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Elevated plasma kidney injury molecule-1 is independently associated with vascular calcification in non-dialysis chronic kidney disease patients of stage G3 to G5

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  • Published: 09 November 2026
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Elevated plasma kidney injury molecule-1 is independently associated with vascular calcification in non-dialysis chronic kidney disease patients of stage G3 to G5
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  • Wenjiao Zhu1,2 na1,
  • Zhiman Lai3 na1,
  • Xiaojie Ke1,2 na1,
  • Miaorong Xue1,2,
  • Yan Wang4,
  • Shaozhen Feng1,2,
  • Jianwen Yu1,2,
  • Jianbo Li1,2,
  • Xiao Yang1,2,
  • Fengxian Huang1,2,
  • Wei Chen1,2,
  • Yuanwen Xu1,2,
  • Shurong Li3 &
  • …
  • Qunying Guo  ORCID: orcid.org/0000-0002-0252-65701,2 

We’re sharing this article early to provide faster access to peer-reviewed, accepted research. It is citable and carries a permanent DOI. This version is subject to further edits and will be replaced automatically by the final Version of Record. All legal disclaimers apply.

Abstract

Background

Plasma kidney injury molecule-1 (KIM-1) is a promising biomarker for cardio-renal diseases, but its associations with vascular calcification (VC) and clinical outcomes in non-dialysis chronic kidney disease (CKD) stages G3 to G5 remain unclear. This study investigated the associations between plasma KIM-1, vascular calcification, and adverse clinical outcomes in this population.

Methods

In a prospective cohort of 221 non-dialysis CKD G3 to G5 patients followed for 1.89 ± 0.96 years, associations between plasma KIM-1 and multiple VC measures-including coronary artery calcification (CAC), thoracic aortic calcification (TAC), abdominal aortic calcification (AAC), carotid artery calcification, and aortic valve calcification (AVC)-were assessed using logistic regression models and reported as odds ratios (ORs) with 95% confidence intervals (CIs). Associations with clinical endpoints, including CKD progression, cardiovascular events, and all-cause mortality, were evaluated using Cox proportional hazards regression models and reported as hazard ratios (HRs) with 95% CIs.

Results

The 221 enrolled patients had a mean age of 51 ± 14 years; 63% were male and 32% had diabetes. Median plasma KIM-1 was 266.10 pg/mL, with significantly higher levels in patients with diabetic kidney disease, glomerular disease, and VC. Elevated KIM-1 was independently associated with severe CAC (OR 32.14, 95% CI 2.36-437.21, p = 0.008) and AAC (OR 2.56, 95% CI 1.01–6.48, p = 0.047) after multivariable adjustment with confounders including estimated glomerular filtration rate (eGFR). Higher KIM-1 was also linked to faster eGFR decline (5.07 vs. 3.12 mL/min/1.73 m²/year, p = 0.046) and in associated with the composite clinical endpoint (HR 1.73, 95%CI 1.05–2.86, p = 0.031).

Conclusion

Elevated plasma KIM-1 was associated with severe coronary artery calcification, abdominal aortic calcification, and adverse clinical outcomes in non-dialysis CKD G3 to G5 patients.

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Abbreviations

AAC:

Abdominal aortic calcification

ALB:

Albumin

ALP:

Alkaline phosphatase

AVC:

Aortic valve calcification

BMI:

Body mass index

BUN:

Blood urea nitrogen

CKD:

Chronic kidney disease

CAC:

Coronary artery calcification

CT:

Computed tomography

CI:

Confidence interval

cTnT:

Cardiac troponin T

CVD:

Cardiovascular disease

CRP:

C-reactive protein

DKD:

Diabetic kidney disease

DBP:

Diastolic blood pressure

ECG:

Electrocardiogram

ELISA:

Enzyme-linked immunosorbent assay

ESRD:

End-stage renal disease

eGFR:

estimated glomerular filtration rate

EF:

Ejection fraction

FSGS:

Focal segmental glomerulosclerosis

FIB:

Fibrinogen

Hb:

Hemoglobin

HUs:

Hounsfield units

HR:

Hazard ratio

HF:

Heart failure

HDL-c:

High density lipid -cholesterol

iPTH:

intact parathyroid hormone

KIM-1:

Kidney injury molecule-1

LDL-c:

Low density lipid -cholesterol

NT-proBNP:

N-terminal pro-B-type natriuretic peptide

PH:

Proportional hazard

ROC:

Receiver operating characteristic

SBP:

Systolic blood pressure

PLT:

Platelet

TCHO:

Total cholesterol

TG:

Triglyceride

TAC:

Thoracic aortic calcification

VC:

Vascular calcification

WBC:

White blood cell

Acknowledgements

We would like to express our sincere gratitude to Naya Huang, Xi Xia, Qiong Wen, Xionghui Chen, Xin Wang, Zhijian Li, and Haiping Mao for providing strong support for this research.

Funding

This work was supported by the Natural Science Foundation of Guangdong Province (Grant nos. 2022A1515010433, 2021A1515010427, and 2023A1515012625), Guangdong Provincial Key Laboratory of Nephrology, and NHC Key Laboratory of Clinical Nephrology (Sun Yat-Sen University).

Author information

Author notes
  1. Wenjiao Zhu, Zhiman Lai and Xiaojie Ke contributed equally to this work.

Authors and Affiliations

  1. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China

    Wenjiao Zhu, Xiaojie Ke, Miaorong Xue, Shaozhen Feng, Jianwen Yu, Jianbo Li, Xiao Yang, Fengxian Huang, Wei Chen, Yuanwen Xu & Qunying Guo

  2. NHC Key Laboratory of Clinical Nephrology, Guangdong Provincial Key Laboratory of Nephrology, Sun Yat-sen University, Guangzhou, China

    Wenjiao Zhu, Xiaojie Ke, Miaorong Xue, Shaozhen Feng, Jianwen Yu, Jianbo Li, Xiao Yang, Fengxian Huang, Wei Chen, Yuanwen Xu & Qunying Guo

  3. Department of Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China

    Zhiman Lai & Shurong Li

  4. Department of Ultrasound, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China

    Yan Wang

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Corresponding authors

Correspondence to Yuanwen Xu, Shurong Li or Qunying Guo.

Ethics declarations

Ethic approval and consent to participate

Study approval statement: This study protocol was reviewed and approved by the Ethics Committee of the First Affiliated Hospital of Sun Yat-sen University (approval number [2022] 656). The study was conducted in accordance with the principles of the Declaration of Helsinki. Consent to participate statement: Written informed consent was obtained from each enrolled patient.

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The authors declare no competing interests.

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12882_2026_5476_MOESM1_ESM.pdf (download PDF )

Supplementary Material 1 Supplementary Table. 1 Supplementary Table. 2 Supplementary Table. 3 Supplementary Fig. 1 Supplementary Fig. 2 Supplementary Fig. 3.

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Cite this article

Zhu, W., Lai, Z., Ke, X. et al. Elevated plasma kidney injury molecule-1 is independently associated with vascular calcification in non-dialysis chronic kidney disease patients of stage G3 to G5. BMC Nephrol (2026). https://doi.org/10.1186/s12882-026-05476-x

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  • Received: 02 March 2026

  • Accepted: 23 October 2026

  • Published: 09 November 2026

  • DOI: https://doi.org/10.1186/s12882-026-05476-x

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Keywords

  • Chronic kidney disease
  • Plasma kidney injury molecule-1
  • Coronary artery calcification
  • Abdominal aortic calcification
  • Adverse clinical outcomes

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  1. Qunying Guo View author profile

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