---
title: "Biallelic EXOSC3 Variants Cause Early-Onset Eculizumab-Resistant Renal Thrombotic Microangiopathy"
id: "kidney-international-0-biallelic-pathogenic-variants-in-exosc3-mediate-renal-thrombotic"
canonical_url: "https://medichelpline.com/clinical-feed/kidney-international-0-biallelic-pathogenic-variants-in-exosc3-mediate-renal-thrombotic"
content_type: "clinical_feed_article"
specialty: "Nephrology"
source_name: "Kidney International"
source_url: "https://www.kidney-international.org/article/S0085-2538(26)00598-3/fulltext?rss=yes"
published_at: "2026-07-22T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Biallelic EXOSC3 Variants Cause Early-Onset Eculizumab-Resistant Renal Thrombotic Microangiopathy
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/kidney-international-0-biallelic-pathogenic-variants-in-exosc3-mediate-renal-thrombotic
- **Specialty:** [Nephrology](https://medichelpline.com/clinical-feed/nephrology.md)
- **Primary Source:** Kidney International
- **Source URL:** [Original Journal Publication](https://www.kidney-international.org/article/S0085-2538(26)00598-3/fulltext?rss=yes)
- **Published At:** 2026-07-22T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- This study identifies a strong association between biallelic pathogenic variants in **EXOSC3** and early-onset renal **thrombotic microangiopathy (TMA)** in children with pontocerebellar hypoplasia 1b (PCH1b). - Among 34 children with PCH1b due to EXOSC3 variants, 13 developed biochemical and clinical features of TMA (microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury), typically presenting at a median age of 6 months. - All TMA episodes in the cohort were preceded within 10 days by an infectious trigger in the reported episodes, most commonly respiratory infections. - Kidney histology from one post-mortem sample confirmed platelet- and fibrin-rich thrombi within glomerular capillaries and arterioles consistent with TMA. - No evidence of complement dysregulation was detected in tested patients; 5 children received **eculizumab**, with three treated long-term—one had no response and two relapsed while on treatment, indicating **eculizumab resistance** in EXOSC3-TMA. - Clinical outcomes were severe: 11 of the cohort with TMA died during follow-up (mean age at death 10 months); 8/13 showed renal recovery after episodes, while two progressed to end-stage kidney disease requiring long-term renal replacement. - A tamoxifen-inducible whole-body Exosc3 conditional knockout mouse (Exosc3KO) produced rapid weight loss, aplastic anemia, bone marrow hypocellularity, cell-cycle arrest at G0/G1, and increased apoptosis in rapidly dividing tissues; mice died a median of 8 days after recombination. - In Exosc3KO mice there was prominent pathology in bone marrow, thymus and large intestine but no renal TMA was observed in the acute timeframe examined, suggesting species or model differences or requirement for an infectious trigger. - Mechanistic interpretation: loss of EXOSC3 impairs RNA exosome function and ribosome biogenesis, triggers nucleolar stress with cell-cycle arrest and apoptosis in proliferative tissues; authors propose a “vascular ribosomopathy” as a shared mechanism with Shiga-toxin HUS. - Clinical implications: consider screening for TMA in children with PCH1b during or after infection; perform genetic testing for **EXOSC3** in eculizumab-resistant pediatric TMA, especially when a neurodevelopmental syndrome is present. Eculizumab has no role in EXOSC3-TMA based on these data.
