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The Role of Platelets in Chronic Kidney Disease and Renal Fibrosis

The Role of Platelets in Chronic Kidney Disease and Renal Fibrosis - PICKS (Platelets in Chronic Kidney Disease Study)

Status
Active, not recruiting
Phases
Unknown
Study type
Observational
Source
NL-OMON
Registry ID
NL-OMON57408
Enrollment
20
Registered
2025-02-17
Start date
2025-02-24
Completion date
Unknown
Last updated
2025-09-08

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Renal Fibrosis tubulointerstitial fibrosis

Interventions

None listed

Sponsors

Amsterdam UMC
Lead Sponsor

Eligibility

Age
18 Years to 64 Years

Inclusion criteria

Inclusion criteria: - Male and female - Age 18-55 years old - In healthy condition

Exclusion criteria

Exclusion criteria: - Refusal to become volunteer in this study. - Using antiplatelets drugs

Design outcomes

Primary

MeasureTime frame
We will conduct an in vitro study by isolating platelets and monocytes from volunteer blood to observe their effects on cells. Since participants are not direct subjects of our research, the data we will obtain are in vitro data related to changes in epithelial-to-mesenchymal transition (EMT) in epithelial cells, molecular changes in endothelial cells, monocyte adhesion, and migration after platelet stimulation. Therefore, there are no data related to primary outcomes that can be observed directly in participants. The primary outcomes of this study focus on investigating the influence and mechanisms of platelets in fibrosis and inflammation. Specifically, we aim to determine whether activated platelet stimulation induces fibrosis through epithelial-to-mesenchymal transition (EMT) and whether inhibiting platelet activation can mitigate fibrosis and EMT. Additionally, we intend to explore the molecular pathways potentially involved in these processes. Another key focus is the impact of activated platelet stimulation on endothelial integrity and its effects on monocyte/macrophage adhesion and transendothelial migration. We will also examine the mechanisms of platelet-macrophage interactions that contribute to inflammation, such as extracellular trap formation.

Countries

Netherlands

Outcome results

None listed

Source: NL-OMON (via WHO ICTRP)