ArticleJournal of veterinary internal medicine
Apoptosis Inhibitor of Macrophages in Cats: A Potential Link Between an Exon 3 Variant Allele and Progression of Naturally Occurring Chronic Kidney Disease.
Article in Journal of veterinary internal medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled 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.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- 2026 iCatCare consensus guidelines on the diagnosis and management of chronic kidney disease in cats.Journal of feline medicine and surgery · 2026Guideline
- Apoptosis inhibitor of macrophage (AIM/CD5L) as a potential immunomodulator in feline injection-site sarcoma: a hypothesis on tumor-macrophage interactions.The veterinary quarterly · 2026Review
- Prevalence of theJournal of feline medicine and surgery · 2026Article
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
Abstract
backgroundThe protein apoptosis inhibitor of macrophages (AIM) is involved in kidney repair. An AIM (fAIM) genetic variant in cats resulting in a domain duplication might abrogate fAIM's protective effect on kidney function.
objectivesTo confirm that the domain duplication previously described in fAIM results from an exon duplication at the genomic level and to determine if cats with chronic kidney disease (CKD) harboring the variant fAIM allele are at higher risk for a decline in renal function relative to fAIM wild-type cats. ANIMALS: Medical records (n = 172) and genomic DNA samples (n = 100) from cats presented to Washington State University and having a diagnosis of CKD were analyzed.
methodsSequencing and PCR were used to determine fAIM genotype. Based on serum creatinine (SCr) concentrations, cats were phenotyped according to IRIS CKD staging. The phenotype-genotype association was tested using Fisher's exact test.
resultsThe 4-domain variant of fAIM was confirmed to be a result of exon 3 duplication and is present in 62% of the DNA samples from cats. Medical records of cats (n = 50) with CKD met the inclusion criteria. Cats homozygous for the exon 3 fAIM variant allele are more likely to have worse IRIS stage (p = 0.01) and more likely to have experienced renal function deterioration (increasing SCr concentration) than fAIM wild-type cats (p = 0.03). CONCLUSIONS AND CLINICAL IMPORTANCE: The fAIM homozygous variant genotype is associated with declining kidney function in cats with CKD, presumably from deficient fAIM-mediated renal tubular repair.
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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 Socratic graph.