## Clinical Analysis & Structured Key Points
Skip to Main Content Skip to Main Menu Submit Log in Register Skip menu Articles Publish Topics About Contact Subscribe Direct Link Advanced search RESEARCH LETTERArticles in PressJuly 22, 2026Open Access Biallelic pathogenic variants in EXOSC3 mediate renal thrombotic microangiopathy of the kidney Patrick R. Walsh1,2 ∙ Uttiya Basu3 ∙ Tahsin Stefan Barakat4 ∙ … ∙ Petya Markova13 ∙ Kevin Marchbank1,2 ∙ David Kavanagh1,2 Send email to David.Kavanagh@ncl.ac.uk … Show more Affiliations & Notes Article Info Download PDF Cite Share Set Alert Get Rights Reprints Previous article Next article Show Outline Abstract Introduction Thrombotic microangiopathy (TMA) is characterized by the classical triad of microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury. Complement inhibition with eculizumab is highly efficacious in TMA secondary to complement dysregulation. However, there are a growing number of eculizumab nonresponsive TMAs reported. Recently a syndromic form of TMA due to recessive variants in RNA exosome components (EXOSC3, EXOSC5) has been identified. The underlying pathogenesis remains unclear. Methods We identified 34 children across Europe with pontocerebellar hypoplasia 1b (PCH1b) due to EXOSC3 rare variants and reviewed their clinical history for signs of TMA. To further examine the pathogenesis, a tamoxifen-inducible whole body Exosc3 conditional knockout mouse model (Exosc3KO) was used. Results Thirteen (eight male, five female) cases of EXOSC3-TMA were identified. In the United Kingdom the incidence of EXOSC3-TMA was 0.004/million/year. Three children received long-term eculizumab therapy, one child failed to respond and two relapsed on treatment. Exosc3KO demonstrated cell cycle arrest and apoptosis resulting in death in a median of eight days with sequelae noted in actively dividing cells in the bone marrow and large intestine. In this timeframe no kidney pathology was identified. Conclusions EXOSC3-TMA is a severe, early-onset, C5 inhibitor resistant TMA. EXOSC3-TMA should be considered in eculizumab resistant pediatric TMA, particularly in the context of neurodevelopmental disease. Graphical abstract Key words Haemolytic Uraemic Syndrome Thrombotic microangiopathy Complement EXOSC3 eculizumab-resistant Shiga-toxin Introduction The haemolytic uraemic syndromes (HUS) display the pathological features of thrombotic microangiopathy (TMA) and present with microangiopathic haemolytic anaemia (MAHA), thrombocytopenia and acute kidney injury.1 TMA can broadly be divided into primary, secondary and infection-associated TMAs. Complement mediated atypical HUS (CaHUS) is the most common primary TMA.2 CaHUS management has been revolutionized by the introduction of the terminal complement inhibitor, eculizumab.2 Real-world use has identified a growing number of eculizumab-resistant TMAs. These include primary/genetic, which can occur in isolation (e.g. DGKE3) or as part of a syndrome (e.g. MMACHC, TSEN22), secondary TMAs4 and infection-associated (e.g. Shiga-toxin mediated HUS (STEC-HUS5)). Overall, STEC-HUS is the most common form of TMA.1 Shiga toxin is a ribosome-inactivating toxin that causes N-glycosidic cleavage of the 28S subunit, thereby inactivating ribosomal function, resulting in cell stress responses that culminate in cycle arrest and apoptosis.6 Recently, TMA has been reported in individuals with the neurodevelopmental condition, pontocerebellar hypoplasia 1b (PCH1b; MIM 614678) due to biallelic pathogenic variants in the RNA exosome component, EXOSC3.2,7 PCH1b is phenotypically variable, but typically presents with contractures and hypotonia at or shortly after birth, reduced or absent deep tendon reflexes, and feeding difficulties. As children develop additional delayed/absent motor and speech development, cognitive deficit, progressive microcephaly and muscle atrophy become apparent. Neuroimaging demonstrates hypoplastic and progressively atrophic cerebellum and pons. The life expectancy of PCH1b is variable from death in infancy through to early adulthood, most commonly due to respiratory failure.8 The RNA exosome is a conserved multi-protein complex (EXOSC1-9) that processes, degrades and modifies many forms of transiently expressed RNA with the help of different cofactors.9 One of the major functions of the RNA exosome is 3’ trimming of precursor ribosomal RNA during ribosome biogenesis.10 Failure of the exosome (and therefore ribosome biogenesis) leads to activation of the nucleolar stress response, characterized by upregulation of cell cycle regulators, cell-cycle arrest and apoptosis.11 In this study, we confirm the association of biallelic mutations in EXOSC3 with TMA and demonstrate that conditional knock-out of Exosc3 in mouse leads to downstream effects of ribosomal dysfunction in rapidly dividing tissues, giving broader insights into the pathogenesis of TMA. Methods Patients with PCH1b with confirmed EXOSC3 rare