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Rigshospitalet - a part of Copenhagen University Hospital
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Apolipoprotein M in patients with chronic kidney disease

Research output: Contribution to journalJournal articleResearchpeer-review

  1. Aging suppresses sphingosine-1-phosphate chaperone ApoM in circulation resulting in maladaptive organ repair

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Elevated suPAR Is an Independent Risk Marker for Incident Kidney Disease in Acute Medical Patients

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Reduced apolipoprotein M and adverse outcomes across the spectrum of human heart failure

    Research output: Contribution to journalJournal articleResearchpeer-review

  4. Automatically generated smartphone data and subjective stress in healthy individuals - a pilot study

    Research output: Contribution to journalJournal articleResearchpeer-review

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BACKGROUND AND AIMS: Plasma apolipoprotein M (APOM) is bound to HDL-particles and has anti-atherogenic effects. The present study explored whether plasma APOM is reduced in patients with chronic kidney disease (CKD), and associated with cardiovascular disease (CVD). In addition, we tested the hypothesis that the excretion of APOM into the urine is increased in patients with kidney disease.

METHODS: Plasma samples were collected from a cohort of patients with CKD stages 1 to 5D (N = 409) and controls (N = 35). Urine was collected from 47 subjects. Plasma APOM was measured with sandwich ELISA and urine APOM with competitive ELISA.

RESULTS: Plasma APOM levels were reduced in patients with CKD stages 3-5D as compared to patients with CKD stages 1 + 2 and controls (p < 0.01). CKD patients with known CVD displayed even further reduction in plasma APOM levels than CKD patients without known CVD (p < 0.001). Fast-phase liquid chromatography showed that plasma APOM was primarily associated with HDL-cholesterol (HDL-C) across CKD stages. Accordingly, when plasma APOM values were corrected for HDL-C, a significant difference only persisted between patients with CKD stage 3 and stages 1 + 2 (p < 0.05), and the difference between CKD patients with and without known CVD disappeared. Urine APOM/creatinine ratio was not significantly increased in patients with kidney disease.

CONCLUSIONS: The results show that the difference in plasma APOM levels observed between patients with mild and advanced CKD may mainly be due to differences in plasma HDL-C. Whether APOM plays a role in human uremic atherogenesis warrants further experimental studies.

Original languageEnglish
JournalAtherosclerosis
Volume275
Pages (from-to)304-311
Number of pages8
ISSN0021-9150
DOIs
Publication statusPublished - Aug 2018

ID: 55401871