ReviewJournal of clinical medicine research2025
Acute Kidney Injury in Autoimmune-Mediated Rheumatic Diseases.
Review in Journal of clinical medicine research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- [Management of emergencies in rheumatology].Zeitschrift fur Rheumatologie · 2026Review
- [Management of emergencies in rheumatology].Medizinische Klinik, Intensivmedizin und Notfallmedizin · 2026Review
- Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity.bioRxiv : the preprint server for biology · 2025Article
- Prevalence and Pathogenetic Mechanisms of Chronic Kidney Disease in Autoimmune-Mediated Systemic Diseases.Journal of clinical medicine research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is increasingly affecting hospitalized patients worldwide. Patients with inflammatory rheumatic diseases, although primarily impacted by functional impairment and sometimes structural damage to joints, bones, and muscle tissue, may also develop AKI during the course of their disease. This narrative review aimed to summarize potential causes of AKI and the associated disease patterns. The following databases were searched for references: PubMed, Web of Science, Cochrane Library, and Scopus. The search period covered from 1958 to 2024. Certain inflammatory rheumatic diseases increase the risk of AKI due to specific types of kidney disease. However, the most common conditions, such as rheumatoid arthritis and spondylarthritis, rarely cause AKI directly. Among the medications used for pain and sometimes disease activity control, nonsteroidal anti-inflammatory drugs (NSAIDs) can potentially induce AKI, even progressing to acute tubular necrosis. There is evidence that certain rheumatic diseases are associated with increased risk of AKI, independently of directly affecting kidney function or structure. However, the data on this topic are quite limited. AKI is a potentially significant issue for patients with inflammatory rheumatic diseases. Additional data on the increased risk of AKI, independent of direct kidney involvement, are needed.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.