variants were identified (n=34) through pan-European registries and the UK national aHUS service (www.atypicalhus.co.uk) and assessed for TMA. Where available samples were tested for known genetic and acquired (factor H autoantibodies) causes of CaHUS. Mouse model of Exosc3 Knock-out To explore the role of the Exosc3, a conditional inducible mouse knock-out model harbouring a “conditional by inversion” Exosc3 allele was used (Exosc3tm1.1Uba/tm1.1Uba.Rosa26CreERT2/ERT2, herein Exosc3fl)12 (Supplementary Figure S1). Adult Exosc3fl (>6 weeks) were treated with intraperitoneal tamoxifen. This resulted in disruption of Exosc3 (designated Exosc3KO herein (Supplementary Figure S1). Green fluorescence protein (GFP) expression in splenocytes was assessed with flow cytometry to confirm recombination (Supplementary Figure S2). Haematology and biochemical analysis Blood was collected for biochemical and haematological analysis including haemoglobin, reticulocyte percentage (Supplementary Figure S3), leukocyte, platelet count (Supplementary Figure S4) and blood urea nitrogen (Supplementary Methods). Cell cycle analysis Mice were treated with Bromodeoxyuridine and bone marrow cells isolated. Cell cycle was analyzed using flow cytometry (supplementary methods) Apoptosis analysis Mice were treated and bone marrow cells isolated. Apoptosis was analyzed using flow cytometry (supplementary methods) Results Clinical Presentation TMA was detected in 13/34 children (8 male, 5 female) with biallelic EXOSC3 variants (Table 1). Between January 2013-January 2024, three cases of EXOSC3-TMA were identified in the UK giving an incidence of 0.004/million/year, for comparison the incidence of CaHUS is 0.41/million/year.2 Ten patients with TMA were identified though European networks; additionally, two patients with haematuria and proteinuria and one patient with nephrotic syndrome were identified. The median age of initial presentation with TMA was 6 months (range 2-20 months) (Table 1). In total, 17 episodes of TMA occurred; all episodes were triggered within 10 days of preceding infection, most commonly respiratory (n=11). TMA was diagnosed by a combination of MAHA, thrombocytopenia and acute kidney injury (AKI) in all patients (Table 1). Hypertension was reported in 10/13 and 5/13 required dialysis at presentation. No evidence of complement dysregulation was detected (Supplementary Table S1). A single post-mortem kidney sample (patient IX) confirmed pathological features of TMA demonstrating widespread congestion within the glomeruli with dilated capillary loops and multiple thrombi within glomerular capillaries and arterioles (Figure 1a). Figure viewer Figure 1 (a) Kidney biopsy from EXOSC3-TMA (patient IX). CD42b (i) and CD61 (ii) immunohistochemistry demonstrating platelet-rich thrombi within arteriole and glomerular capillaries. MSB highlighting glomerular thrombi and thrombus in arteriole (red-fibrin) with congested glomerular erythrocytes (yellow) (iii) H&E demonstrating fibrin-rich thrombi within glomeruli (iv) (b) Age at presentation and clinical course. Presentation with TMA TMA Outcome Patient number EXOSC3 Variants TMA presentation (months) Infective trigger Creatinine (μmol/L) Haemoglobin (g/L) Platelets (109/ml) LDH (iU/ml) Blood film Renal diagnosis Medical management Dialysis (days) Outcome Days to platelet normalisation I Asp132Ala; Glu114_Pro115delinsAla 6 Respiratory 83 82 37 3934 MAHA TMA Eculizumab 3 Recovery 12 II Gly31Ala; Asp132Ala 8 RSV 88 77 37 9478 MAHA TMA FFP and Eculizumab 14 Recovery, 1 relapse 14 III Gly31Ala; Gly31Ala 2 Respiratory 172 61 69 962 MAHA TMA Eculizumab 15 Recovery 4 IV Gly31Ala; Gly31Ala 5 Gastroenteritis 134 66 67 2298 ND TMA FFP N Death N/A V Asp132Ala; Asp132Ala 2 RSV 38 55 88 1659 MAHA TMA Supportive N Recovery 4 VI 99fsX11; Gly191Asp 20 Respiratory 117 87 58 1670 MAHA TMA FFP (first presentation), Eculizumab subsequent presentations N Recovery, 3 relapses 6 VII Gly31Ala; Gly31Ala 2 Gastroenteritis 140 72 112 4451 ND TMA FFP N Death N/A VIII Gly31Ala; Gly31Ala 3 Influenza 378 89 61 4419 MAHA TMA FFP N Death N/A IX Gly31Ala; Gly31Ala 5 Respiratory 265 67 74 3891 MAHA TMA FFP ESKD ESKD 7 X Gly31Ala; Gly31Ala 6 Respiratory 137 88 67 2298 MAHA TMA FFP N Recovery 7 XI Gly31Ala; Gly31Ala 6 Influenza A 101 89 86 1091 ND TMA Supportive N Recovery Not available XII Gly31Ala; Gly31Ala 3 Gastroenteritis 84 84 34 2332 MAHA TMA Supportive N Recovery Not available XIII Gly31Ala; Gly31Ala 2 Bordetella pertussis 132 78 80 1857 MAHA TMA Eculizumab ESKD ESKD No recovery XIV Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A Nephrotic Syndrome N/A N/A N/A N/A XV Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A Haematuria and proteinuria N/A N/A N/A N/A XVI Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A Haematuria and proteinuria N/A N/A N/A N/A XVII Asp132Ala; Val80Phe N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XVIII Asp132Ala; Val80Phe N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XIX