Kidney Week

Abstract: SA-PO1104

Effects of Kidney Diseases on Platelet Activation

Session Information

• Pathology and Lab Medicine: Clinical
  October 27, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Pathology and Lab Medicine

• 1502 Pathology and Lab Medicine: Clinical

Authors

• Ikegaya, Naoki, Yaizu City Hospital, Yaizu, Japan

Naoki Ikegaya,

• Yoshida, Takuya, University of Shizuoka, Shizuoka, Japan

Takuya Yoshida,

• Kumagai, Hiromichi, University of Shizuoka, Shizuoka, Japan

Hiromichi Kumagai,

• Yamamoto, Tatsuo, Fujieda City Hospital, Fujieda , Japan

Tatsuo Yamamoto,

• Seki, George, Yaizu City Hospital, Yaizu, Japan

George Seki,

• Hishida, Akira, Yaizu City Hospital, Yaizu, Japan

Akira Hishida,

Background

Platelet activation can lead to intravascular thrombosis formation. Immature platelets comprise the youngest component of circulating platelet pool and actively participate in thrombosis formation. Although patients with kidney diseases are at increased risk of altered coagulation of both thrombotic and bleeding, little data on the presence of immature platelets in kidney diseases are available. We investigated the relationship between renal function and immature platelets count (IPC) and evaluated effects of endothelial dysfunction, inflammation and thrombopoietin on IPC in patients with kidney diseases.

Methods

First, we measured IPC in patients with 235 chronic kidney diseases, 32 patients with acute kidney injury (AKI), and 75 patients with hemodialysis (HD). Immature platelets were measured with an automated hematoanalyzer that uses fluorescent dyes containing polymethine and oxazine. Second, we analyzed serum interleukin-6, thrombopoietin, and thrombomodulin in HD patients and evaluated the correlation between IPC and them.

Results

In patients with CKD, IPC had a tendency to decrease with the deterioration of renal function, but was not significantly correlated with eGFR (G1+2: n=69, 0.71±0.33, G3: n=83, 0.66±0.35, G4+5: n=83, 0.62±0.38×10⁴ /μL). Patients with HD showed significantly lower IPC than patients with CKD (0.47±0.33×10⁴ /μL, p < 0.05). On the other hand, patients with AKI showed significantly higher IPC than other groups at the peak of serum creatinine (0.99±0.76×10⁴ /μL, p < 0.05). Among HD patients, patients with catheters showed significantly increased IPC compared to patients with fistulas (0.69 vs. 0.38×10⁴ /μL, p < 0.05). Second, IPC was not correlated with thrombopoietin (r=-0.159) and IL-6 (r=0.223), but significantly related with thrombomodulin (r=0.359, P< 0.01) in HD patients.

Conclusion

HD patients showed decreased platelet activation compared to non-HD patients, suggesting that uremia might decrease the activation of platelets. In AKI patients, there was a transient platelet activation in the course of AKI. Microvascular endothelial dysfunction might cause platelet activation and intravascular thrombus formation.