Evidence map›Paper›PMID 42100066›Full record

ArticleMediterranean journal of rheumatology2026

KIM-1: A Non-Invasive Marker for Kidney Injury and Treatment Efficacy in FMF.

Oktay Bagdatoglu, Esra Fırat Oguz, Ahmet Kor, Sukran Erten, Mıne Sebnem Karakan

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Article in Mediterranean journal of rheumatology, 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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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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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

5 authors.

Oktay BagdatogluDepartment of Nephrology Clinic, Republic of Turkey Ministry of Health Ankara Bilkent City Hospital, Ankara, Türkiye.
Esra Fırat OguzDepartment of Biochemistry Clinic, Republic of Turkey Ministry of Health Ankara Bilkent City Hospital, Ankara, Türkiye.
Ahmet KorDepartment of Rheumatology Clinic, Republic of Turkey Ministry of Health Aksaray Training and Research Hospital, Aksaray, Türkiye.
Sukran ErtenDepartment of Rheumatology Clinic, Ankara Yıldırım Beyazıt University-Ankara Bilkent City Hospital, Ankara, Türkiye.
Mıne Sebnem KarakanDepartment of Nephrology Clinic, Republic of Turkey Ministry of Health Ankara Bilkent City Hospital, Ankara, Türkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Familial Mediterranean Fever (FMF) arises from mutations in the MEFV gene, which encodes the immune-regulatory protein pyrin. Early detection of FMF-associated kidney injury and identification of noninvasive biomarkers to monitor disease progression and treatment response are critical. This study aimed to measure serum Kidney Injury Molecule-1 (sKIM-1) levels in FMF patients, assess its potential as an early indicator of renal damage, and evaluate its utility in monitoring treatment efficacy. Methods: Fifty FMF patients and 36 healthy controls were enrolled. Serum KIM-1 levels were determined by ELISA. Clinical and laboratory data were extracted from patient records. The relationships between sKIM-1, urine protein/creatinine ratio (UPCR), and estimated glomerular filtration rate (eGFR) were analyzed. Subgroup analyses compared sKIM-1 levels in patients treated with anakinra or canakinumab. Results: Median sKIM-1 was significantly higher in FMF patients than controls [571.30 pg/mL (562.50-586.90) vs. 562.40 pg/mL (558.10-580.40), p=0.040]. No correlation was observed between sKIM-1 and UPCR (p=0.547) or eGFR (p=0.232) in the FMF group. Canakinumab-treated patients exhibited significantly lower sKIM-1 levels [561.10 pg/mL (556.10-567.00) vs. 575.4 pg/mL (564.00-591.20), p=0.036], whereas anakinra treatment showed no significant difference [561.20 (558.40-595.70), 572 (564.60-588), (p=0.430)]. Conclusion: Elevated sKIM-1 in FMF patients and its reduction with canakinumab support KIM-1 as a noninvasive biomarker of renal involvement in FMF. These findings suggest KIM-1 may serve as a tool for monitoring disease activity and treatment response.

Indexed as

canakinumabFamilial Mediterranean FeverGFRKidney Injury Molecule 1KIM-1

Identifiers

PMID42100066
PMCPMC13145288

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