Asp132Ala; Asp132Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XX Asp132Ala; Asp132Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXI Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXII Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXIII Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXIV Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXV Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXVI Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXVII Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXVIII Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXIX Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXX Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXXI Asp132Ala; Asp132Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXXII Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXXIII Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A XXXIV Gly31Ala; Gly31Ala N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A N/A Table 1 Demographic, genetic, and laboratory characteristics at presentation. TMA – Thrombotic microangiopathy, RSV - Respiratory syncytial virus, LDH - Lactate dehydrogenase, MAHA - Microangiopathic hemolytic anemia, FFP- Fresh frozen plasma, ESKD – End stage kidney disease ND - Not done Open table in a new tab PCH1b was present in all patients, characteristic symptoms included developmental delay, hypotonia, feeding difficulties, and hypo/areflexia (Supplementary Table S1). Eleven children with TMA died during follow-up, with a mean age at death of 10 months (range 2-43 months). Ten patients carried homozygous and three compound heterozygous EXOSC3 variants (Table 1). One novel in frame deletion (c.341_343del) was identified, the remaining variants have all been identified in individuals with PCH1b.13,14 Two missense variants, which are known to cause loss of RNA processing function in model organisms,15 p.Gly31Arg (allelic frequency (A.F.) 73%) and p.Asp132Ala (A.F. 15%) accounted for 88% of the EXOSC3 alleles in the TMA subgroup. This was not significantly different to the non-TMA cohort (A.F. 76% p=0.76, and 17% p=1.0, respectively). Outcome Following the initial diagnosis of TMA, 3/13 died within a week of presentation with evidence of ongoing TMA, 8/13 patients had evidence of renal function recovery, two patients (IX and XIII) required long-term renal replacement (Figure 1b). Treatment strategies included supportive measures (diuretics, fluid management), fresh frozen plasma (n=7) and eculizumab (n=5). Eculizumab was used at initial presentation in four cases (I, II, III and XIII) and following relapse in one (VI). Two patients received limited doses of eculizumab (I received one and III received two doses), which were discontinued in both cases due to the poor neurological prognosis from underlying PCH1b. Three children were treated with long-term eculizumab, one had no response (XIII) and two experienced relapsed despite treatment (II and VI) (Figure 1b). Exosc3KO mouse (Figure 2) Following Cre-recombination (Supplementary Figure S2), Exosc3KO developed rapid weight loss necessitating euthanize, at a median of 8 ±2 days (Figure 2a). Post-mortem haematological examination of Exosc3KO, compared to Exosc3fl (Figure 2c.i-v), revealed aplastic anaemia (mean haemoglobin 89g/l vs 126g/l, white cell count 2.50x106 vs. 7.18x106 cells/ml and platelet 6.12x108 vs. 1.36x109 cells/ml), with decreased total marrow cell count (4.6x106 vs. 2.5x107 cells) and reduced reticulocyte percentage (0.45% vs. 3.48%). Additionally, analysis of bone marrow isolates demonstrated cell cycle arrest at G0/G1 (Supplementary Figure S5) and increases in both early and late apoptosis (Supplementary Figure S6). Histological examination demonstrated the downstream effects of ribosomal dysfunction in affected tissues,16 with hypocellular bone marrow, thymus and large intestine (i.e. rapidly dividing cells). There was no evidence of renal disease in this period (Figure 2b.i & 2c.vi). Figure viewer Figure 2 (a) Mouse survival following recombination. Exosc3KO (n=12) mice demonstrated weight loss, diarrhoea and deterioration in their clinical score, compared to mice with no Cre expression (n=13). (b) H&E staining of selected organs in Exosc3KO 40x (left) and 400x (Right). (i) Kidney demonstrating normal morphology. (ii) Thymus, showing atrophy with loss of cortical and medullary architecture. (iii) Bone marrow showing decrease cell number. (iv) Large intestine, demonstrating proliferative colitis with eosinophilic material and sloughed cells in the lumen. Results indicating evidence of cell death in rapidly dividing cell types. (c) Haemoglobin, leucocyte, platelet, reticulocyte count, bone marrow cell count and blood urea nitrogen levels from mice at time of death. (i) Haemoglobin measured using CHEM8+ cartridges and iSTAT (Abbott). (ii)Reticulocyte percentage, platelet and leucocyte count determined by flow cytometry. Reticulocyte