT genes. A balance between these two signaling pathways is essential to control survival of the early nephron progenitor cells. The X file format reference defined by DirectX 9 contains reference information for.

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