ArticleBMC nephrology2018
A rare case of Alport syndrome, atypical hemolytic uremic syndrome and Pauci-immune crescentic glomerulonephritis.
Article in BMC nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
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
5 citing papers in PubMed, 10 citations in OpenAlex.
- A rare case of dual glomerular pathology: Alport syndrome and immune complex-mediated MPGN.BMC nephrology · 2025Article
- A case of Alport syndrome with pregnancy-related atypical hemolytic uremic syndrome and crescentic glomerulonephritis.Clinical nephrology. Case studies · 2023Article
- A rare complication of pauci-immune crescentic glomerulonephritis in a child: Answers.Pediatric nephrology (Berlin, Germany) · 2021Article
- FHR-5 Serum Levels andFrontiers in immunology · 2021Article
- Deposition of the Membrane Attack Complex in Healthy and Diseased Human Kidneys.Frontiers in immunology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRenal thrombotic microangiopathy (TMA) is occasionally seen in biopsies with pauci-immune necrotizing crescentic glomerulonephritis (PCGN). Recent study indicated that the complement activation is more prominent in the ANCA-negative glomerulonephritis. CASE PRESENTATION: We report a case of concurrent TMA and PCGN without ANCA positivity. Interestingly, our patient also had biopsy features supportive of Alport syndrome (AS). Genetic studies identified variants and polymorphisms in alternative complement pathway genes that confer substantial risk of developing atypical hemolytic uremic syndrome (aHUS).
conclusionsAbnormal activation in complement pathway may represent a common pathogenic link between these three distinct entities.
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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.