percentage calculated using Retic-Count (BD biosciences), (iii) platelets confirmed using anti-CD41 (BD biosciences), (iv) Leucocytes identified using anti-CD45 (BD biosciences), (v). Bone marrow cell count measured following extraction from both femurs and one humerus, cells were treated with red cell lysis buffer and washed, cells were resuspended in 1ml of PBS and counted using Anvajo cell counter, (vi) Blood urea nitrogen measured using CHEM8+ cartridges and iSTAT (Abbott). Together results indicate aplastic anaemia following Exosc3 depletion. Readings for individual mice displayed with bars indicating mean. Unpaired T test was used to compare between the two groups. The results quantify the reduced bone marrow cell count seen in H&E staining * p <0.05, ** p<0.01, *** p<0.005, **** p<0.0001 Discussion Previous case reports have identified TMA in patients with pathogenic variants RNA exosome components, EXOSC3 and EXOSC5.2,7,17 This is the first systematic analysis of a large cohort of patients with biallelic pathogenic variants in EXOSC3 to confirm this strong association with TMA. These findings indicate a previously unrecognized function of the RNA exosome in the kidney. Eculizumab has proven highly effective for the management of TMA driven by terminal complement dysregulation.2 However, there are a growing number of TMAs that are not caused by complement dysregulation (e.g. MMACHC, INF2, DGKE). This study demonstrates that eculizumab has no role in the management of EXOSC3-TMA. To investigate the potential mechanism of Exosc3-TMA using mice, a conditional whole-body Exosc3 knock-out was utilized. When Exosc3KO was induced in adult mice, they demonstrated evidence of widespread ribosomal dysfunction in rapidly dividing tissues. This has previously been demonstrated in both tissue specific (Brain and Erythroid progenitors) Exosc3KO mice18,19 and other model organisms.11,20 The RNA exosome is essential for trimming precursor ribosomal RNA during ribosome biogenesis. In the absence of a functioning exosome, ribosome biogenesis is disrupted, and these precursors accumulate.10 This triggers the nucleolar stress response, characterized by upregulation of cell-cycle regulators, cell-cycle arrest and apoptosis.21 Ribosomal inactivation is also central to the pathogenesis of STEC-HUS.22,23 Our study highlights a potential common disease process, a “vascular ribosomopathy”, in these two conditions; further investigation will be required to understand the overlapping pathogenesis and how this could be utilized to aid better understanding of STEC-HUS. Unlike the human phenotype, disruption of Exosc3 function via Exosc3KO did not induce TMA in mice; potentially explained by differences in the mouse model vs. human phenotype. For example, age of mice, genetic background (knock-out vs. hypomorphic allele) and requirement for an infectious trigger. In the human cohort, all patients presented under 2 years of age. In this study adult mice were used, this was to prevent any potential complication from a developmental phenotype, specifically neurodevelopmental and non-uniformity with respect to tamoxifen response.24 Complete disruption of Exosc3 in the Exosc3KO mice resulted in overwhelming cell-cycle arrest and apoptosis in rapidly dividing tissues (bowel and bone marrow). All reported cases of EXOSC3-mediated disease, including in our cohort, occur due to at least one missense variant that disrupts, but does not eliminate the exosome’s function. No biallelic null variants have been described15 and constitutive Exosc3 knock-out in mice is embryonic lethal,18 together underscoring the need for residual exosome function. To further investigate the TMA phenotype, a patient specific model will need to be developed. Additionally, a viral stressor may be required to uncover the kidney phenotype in a mouse model; in humans with EXOSC3-TMA an infection is required to trigger TMA. We propose that during basal conditions the RNA exosome can perform sufficient RNA processing to maintain the health of the endothelium. However, during the stress of infection this processing ability, and specifically ribosome biogenesis, is overwhelmed, resulting in an endothelial cell activation and the clinical phenotype of TMA. In summary, this study establishes that biallelic variants in EXOSC3 predispose to TMA. We demonstrate that terminal complement blockade has no role in the management of children with EXOSC3-TMA. Screening for TMA should be considered in children with PCH1b, particularly during and shortly after acute infection. Genetic sequencing of EXOSC3 should be undertaken in children with eculizumab-resistant TMA, especially in the setting of neurodevelopmental conditions. Conflict of Interest KJM has received research funding from Gemini Therapeutics, Idorsia Pharmaceuticals Ltd., and Catalyst Biosciences as well as consultancy income from Freeline Therapeutics,
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