ReviewNature reviews. Nephrology2015
Podocyte dysfunction in atypical haemolytic uraemic syndrome.
Review in Nature reviews. Nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 65 citations in OpenAlex.
- Terminal complement inhibition in atypical haemolytic uremic syndrome: a single-centre experience.Frontiers in pharmacology · 2025Article
- Breaking the cycle: immune complexes, complement activation, and novel immunotherapies in lupus nephritis.Frontiers in immunology · 2025Review
- Article
- Clinical and biochemical footprints of inherited metabolic diseases. XIV. Metabolic kidney diseases.Molecular genetics and metabolism · 2023Article
- Clinical features and outcomes of patients with diacylglycerol kinase epsilon nephropathy: a nationwide experience.Pediatric nephrology (Berlin, Germany) · 2023Article
- Clinical features and management of atypical hemolytic uremic syndrome patient withFrontiers in pediatrics · 2023Review
- Diacylglycerol kinase epsilon protects against renal ischemia/reperfusion injury in mice through Krüppel-like factor 15/klotho pathway.Renal failure · 2022Article
- A Life-Threating Postpartum Atypical Hemolytic-Uremic Syndrome with Multiorgan Involvement.Journal of clinical medicine · 2022Article
- Kidney thrombotic microangiopathy in lupus nephritis: Impact on treatment and prognosis.Lupus · 2022Article
- IgA nephropathy and atypical hemolytic uremic syndrome: a case series and a literature review.Journal of nephrology · 2022Review
- Thrombotic microangiopathy triggered by podocytopathy.Clinical nephrology. Case studies · 2021Article
- Immune-complex glomerulonephritis with a membranoproliferative pattern in Frasier syndrome: a case report and review of the literature.BMC nephrology · 2020Review
- Whole exome sequencing revealed a novel homozygous variant in the DGKE catalytic domain: a case report of familial hemolytic uremic syndrome.BMC medical genetics · 2020Article
- Podocytes Produce and Secrete Functional Complement C3 and Complement Factor H.Frontiers in immunology · 2020Article
- Case Report: Denys-Drash Syndrome WithFrontiers in pediatrics · 2020Article
- Differential contribution of C5aR and C5b-9 pathways to renal thrombic microangiopathy and macrovascular thrombosis in mice carrying an atypical hemolytic syndrome-related factor H mutation.Kidney international · 2019Article
- Atypical hemolytic uremic syndrome: a syndrome in need of clarity.Clinical kidney journal · 2019Article
- Advances in our understanding of the pathogenesis of hemolytic uremic syndromes.American journal of physiology. Renal physiology · 2018Review
- The Phenotypic Spectrum of Nephropathies Associated with Mutations in Diacylglycerol KinaseJournal of the American Society of Nephrology : JASN · 2017Article
- Complement C5-inhibiting therapy for the thrombotic microangiopathies: accumulating evidence, but not a panacea.Clinical kidney journal · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Genetic or autoimmune defects that lead to dysregulation of the alternative pathway of complement have been associated with the development of atypical haemolytic uraemic syndrome (aHUS), which is characterized by thrombocytopenia, haemolytic anaemia and acute kidney injury. The relationship between aHUS, podocyte dysfunction and the resultant proteinuria has not been adequately investigated. However, the report of mutations in diacylglycerol kinase ε (DGKE) as a cause of recessive infantile aHUS characterized by proteinuria, highlighted podocyte dysfunction as a potential complication of aHUS. DGKE deficiency was originally thought to trigger aHUS through pathogenetic mechanisms distinct from complement dysregulation; however, emerging findings suggest an interplay between DGKE and complement systems. Podocyte dysfunction with nephrotic-range proteinuria can also occur in forms of aHUS associated with genetic or autoimmune complement dysregulation without evidence of DGKE mutations. Furthermore, proteinuric glomerulonephritides can be complicated by aHUS, possibly as a consequence of podocyte dysfunction inducing endothelial injury and prothrombotic abnormalities.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.