Evidence map›Paper›PMID 41788457›Full record

ArticleClinical medicine insights. Case reports2026

Immunoglobulin A Nephropathy With Associated Thrombotic Microangiopathy: Biopsy and Clinical Case Series.

Ryan Fekrat, Arif Nihat Demirci, Caroline Gee, Sohrab Kharabaf, Mina Tadros, Matthew Nguyen, Dao Le, Omid Vadpey, Jonathan Zuckerman, Ramy Hanna

Abstract readCase Reports
In one paragraph

Article in Clinical medicine insights. Case reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Ryan FekratDepartment of Medicine, Division of Nephrology, Hypertension, and Renal Transplant, University of California, Irvine, USA.ORCID https://orcid.org/0009-0007-3373-2848
Arif Nihat DemirciDepartment of Medicine, Division of Nephrology, Hypertension, and Renal Transplant, University of California, Irvine, USA.ORCID https://orcid.org/0009-0000-9423-0867
Caroline GeeDepartment of Medicine, Division of Nephrology, Hypertension, and Renal Transplant, University of California, Irvine, USA.
Sohrab KharabafDepartment of Medicine, Division of Nephrology, Hypertension, and Renal Transplant, University of California, Irvine, USA.ORCID https://orcid.org/0000-0002-1215-4424
Mina TadrosDepartment of Medicine, Division of Nephrology, Hypertension, and Renal Transplant, University of California, Irvine, USA.
Matthew NguyenDepartment of Medicine, Division of Nephrology, Hypertension, and Renal Transplant, University of California, Irvine, USA.
Dao LeDepartment of Medicine, University of California, Irvine, USA.
Omid VadpeyDepartment of Medicine, University of California, Irvine, USA.
Jonathan ZuckermanDavid Geffen School of Medicine, Department of Pathology and Lab Medicine, University of California, Los Angeles, USA.
Ramy HannaDepartment of Medicine, Division of Nephrology, Hypertension, and Renal Transplant, University of California, Irvine, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: IgA nephropathy (IgAN) with concurrent thrombotic microangiopathy (TMA) is an unusual combination of pathological findings that is associated with severe hypertension, proteinuria, and lower estimated glomerular filtration rate (eGFR). This series presents 7 patients with kidney biopsies demonstrating IgAN and concomitant TMA and presents a link by way of complement disorder. Case presentation: Seven patients all presented as IgAN with associated TMA coinciding with hypertension, proteinuria, and low eGFR. Six patients showed tubular atrophy or interstitial fibrosis and 5 of those 6 showed >50% of renal cortex containing tubular atrophy or interstitial fibrosis. Variations of low serum C3, high serum C4, elevated IgA or IgM proteins, and elevated CH50 were found in 6 of the 7 patients. Conclusions: Chronic changes seen like interstitial fibrosis and tubular atrophy appear to show a subacute or chronic nature of IgAN with TMA. The low serum C3, high C4, elevated CH50, suggests complement activation in endothelial and mesangial from IgG-IgA complexes known to occur in IgAN. This phenotype of IgAN with TMA may represent a more unique IgAN phenotype with a more severe clinical course and be indicative of underlying complement dysregulation.

Indexed as

case reportcase seriescomplement dysregulationimmunoglobulin A (IGA) nephropathythrombotic microangiopathy (TMA)

Identifiers

PMID41788457
PMCPMC12957606

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